Volume 181 Issue 9

Hypothermia is now standard care for some types of cardiac arrest Out-of-hospital cardiac arrest is a leading cause of unexpected death in the developed world, occurring in about 1 in 1500 adults each year.1 Successful recovery from out-of-hospital cardiac arrest depends on the rapid activation of the “chain of survival”: an immediate call to the ambulance service, bystander delivery of external cardiac massage and expired-air breathing, defibrillation and the provision of advanced life support by paramedics.2 Unfortunately, survival with good neurological outcome at hospital discharge is rare after out-of-hospital cardiac arrest. Studies in Perth and Melbourne show that less than 5% of these patients survive to hospital discharge.3,4 As the average response time of ambulances in most Australian cities is between 7 and 12 minutes, considerable neurological injury occurs during this prolonged period of cardiac arrest, even with bystander cardiopulmonary resuscitation. While paramedics may restore spontaneous circulation and transport some patients alive to an emergency department, most remain comatose because of the severe anoxic brain injury.4 To improve outcome, considerable emphasis has been placed on shortening the time between cardiac arrest and defibrillation. As decreasing ambulance response times towards 5 minutes would be prohibitively expensive, alternative approaches to earlier defibrillation have been proposed. These include fire-fighters co-responding with ambulance services to patients with suspected cardiac arrest,5 or installation of automatic defibrillators in public places.6 On the other hand, recent data from Canada have cast doubt on the effectiveness of paramedic advanced life-support programs, which did not improve survival rates when introduced.7 What therapies are available after arrival at the hospital? In most cases, no immediate cardiology intervention is required, and treatment has therefore been largely supportive until the neurological outcome could be determined. Common intensive care practice has been to defer neurological assessment for at least 3 days, to allow more accurate clinical assessment.8 Recently, an “old” therapy for anoxic brain injury — therapeutic hypothermia — has been re-introduced into clinical practice. In this issue of the Journal, Williamson and colleagues (page 500) describe the use of this therapy in a patient who was comatose after near-drowning.9 The use of mild therapeutic hypothermia after cardiac arrest was first described in the 1950s, but later abandoned without being formally tested in clinical trials.10 Interest in hypothermia was revived in the early 1990s when animal studies and preliminary clinical studies suggested benefit. Subsequently, two prospective, randomised, controlled clinical trials have been conducted.11,12 In a recent Australian trial, patients who remained comatose after resuscitation from out-of-hospital cardiac arrest were treated with either 12 hours of therapeutic hypothermia (33°C) or standard care.11 At hospital discharge, 49% of those treated with hypothermia were discharged home or to rehabilitation, compared with 24% of those treated with standard care. In a European study, 55% of patients treated with hypothermia (33°C for 24 hours) had a favourable outcome at 6 months, compared with 39% of those treated with standard care.12 Subsequently, the International Liaison Committee on Resuscitation (which includes the Australian Resuscitation Council) endorsed the use of therapeutic hypothermia for patients with anoxic brain injury after out-of-hospital cardiac arrest, particularly when the initial cardiac rhythm is ventricular fibrillation (Box).13 Therefore, this treatment should now be regarded as a standard of care for this condition. However, a number of issues require further consideration if therapeutic hypothermia is to be applied more widely. Firstly, uncertainty remains about the effectiveness of this therapy in patients with out-of-hospital cardiac arrest due to causes other than ventricular fibrillation. Patients with asystolic out-of-hospital cardiac arrest have a dismal prognosis,14 as do those with coma after near-drowning, hanging, or other causes of asphyxia. Clinical data on the effects of therapeutic hypothermia in these groups are lacking. The role that therapeutic hypothermia played in the recovery of the patient reported by Williamson and colleagues is uncertain. Secondly, a protocol needs to be established in the emergency department for the rapid induction of hypothermia in patients who are unconscious after out-of-hospital cardiac arrest. In most hospitals, this will require consensus to be reached between emergency physicians, intensive care physicians and cardiologists on the indications for the provision of this treatment. Finally, there are technical issues to be considered in the rapid induction of hypothermia. In previous studies, hypothermia was induced through surface cooling with ice packs and/or refrigerated air blankets.11,12 This approach is slow and logistically difficult in busy emergency departments. Other technologies for the rapid induction of hypothermia are therefore under investigation.10 Currently, we are exploring the use of a rapid intravenous infusion of large-volume (30 mL/kg), ice-cold crystalloid fluid to induce hypothermia. Preliminary data suggest that this is relatively simple, effective, inexpensive and not associated with pulmonary complications.15 As there is often a delay between resuscitation and emergency department initiation of hypothermia, cooling in the ambulance would be ideal. In a study supported by the National Heart Foundation, paramedics in Melbourne are now infusing large-volume (2000 mL), ice-cold crystalloid fluid, together with a muscle relaxant, immediately after out-of-hospital cardiac arrest to induce hypothermia as soon as possible after resuscitation. If this is confirmed as feasible, further studies are planned which will examine the use of therapeutic hypothermia after asystolic and asphyxial cardiac arrest. Recommendations on therapeutic hypothermia from the International Liaison Committee on Resuscitation In October 2002, the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation recommended: Unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32°C–34°C for 12–24 hours when the initial rhythm was ventricular fibrillation. Such cooling may also be beneficial for other rhythms or in-hospital cardiac arrest. Preliminary data from clinical trials of perinatal asphyxia indicate that induced hypothermia is feasible and safe, but data on long-term neurological morbidity are not yet available. Until additional paediatric data become available, clinicians should tailor therapy for individual patients based on their assessment of the risks and benefits of hypothermia.

Stephen A Bernard MD, FACEM, FJFICM

The justice system could go further in supporting the needs of those it detains after they are returned to the community Nearly 20 years ago, public attention was drawn to the previously hidden tragedy of deaths in prison and police custody. Initially, attention was focused on deaths of Indigenous people. However, it quickly became apparent that the death rate for all people held in custody was much higher than that for the general population. The result was a detailed investigation into the causes of the problem, in the form of the Royal Commission into Aboriginal Deaths in Custody.1 The Royal Commission made over 300 recommendations on penal policy, cell design, custody management regimens, treatment programs, services to Indigenous offenders and a host of other topics. In addition, the Deaths in Custody Monitoring Program was established at the Australian Institute of Criminology (AIC) to scrutinise and report on deaths in prison or police custody.2 In parallel with the acknowledged problem of deaths in custody, there is an equally significant tragedy in the form of high death rates among released prisoners3-5 and offenders in the community.6,7 In the decade after the Royal Commission (1990 to 1999), the AIC monitoring program recorded 628 deaths in police or prison custody. Over the same period, in Victoria alone, 820 men and women who had been released from prison died unnatural deaths.4 The study by Coffey and colleagues in this issue of the Journal (page 473) shows that the problem is not confined to adult offenders but affects juveniles as well.8 The high rate of unnatural deaths among offenders living in the community is a major public health issue, but what can we do to reduce these rates? One of the groups at greatest risk is injecting drug users — over half of the unnatural deaths examined in the earlier Victorian study were heroin related,4 and drug-related offences were an indicator of high mortality risk in the study by Coffey et al.8 Drug treatment and maintenance (methadone) programs lower the risk of death by overdose.9 However, many of those at greatest risk are profoundly alienated from society, and we need to find ways to engage them. For example, heroin-dependent Indo-Chinese offenders frequently face rejection by their families and community, and are isolated from the mainstream community as well. Female offenders often come from backgrounds of extensive sexual and physical abuse, their heroin dependency is often supported by prostitution,5 and any interventions need to take account of their responsibilities as parents.10 Treatment and maintenance programs need to be delivered in ways that meet the material, social and cultural needs of those at risk. Overdose risk can be dramatically lowered by behaviour changes, like not using drugs by yourself, being aware of variations in the purity of heroin, and not taking heroin in conjunction with alcohol or benzodiazepines. Again, the problem is partly that those at greatest risk are also the most difficult to communicate with, and tend to be unrealistic in judging risks to themselves. Peer-based education and information dissemination programs have shown they can transmit the key messages about risk reduction to this group (eg, how to avoid overdose and recognise its signs),9 but, again, a range of approaches tailored to the needs of specific groups at risk is required. Such approaches could include maximising the effectiveness of needle and syringe program workers by having them provide standardised, evidence-based messages and materials on safe injecting, overdose prevention and support options.9 The importance of heroin as a cause of unnatural death should not obscure the other dangers that offenders face. Individuals who have the combination of mental disorder and drug and alcohol misuse experience much higher risks of both overdose and suicide and can find it difficult to obtain the kind of treatment and support services that might alleviate their problems. Older offenders are at increased risk of a variety of general health problems, such as diabetes, cancer and liver disease, and there need to be programs that link at-risk offenders with healthcare and support services.11 People who are released from custody are at greatly increased risk, in part because their tolerance for heroin is reduced, and also because return to the community can be a time of great emotional stress. Prisoner release support programs like the Victorian Bridging the Gap program have shown that the period before release can be an important “window of opportunity” when offenders are motivated to plan for their release.12 A key feature of this program is intensive, outreach-based support, with the support agency helping the releasee to identify his or her specific needs and brokering access to material support, healthcare and social services. Releasees who participated in Bridging the Gap had improved outcomes as measured by accommodation stability and engagement in drug-treatment programs, and these in turn translated into lower rates of reoffending.12 Finally, we need to attend to an important lesson from the Royal Commission. Despite real improvements in custodial management, the number of deaths of Indigenous people in custody has continued to increase because there are now more Indigenous people in custody.2 The high rate of unnatural deaths among offenders is a public health problem that requires changes in the way that healthcare services are delivered to this vulnerable population. However, we also need to recognise that the justice system has a key role to play in ensuring that its goals of punishing offenders and preventing crime are properly balanced by a consideration of the health and support needs of the people who are the subjects of its interventions.

Stuart Ross

Despite well publicised claims of the therapeutic value of dietary supplements and other new treatments, the evidence for their effectiveness is modest The distinction between conventional and alternative medicine is often based on the presence or absence of scientific evidence. However, this evidence is expensive to gather, and often difficult to interpret and reduce to practical advice. Age-related macular degeneration (ARMD), the dominant and rapidly increasing cause of permanent visual loss in Australia, is an important case in point. Its prevalence rises from 0.7% in the 65–74-years age group to 5.4% at 75–84 years and 18.5% in people over 85.1 Definitive treatment does not yet exist. While we have some knowledge of risk factors, this knowledge is imperfect and has recently been muddied by well publicised claims (discussed below) that, although evidence-based, are preliminary and need to be interpreted with caution. The early signs of ARMD include hypo- or hyperpigmentation of the retina and large yellow drusen (> 63 μm) or soft drusen with indistinct margins.2 A few small hard drusen can be found in almost everyone over 50 years of age, and, in contrast to large or soft drusen, do not appear to progress with age.1 Loss of vision from ARMD occurs either as a result of choroidal neovascularisation with exudation and haemorrhage (the “wet” form) or by slow atrophy of the retinal-pigment epithelium and overlying receptors (the “dry” form). Wet ARMD is twice as common as the dry type and causes rapid vision loss. About 10% of patients with wet ARMD who present early with distorted vision and an eccentric neovascular lesion can be treated successfully with laser photocoagulation.3 However, the recurrence rate is over 60%, and further vision is then usually lost. Another small proportion of patients can be treated with photodynamic therapy (involving low-intensity red laser treatment after intravenous verteporfin infusion), but the functional benefit is usually modest.4 There is no treatment yet for the dry form of ARMD. Elderly people fear blindness and the loss of independence greatly, and the prevalence of ARMD is rising dramatically. It is no surprise that recent studies of possible risk factors have attracted a lot of public interest. People with an ARMD-affected first-degree relative have a 50% lifetime risk of experiencing advanced ARMD and vision loss, and tend to develop it earlier.5 Smoking is associated with a fourfold increase in the risk of ARMD and visual loss and, again, tends to promote earlier occurrence.6 Weaker associations have been found with obesity, hypertension, macro-vascular disease, raised cholesterol and fibrinogen levels, cumulative light exposure and cataract surgery. Dietary associations have also been found both with the signs of ARMD and with progression to vision loss.7-9 In a well conducted, prospective study, dietary fat intake was systematically analysed after correcting for other risk factors.9 Vegetable fat intake had the strongest relationship with ARMD progression, with a relative risk of 3.82 for the highest fat-intake quartile compared with the lowest quartile. Higher intakes of total fat and of saturated, monounsaturated, polyunsaturated and transunsaturated fats all raised the relative risk of ARMD progression about twofold. Weekly fish intake and eating nuts two to three times a week were mildly protective. The implication is that a large shift away from vegetable oils, margarine and fat-containing processed foods might reduce this epidemic of blindness in the elderly. Some of these measures conflict with conventional advice on controlling cardiovascular conditions and need further research.10 Definitive evidence for the effectiveness of certain interventions might be obtained by randomly assigning those in the top quartile of risk to receive either a diet with low vegetable fat, fish, nuts and fruit, or a normal diet. There is also evidence from a randomised controlled trial that high-dose dietary supplements of the antioxidants vitamin C, vitamin E, beta-carotene and zinc can reduce the risk of progression from large or soft drusen to advanced ARMD and visual loss by about 20% compared with controls over 6 years.11 However, high-dose zinc can cause gastric irritation or anaemia, and beta-carotene may possibly be associated with an increased risk of lung cancer among smokers. Uncontrolled studies suggest the antioxidants selenium, lutein and zeaxanthin, which localise in the normal macula, may also help. There are as yet no studies to show whether dietary supplements are protective in patients with only small drusen or in the 20% of patients who are at genetic risk. It is not yet known whether major dietary adjustment and/or introduction of dietary supplements for large numbers of elderly people will be justified in terms of preventing blindness. On present evidence, we should identify people at increased risk of ARMD (ie, those with a family history, large or soft drusen, or vision loss in one eye from ARMD), encourage them to stop smoking, and promote a diet that includes vegetables, fish and nuts and reduces fatty foods laced with vegetable oils. Antioxidant supplements should be recommended if a fresh diet is impractical and if retinal signs of progression are present. For people of advanced age with a lower risk of ARMD, we might compliment them on reaching seniority and note that, in the dietary supplement study mentioned above,11 only 1.3% of patients with small drusen experienced ARMD progression over a 6-year period. Retinal images showing age-related macular degeneration (ARMD) A. “Dry” ARMD. Large soft macular drusen, signifying a high risk of progressive visual loss. B. “Wet” ARMD. Arrowed area delineates advanced wet macular degeneration with subretinal exudation and neovascular scar tissue. These changes result in blindness.

Ian J Constable FRANZCO, FRACS, FRCS

Objective: To examine predictors of death in young offenders who have received a custodial sentence using data routinely collected by juvenile justice services.Design: A retrospective cohort of 2849 (2625 male) 11–20-year-olds receiving their first custodial sentence between 1 January 1988 and 31 December 1999 was identified.Main outcome measures: Deaths, date and primary cause of death ascertained from study commencement to 1 March 2003 by data-matching with the National Death Index; measures comprising year of and age at admission, sex, offence profile, any drug offence, multiple admissions and ethnic and Indigenous status, obtained from departmental records.Results: The overall mortality rate was 7.2 deaths per 1000 person-years of observation. Younger admission age (hazard ratio [HR], 1.4; 95% CI, 1.0–1.9), repeat admissions (HR, 1.8; 95% CI, 1.1–2.9) and drug offences (HR, 1.5; 95% CI, 1.0–2.1) predicted early death. The role of ethnicity/Aboriginality could only be assessed in cohort entrants from 1996 to 1999. The Asian subcohort showed higher risk of death from drug-related causes (HR, 2.5; 95% CI, 1.1–5.5), more drug offences (relative risk ratio [RRR], 13; 95% CI, 8.5–20.0) and older admission age (oldest group v youngest: RRR, 9.3; 95% CI, 1.3–68.0) than non-Indigenous Australians. Although higher mortality was not identified in Indigenous Australians, this group was more likely to be admitted younger (oldest v youngest: RRR, 0.31; 95% CI, 0.15–0.63) and experience repeat admissions (RRR, 1.6; 95% CI, 1.0–2.4).Conclusions: Young offenders have a much higher death rate than other young Victorians. Early detention, multiple detentions and drug-related offences are indicators of high mortality risk. For these offenders, targeted healthcare while in custody and further mental healthcare and social support after release appear essential if we are to reduce the mortality rate in this group.

Carolyn Coffey BSc, GradDipEpi · Andrew W Lovett FRACP · Eileen Cini BSc(Hons) · George C Patton MD, FRANZCP · Rory Wolfe PhD · Paul Moran MD, MRCPsych

Objective: To determine trends in use of Australian acute hospital inpatient services by older patients.Design and data sources: Secondary analysis of hospital data from the Australian Institute of Health and Welfare in the period 1993–94 to 2001–02, with population data for this period from the Australian Bureau of Statistics.Outcome measures: Population-based rates of hospital separations and bed utilisation.Results: The Australian aged population (65 years and older) increased by 18% compared with total population growth of 10%, yet the proportion of hospital beds occupied by older patients remained stable at 47%. The most substantial changes were observed in the population aged 75 years and older, with separations increasing by 89%, length of stay reducing by 35% and bed utilisation increasing by 23%. However, rates of bed utilisation (in relation to population) declined among older groups (10% decline in per capita use in population 75 years and older), but increased in the younger population (1% increase in per capita use in people younger than 65 years).Conclusion: Important trends in use of inpatient services were identified in this study. These trends are contrary to common perception. Ageing of the Australian population was not associated with an increase in the proportion of hospital beds used by older patients.

Len C Gray PhD, FRACP · Margaret A Yeo MPH, BSc(Hons) · Stephen J Duckett PhD, FCHSE

Objective: To describe the impact of a hepatitis A vaccination program for Indigenous children in north Queensland.Design: Enhanced surveillance of all notified cases of hepatitis A in north Queensland from 1996 to 2003.Setting: North Queensland; population, 596 500 people, including about 6900 Indigenous children aged under five years.Interventions: Hepatitis A vaccine was provided to Indigenous children in north Queensland from February 1999; two doses were recommended (at 18 months and 2 years of age), as was catch-up vaccination up to the sixth birthday.Results: In the 4 years 1996–1999, 787 cases of hepatitis A were notified in north Queensland, 237 (30%) of which were in Indigenous people. The average annual notification rates in Indigenous and non-Indigenous people during this period were 110 and 25 cases per 100 000 persons, respectively. In the first 4 years after introduction of the vaccination program (2000–2003), 66 cases of hepatitis A were notified. Only nine of the 66 (14%) were in Indigenous people. The average annual notification rates in Indigenous and non-Indigenous people in 2000–2003 were 4 and 2.5 cases per 100 000 persons, respectively.Conclusion: Hepatitis A seems to have been eradicated from Indigenous communities in north Queensland very soon after the vaccination program began. The rapid decline in notifications in non-Indigenous as well as Indigenous people suggests the program quickly interrupted chains of transmission from Indigenous children to the broader community. To our knowledge this is the first evidence that a hepatitis A vaccination program targeting a high-risk population within a community can reduce disease in the broader community. Hepatitis A vaccine should be provided to other high-risk Indigenous children elsewhere in Australia.

Jeffrey N Hanna MPH, FAFPHM · Susan L Hills MTH, FAFPHM · Jan L Humphreys

Objective: To determine the postnatal vitamin D status and bone health of women identified as vitamin D-deficient in pregnancy, and of their infants.Design and participants: Retrospective audit conducted between 27 August and 5 November 2003. The study included women delivering between August and October 2002 at the Royal Women’s Hospital, Melbourne, who had had a 25-hydroxyvitamin D (25-[OH]D) level < 30 nmol/L in pregnancy, and their infants at age 4–10 months.Setting: The outpatient clinic at the Royal Children’s Hospital, Melbourne.Main outcome measures: Maternal and infant serum levels of vitamin D, total alkaline phosphatase (tALP), parathyroid hormone (PTH), calcium and phosphorus; x-ray results in children with clinical or laboratory findings suggestive of rickets.Results: Of 69 mother–infant pairs invited to participate, 47 (68%) attended. All 47 women had 25-(OH)D levels < 50 nmol/L, and 39 (83%) had levels < 30 nmol/L. Vitamin D supplements had been prescribed in pregnancy for 35 women (74%), and 19/35 reported having taken them as prescribed. None had continued to take supplements postnatally, but one had recently started taking them again. Among 45 infants from whom blood samples were successfully obtained, 18 (40%) had 25-(OH)D levels < 50 nmol/L, and 14 (31%) had levels < 30 nmol/L. Twelve of 16 breastfed infants had 25-(OH)D levels < 30 nmol/L, compared with 2/29 fed formula milk (P = 0.001).Conclusions: Most mothers who had been vitamin D-deficient in pregnancy were also deficient postnatally, indicating that treatment offered, counselling and/or treatment compliance were inadequate. Their infants, especially if breastfed, were at high risk of vitamin D deficiency and increased bone formation. Breastfed infants of mothers at high risk of vitamin D deficiency should receive vitamin D supplements.

Katherine Thomson MB BS · Margaret R Zacharin MB BS, FRACP · Ruth Morley BA, MB BChir, FRCPCH · Sonia R Grover MB BS, FRACOG

Recent data from Australia, the United States and Europe show increased self-reported energy intake associated with obesity, in contrast to earlier suggestions that the obesity epidemic has occurred despite minimal or no increase in per capita energy intake from food. The effect of increased energy intake is compounded by sedentary lifestyles. Both physical activity and nutrition must be addressed to reduce the prevalence of obesity and improve the health of Australians. During the past decade, several authors from the United States and the United Kingdom have suggested that the obesity epidemic has occurred despite minimal or no increase in per capita energy intake and/or energy from the food supply.1,2 This has been described as the “American paradox”,2 and cited as evidence that the obesity epidemic is due to decreased physical activity and not to changes in eating patterns.3 There are dangers inherent in this viewpoint. According to the International Obesity Taskforce (IOTF), the food industry seeks to focus on inactivity and promote sports to divert attention from the role of foods and drinks.4,5 The IOTF asserts that the causes of the obesity epidemic are twofold: an abundance of energy-dense foods and drinks, leading to a pervasive “passive over-consumption” of energy; and an environment that limits opportunities for physical activity, leading to an almost universal sedentary state.4 Energy intakeTrends in energy consumption are difficult to establish because of a variety of measurement issues. People under-report their energy intake, and higher BMI is associated with a greater degree of under-reporting.6 This introduces a systematic bias, resulting in the paradoxical observation that obese individuals appear to eat less than lean people. Techniques have been developed to reduce this bias by excluding the most blatant under-reporters. The Australian Food and Nutrition Monitoring Unit undertook a bridging study to compare the food and nutrient intake data from the 1983 and 1995 Australian national nutrition surveys and the 1985 Australian Council for Health, Physical Education and Recreation (ACHPER) study.7 For these studies, energy intake was estimated from 24-hour intake and food frequency data, collected by dietitians at in-home interviews. After adjusting for differences in the food composition databases and demographic changes in the Australian population, the study found that mean energy consumption of Australian adults living in capital cities increased significantly by around 3%–4% (about 350 kJ/day) between 1983 and 1995.7 Between 1985 and 1995, mean energy intake increased greatly and significantly by 11% for girls and 15% for boys aged 10–15 years. The major source of increased energy intake was carbohydrate. Absolute fat intake did not increase among children, and declined slightly among adults.7 Fat as a percentage of energy decreased because of the increase in energy intake. An energy imbalance of 3%–4% in adults (about 350 kJ/day, equivalent to a slice of bread, or 30 minutes of sitting instead of brisk walking) would produce weight gain of about 1 kg per year until equilibrium is again reached, when the higher energy expenditure at a higher body mass equals energy intake. The Australian intake data are supported by recent data from the US. A significant increase in total energy intake between 1971 and 2000, particularly from carbohydrate, has been reported in the US, based on intake data from the National Health and Nutrition Examination Survey (NHANES).8 Data on food supply in the US and Europe also indicate that energy supply has increased.9,10 In Europe, data from the MONICA study indicate that per capita energy supply correlates with prevalence of obesity.10 In that study, trends in total energy supply per capita explained 41% of the between-population trends in BMI. Energy supply combined with prevalence of ex-smokers (who are more likely to be overweight) explained 69% of the between-country differences in change of prevalence of overweight. An economic analysis of factors underlying the trends in obesity in the US found that the per capita increase in the numbers of restaurants accounted for 61% of the increase in BMI and 65% of the increase in the percentage of the population who are obese.11 Energy expenditureAlthough it is not possible to measure energy expenditure at a population level, it has been suggested that population Total Daily Energy Expenditure (see Box) has declined.1,2,12 However, all of these reviews rely on the argument, based on the UK data,1 that energy intake has not increased and therefore energy expenditure must have decreased. Objective analysis of Total Daily Energy Expenditure and Activity Energy Expenditure in free-living individuals is possible using doubly-labelled water techniques. A large review of objective studies of energy expenditure found that Resting Energy Expenditure, Activity Energy Expenditure and Total Daily Energy Expenditure are all substantially and progressively higher with obesity. For BMI categories ranging from < 25 to > 35 kg/m2, Total Daily Energy Expenditure ranges from 9.5 to 13.5 MJ/day for women and from 12.9 to 17.5 MJ/day for men.13 This contradicts the popular view that obesity is due to “low metabolism” and is maintained despite a low level of food intake. After adjustment for body size, energy expenditure of obese individuals is similar to that of lean individuals. Population body mass has increased, so population per capita Total Daily Energy Expenditure must have increased. Clearly, energy intake must also have increased to maintain energy balance. The recent studies quoted above, based on both food supply and self-reported intake data in the US, Australia and Europe, confirm this. Physical activityAt an individual level, physical activity is clearly important for weight control. Physical activity is an effective adjunct to dietary management for weight loss and maintenance.14 However, at a population level, measurement of physical activity relies on self-report and suffers from methodological difficulties similar to those for determining nutrition. Prospective observational population studies of the effect on body weight of physical activity measured at baseline are few and the results are inconsistent.15-17 Physical inactivity appears to be both a cause and a consequence of obesity. Many studies have shown that television viewing is associated with obesity, although this is independent of physical activity level.18 However, it is very clear that a sedentary lifestyle is almost universal in developed societies, and that this is related to physical, technological and economic environmental conditions.19 In Australia, population surveys suggest that the proportion of the population reporting undertaking 30 minutes of moderate physical activity daily has declined from 62% in 1997 to 57% in 2000.20 However, there is now consensus that 45–60 minutes of moderate physical activity may be required for some people to prevent weight gain in the current environment of abundant energy-dense food.15,17 Relative contributions to obesityTwo longitudinal studies using objective measures of energy expenditure have attempted to determine the relative contribution of energy intake and expenditure to subsequent risk of obesity. In the first study, involving infants, measured energy intake determined weight gain between 3 months and 12 months, but measured energy expenditure did not.21 The other study showed that, among Pima Indian adults, baseline total energy intake (calculated from energy expenditure measured by using doubly-labelled water) is a predictor of weight gain over 4 months or more.22 However, baseline Activity Energy Expenditure and physical activity were not related to weight gain. As in many other studies, the physical activity level was lower in obese subjects, and the authors concluded that this was secondary to obesity. ConclusionAn increase in energy supply and consumption has made a major contribution to the obesity epidemic. It is probable that population physical activity level has also decreased, as both a cause and a consequence of the obesity epidemic. There are many other benefits of physical activity and healthy eating besides weight management, and both physical activity and nutrition must be addressed together to improve the health of all Australians. This requires multistrategy interventions across a range of sectors, including food producers, manufacturers, wholesalers, retailers, restaurateurs, caterers, transporters, advertisers, urban planners, employers, sporting associations, the fitness industry, community groups, the media, and policymakers at all levels of government, in addition to interventions in schools. A national, coordinated, systematic approach to monitoring overweight and obesity, dietary intake and physical activity is essential to both inform and evaluate interventions. Key evidence-based interventions to address childhood obesity through improved nutrition and increased physical activity are outlined in the National Obesity Taskforce report Healthy weight 2008 — Australia’s future.23 Energy expenditure terminology Total Daily Energy Expenditure is the amount of energy expended by an individual in one day. This is made up of Resting Energy Expenditure and Activity Energy Expenditure. Resting Energy Expenditure is the energy expended by the body in the resting state to maintain itself and digest food. This is made up of Basal Metabolic Rate (energy expended in the rested and fasted state) plus the Thermic Effect of Food (the energy used in digesting food — estimated at ~10% of Total Energy Expenditure). Activity Energy Expenditure is the energy expended by the body in movement, and is the only aspect of energy expenditure that is under conscious control. Activity Energy Expenditure makes up 20%–40% of Total Energy Expenditure, depending on activity level. Physical Activity Level is expressed as the ratio of Total Daily Energy Expenditure divided by Basal Metabolic Rate.

Christina O Stubbs BSc, GradDipDiet, APD · Amanda J Lee BSc, GradDipDiet, PhD

For most warfarin indications, the target maintenance international normalised ratio (INR) is 2–3. Risk factors for bleeding complications with warfarin use include age, history of past bleeding and specific comorbid conditions. To reverse the effects of warfarin, vitamin K1 can be given. Immediate reversal is achieved with a prothrombin complex concentrate (PCC) and fresh frozen plasma (FFP). Vitamin K1 is essential for sustaining the reversal achieved by PCC and FFP. When oral vitamin K1 is used for warfarin reversal, the injectable formulation of vitamin K1 is preferable to tablets because of its flexible dosing; this formulation can be given orally or injected. To temporarily reverse the effect of warfarin when there is a need to continue warfarin therapy, vitamin K1 should be given in a dose that will quickly lower the INR to a safe, but not subtherapeutic, range and will not cause resistance once warfarin is reinstated. Prothrombinex-HT is the only PCC approved in Australia and New Zealand for warfarin reversal. It contains factors II, IX and X, and low levels of factor VII. FFP should be added to Prothrombinex-HT as a source of factor VII when used for warfarin reversal. Simple dental or dermatological procedures may not require interruption to warfarin therapy. If necessary, warfarin therapy can be withheld 5 days before elective surgery, when the INR usually falls to below 1.5 and surgery can be conducted safely. Bridging anticoagulation therapy for patients at high risk for thromboembolism should be undertaken in consultation with the relevant experts.

Ross I Baker PhD, FRACP · Paul B Coughlin PhD, FRACP, FRCPA · Hatem H Salem MD, FRACP, FRCPA · Alex S Gallus FRACP, FRCPA, FRCP · Paul L Harper MD, FRACP, FRCPA · Erica M Wood FRACP, FRCPA

We report a young woman presenting with digital gangrene, paranasal sinusitis, mononeuritis multiplex, and rapidly progressive glomerulonephritis without asthma and eosinophilia — an extremely rare variant of this disease. Churg–Strauss syndrome (CSS), or allergic granulomatosis and angiitis, is a granulomatous vasculitis affecting small- to medium-sized arteries and veins. Although CSS is a systemic disease characterised by asthma and eosinophilia, various limited forms have been described.1 Here, we report a patient with such a limited form of the disease. Clinical recordA 35-year-old woman presented with a 15-day history of gangrene of the fingertips of her left hand, and weakness of the right wrist joint and the left ankle joint. She had a 3-year history of recurrent paranasal sinusitis. There was no history of asthma or any other allergic disorder, parasitic infestation, or smoking. On presentation, the patient had a pulse rate of 78 beats/min, blood pressure of 150/90 mm/Hg, and a temperature of 38.8°C. She had conjunctival pallor, gangrene involving all fingertips of the left hand, palpable purpura on the anterior aspect of the left leg, and 3/5 grade motor weakness of the right wrist joint and left ankle joint on dorsiflexion. The provisional diagnosis was systemic vasculitis syndrome. Blood tests on presentation showed (reference ranges in parentheses) a haemoglobin level of 93 g/L (110–165 g/L), a white blood cell count of 15 × 109 cells/L (4–11 × 109 cells/L), an eosinophil count of 0.15 × 109 cells/L (0–0.4 × 109 cells/L), and erythrocyte sedimentation rate of 35 mm/h (< 15 mm/h). Levels of urea, creatinine and electrolytes, fibrinogen level and prothrombin time, and the results of liver function tests, were within normal ranges. Urinalysis showed 3+ proteinuria (3 g/L) and microscopic analysis showed 30–40 red blood cells per high power field (reference range, < 4). The creatinine clearance rate was 98 mL/min. A chest x-ray demonstrated bilateral ground glass infiltrates, predominantly in the basal zones. High-resolution computed tomography (CT) of the chest revealed bilateral patchy ground glass opacities (Box 1). Spirometry showed a forced vital capacity (FVC) of 65% predicted, a forced expiratory volume (FEV1) of 68% predicted, and FEV1/FVC of 104%. An echocardiogram was normal. A nerve conduction velocity study showed axonal involvement, with reduced nerve conduction velocity in the right radial and left superficial peroneal nerves. CT of the paranasal sinuses showed chronic pansinusitis. Histopathological examination of the open-lung biopsy showed leukocytoclastic vasculitis, granuloma formation, and extravascular eosinophilic infiltration (Box 2). Renal biopsy showed pauci-immune, crescentic glomerulonephritis. Renal vessel Doppler ultrasonography and renal angiography gave normal results and ruled out any renal vessel involvement. The patient tested positive for perinuclear antineutrophilic cytoplasmic antibodies (ANCAs) and negative for cytoplasmic ANCAs by the indirect immunofluorescence method. A more specific enzyme-linked immunosorbent assay (ELISA) for anti-myeloperoxidase was positive, and another, for anti-proteinase 3, was negative. These tests ruled out Wegner’s granulomatosis. Antinuclear factor, anticardiolipin antibodies, hepatitis B surface antigen, and serological tests for hepatitis C and HIV were negative, thus ruling out significant secondary causes of vasculitis. The patient was treated with prednisolone (1 mg/kg per day, orally) and her condition showed marked clinical as well as radiological improvement. She became afebrile after 4 days, normotensive after 4 weeks, and her palpable purpura disappeared after 6 weeks. High-resolution CT of the chest, repeated at 4 and 8 weeks, showed progressive resolution of ground glass infiltrates. Repeat urinalysis showed resolution of proteinuria and haematuria at 8 weeks. The prednisolone dose was tapered over 8 weeks to a maintenance dose of 0.125 mg/kg every second day. Additional management included surgical amputation of all left-hand fingertips and physiotherapy for the motor weakness. DiscussionOur patient presented without the asthma and eosinophilia which are hallmark features of CSS. To the best of our knowledge, this is only the second report of this disease presenting in this way. A previous case report from Turkey described a young patient with CSS but no asthma and eosinophilia.2 CSS with eosinophilia but without asthma is also extremely rare and few cases have been described.3-7 In 1990, the American College of Rheumatology proposed six criteria for classification of CSS. These include asthma, eosinophilia (more than 10%), paranasal sinusitis, pulmonary infiltrates on chest x-ray (may be transient), extravascular eosinophils on biopsy, and mononeuritis multiplex or polyneuropathy.8 A patient is said to have CSS if at least four of these six criteria are met. The presence of any four or more of these criteria yields a sensitivity of 85% and a specificity of 99.7%. Our patient had four of the six features (paranasal sinusitis, mononeuritis multiplex, extravascular eosinophilic infiltration on biopsy, and pulmonary infiltrates on chest radiography). As illustrated by this case, CSS may present without asthma and eosinophilia. Earlier recognition of this disease and treatment with corticosteroids and/or immunosuppressive agents is important to prevent life-threatening visceral involvement. 1 High-resolution computed tomography of the chest, showing bilateral ground glass opacities 2 Open-lung biopsy specimen, showing leukocytoclastic vasculitis, granuloma formation, and extravascular eosinophilic infiltration Magnification × 100; haematoxylin–eosin stain.

Bhavneesh K Sharma MB BS, MD · Mradul K Daga MB BS, MD · Manisha Sharma MB BS, DTCD

Clinical record A 46-year-old English tourist became distressed when caught in a strong rip while swimming at a Sydney beach. An off-duty lifesaver dragged him to shore, where he was found to be apnoeic but had a weak pulse. After a minute of mouth-to-mouth ventilation, his pulse was lost, and chest compressions were begun. Ten minutes after cardiac arrest an ambulance arrived, and a wide complex bradycardia with no pulse was documented. During resuscitation, a total of 3 mg adrenaline, 70 mmol sodium bicarbonate and 1.5 mg atropine was administered. At 26 minutes after the cardiac arrest, the patient regained a pulse and was noted to be in atrial fibrillation. By this point, he was intubated and ventilated. On arrival in the emergency department, his systolic blood pressure was 90 mmHg, pulse rate was 136 bpm and irregular, and core temperature was 34.7°C. Auscultation of the chest revealed coarse bilateral crackles. His pupils were fixed and dilated. Initial arterial blood gases showed a severe mixed respiratory and metabolic acidosis, with a temperature-corrected pH of 6.47 (reference range [RR], 7.35 to 7.45), Pco2 of 98.6 mmHg (RR, 32.0–48.0 mmHg), Po2 of 104 mmHg (RR, 83.0–108 mmHg), arterial lactate level of 29 mmol/L (RR, 0.5–1.6 mmol/L), base excess of –28.1 mmol/L (RR, –2.0 to 2.0 mmol/L), and HCO3 level of 7.1 mmol/L (RR, 22–32 mmol/L). Chest radiography showed changes consistent with aspiration pneumonitis. The ventilator was adjusted to hyperventilate and reverse the respiratory component of the acidosis. Computed tomography of the head and neck revealed no abnormalities. It was decided to use controlled hypothermia to limit further hypoxic brain injury. The patient was packed in ice, and cooled intravenous fluids were administered, aiming for a core temperature of 33°C for a period of 12 hours (Box 1). The patient’s condition improved rapidly. The heart reverted to sinus rhythm spontaneously within a few hours, with no subsequent electrocardiograph or biochemical evidence of myocardial injury. The metabolic and respiratory acidosis normalised over the 10 hours after injury (Box 2). After 12 hours of hypothermia, cooling was ceased, and his core temperature was allowed to rise to 37°C. He was extubated on Day 3 after admission and discharged from hospital on Day 7. Neuropsychological assessment performed 2 weeks after the injury (including Wechsler Memory Scale Three and Delis–Kaplan Executive Function System) revealed relatively intact cognitive function, although there was moderate impairment in new learning ability and capacity for visuospatial information, and slowed information processing. This may be consistent with hypoxic brain injury, but, alternatively, might have been present before the accident. Repeat assessment 5 months after the accident (in the United Kingdom) revealed normal psychometric performance, with persisting impairment of visuospatial processing and organisational abilities. The patient and his family reported he was functioning just as he was before the injury, performing domestic duties and caring for his elderly mother. The World Health Organization reported 409 272 drowning deaths worldwide in the year 2000, making this the second leading cause of unintentional injury death globally, after road traffic accidents.1 The burden of near-drowning morbidity has not been defined but is likely to be high. Acidosis, especially pH < 7.0, usually correlates with a poor outcome. However, in drowning, the prognosis is often less grim, and patient survival has been reported after pH levels as low as 6.29.2 In our patient, the acidosis had both respiratory and metabolic components. The respiratory component, caused by apnoea, was the most readily correctable with gentle hyperventilation to “blow off” excess CO2. This had a rapid effect on the pH. The metabolic component was most probably a result of both physiological and pathological processes — the extreme muscle exertion while struggling in the surf and end-organ hypoxia as his respiration and circulation failed. In intensive care, blood lactate levels > 10 mmol/L are associated with 95% mortality.3 Our patient’s arterial lactate level was 29 mmol/L. We believe one reason for his good outcome was that the acidosis had a different aetiology to that in most intensive-care patients, in whom sepsis, hypoxia and shock predominate. This case therefore highlights the importance of continuing resuscitation efforts despite severe acidosis and fixed dilated pupils in drowning victims, as ultimate neurological recovery is still possible. Hypothermia is not a novel therapy for near-drowning. For over four decades, favourable outcomes have been reported for victims of near-drowning in ice-cold water.4 The effects of hypothermia are thought to be mediated by a reduction in brain metabolic requirements, limiting hypoxic cellular damage. A 1986 trial in Canada used hypothermia in near-drowned children to reduce intracranial pressure and limit brain injury.5 However, the death rate in the hypothermic group was higher than in the normothermic group, with most deaths attributed to neutropenic sepsis. This complication is now thought to occur only in children.6 The study also used lower temperatures and a longer period of hypothermia than is now recommended. This may have contributed to the poorer outcome and subsequent lack of interest in hypothermia for near-drowning. Interestingly, survivors in the study were more likely to be neurologically intact if they had been assigned to the hypothermia group. This suggests that the benefit of hypothermia may be not in preventing death but in improving neurological outcome in survivors. Recent evidence for controlled hypothermia as a neuroprotective therapy has been published in a study assessing its benefits in treating out-of-hospital cardiac arrest.7 This study used moderate (33°C), short-term (12 hours) hypothermia. Based on the favourable outcome of this and similar studies, the 2002 World Congress on Drowning, in Amsterdam, recommended this therapy for near-drowning victims who have restoration of adequate spontaneous circulation and remain comatose.8 A recent ILCOR (International Liaison Committee on Resuscitation) advisory statement also suggested that hypothermia may be beneficial for other rhythms causing cardiac arrest in settings such as drowning.9 We suggest that, in near-drowning cases where the patient remains comatose yet has adequate circulation, controlled hypothermia is an important tool to maximise neurological recovery. Further, severe acidosis should not be seen as a poor prognostic marker and should not preclude ongoing resuscitation efforts. Lessons from practice Severe acidosis or fixed dilated pupils are not useful markers for prognosis in the near-drowned patient. Controlled hypothermia at 33°C for 12 hours should be used in near-drowned patients who have spontaneous circulation but remain comatose. Controlled hypothermia cannot be recommended at present for children because of the risk of neutropenic sepsis. 1 Patient’s temperature over time after near-drowning 2 Arterial pH, lactate level and Pco2 over time after near-drowning* * Shading indicates reference ranges.

Jonathan P Williamson MB BS, BSc(Med) · Stan Braude MD, FRACP · Rowland Illing MRCS · Paul Gertler BA(Hons), MPsych, MAPS

Setting On the round you review a patient who needs long-term intravenous antibiotics. Your registrar says she will put in a “PIC” (percutaneous intravenous catheter) later that day. As you wander off, you wonder how good she is at putting in a PIC line. You wonder who taught her, as you know you didn’t and, indeed, it is many years since you have done one. Doctors in training need to practise to improve, and, whether we like it or not, practice often involves patients.1 While learning, it is possible that errors will occur. It is our responsibility as senior doctors to ensure that our trainees provide safe and good care and receive support in the learning environment. At a certain point, we also need to decide whether they are good enough to work alone. This involves assessing knowledge, skills, communication skills and professional behaviour. Often we rely on our “gut feeling” about whether they are capable. Is this sufficient? The focus of this teaching tips article is on how to decide when trainees are capable of carrying out procedural skills on patients. Skills trainingIt is important to consider what skills you expect your junior doctor or trainee to perform either independently or under your observation, to let them know and to give them training when needed. As many hospitals or training programs now have structured training for common simple skills (eg, suturing) and extensive training and testing of competency for infrequently performed but life-saving skills (eg, intubation), it is initially important to find out what training junior doctors have had in such skills.2 Framework for clinical assessmentA basic framework for determining clinical competence is shown in Box 1.3,4 The four stages move from “knowing” (awareness) up to “doing” (performance). For clinicians who assess junior staff, competence can be viewed as what these staff do in controlled situations, whereas performance is what they actually do when unsupervised.5 As described in “Tips 5”,6 trainees should not only demonstrate technical competence, but also be able to articulate the indications, contraindications and risks of a procedure, and be able to communicate these details to patients and know when to seek assistance. A trainee may be competent to insert a PIC line in a simulated setting, but, to perform well, he or she needs to be able to cope with a variety of situations (eg, patients who are obese, thin, well, unwell, agitated, or receiving anticoagulants) and know when to call for help. As clinicians, we are usually called upon to determine competence (can they do it safely in a supervised environment?) or performance (are they safe to do it alone?) while they work with us. How can we do this? Methods of assessmentMethods that can be used to assess skills include objective, structured clinical examinations, simulated and virtual settings, and “on-the-job” assessment.4,7 Each medical school, medical board, hospital and college uses its own range of tools and uses different methods for different levels (Box 1). Being competent doesn’t guarantee good performance.8 Knowing that trainees passed their medical school course or progressed from internship doesn’t mean they can safely care for patients without supervision. A review of the reliability or validity of these methods of assessment is beyond the scope of this article, but no single method can provide all the data required for deciding something as complex as whether a trainee is capable of delivering professional services.3 Tips for assessing competence and performance in the clinical settingThink about assessable moments. Structure work and teaching so you can observe behaviour. Gather information from multiple sources. Observe often and ask others (colleagues, registrars, nurses, patients). Ask trainees how they think they are going. Tell trainees how they performed, offering timely and constructive feedback and supporting them when things don’t go well. Use a simple rating scale (Box 2) to guide your assessment as to whether further training is required. Get trainees to describe and demonstrate. This will allow you to determine their weaknesses (Box 2). Take-home message In determining whether a trainee is safe to carry out procedures on your patient: Know what you would expect at each level of training. Decide whether you are determining competence (can the trainee do it safely in a supervised environment?) or performance (is he or she safe to do it alone?). In the clinical setting, observe often and ask others. Provide constructive feedback and further training when needed. 1 Framework for clinical assessment* * Adapted from Miller.3,4 2 Competence rating scale* No errors observed. Occasional errors, corrected by trainee. Frequent errors, corrected by trainee. Frequent errors, not corrected by trainee. Trainee unable to proceed without step-by-step instruction. * Adapted from a competence rating scale used in the Royal Australasian College of Surgeons Basic Surgical Skills Course. Student assessment materials. 2000.

Fiona R Lake MD, FRACP · Jeffrey M Hamdorf PhD, FRACS

A series looking at everyday practice in the light of the evidence The health of the first two of Shakespeare’s seven ages of man — “the infant, mewling and puking” and “the whining school-boy”1 — is the domain of paediatricians, paediatric surgeons and general practitioners. Paediatrics is a relatively new discipline. The first Professor of Paediatrics in Australia, Sir Lorimer Dods, was appointed to the University of Sydney in 1949, but it was not until the late 1960s that a common written examination for paediatrics and adult medicine was abandoned, and the medical world formally recognised that children are not just little adults when it comes to health and disease. Today, paediatrics is a vibrant discipline encompassing the whole gamut of medical subspecialties, plus some exclusive to childhood, such as neonatology and child development. 1 Topics covered by the Paediatrics series Problem crying in infancy Acute infectious diarrhoea and dehydration Prevention and treatment of obesity Bedwetting, constipation and toileting issues Autism and language disorders Atopic disease Obstructive and other sleep disorders Developmental, learning and behavioural problems Minor trauma Care of the child in Australian society The differences between the disciplines of paediatrics and internal medicine are far greater than those embodied in the observation that children are not just scaled-down adults. Most of the children admitted for acute care to Australian paediatric hospitals are still cared for by general paediatricians, while it is a long time since generalists fulfilled this role for adults in tertiary hospitals. Subspecialty practice in paediatrics is also different: children’s health problems differ from those of adults, and subspecialty practice is almost exclusively hospital or university based. In this issue of the Journal, we begin a Practice Essentials series on paediatrics that will focus on the common problems confronting paediatricians and, by extension, general practitioners. We could have chosen to cover the recent technological and pharmacological advances in paediatrics (of which there are many), but most, although not all, of these have their origin in adult medicine, partly because of a correct emphasis on the ethical considerations of experimentation in children, and partly because of the commercial considerations of the pharmaceutical and biotechnology industries. The problems we have chosen to feature are low technology and predominantly concern development and neurocognition. In 2002, 62 general paediatricians in Victoria were asked which of the clinical conditions they dealt with were the most difficult.2 The responses were illuminating: 26% listed conduct disorder, 24% family dysfunction, 18% eating disorder, 15% autism spectrum disorder, 13% children at risk, and 13% attention deficit disorder. A previous study looked at how six paediatricians spent their time during 12 months of community paediatric consultation:3 3875 of 14 711 (26.3%) consultations were for attention deficit hyperactivity disorder and learning problems, and 1917 (13.0%) were for intellectual disability. The most common medical condition was asthma (1470 consultations; 10%), followed by constipation and/or encopresis (966; 6.6%), and urinary tract infection and enuresis combined (815; 5.6%). In planning this series, potential topics were focused through the “camera obscura” of a group of general practitioners. The topics chosen reflect very closely the experience of the Victorian general paediatricians, and include developmental and learning problems, autism and language disorders, constipation, bedwetting, and the most common eating disorder — obesity. A complete list of the topics is given in Box 1. Problematic childhood behaviours often make a major contribution to family dysfunction, and problem crying in infancy and sleep disturbance can test the resilience of families and marriages. These disorders often do not have a significant underlying physical problem, but may be symptomatic of difficult family relationships. Paediatricians have to keep in mind that their patients grow up and stewardship will pass into other hands. Equally, we cannot practise in isolation — we need to be aware of the childhood lifestyle disorders that are determinants of adult disease. The child is indeed “father of the man”.4 The pandemic of obesity facing Australia and other developed countries has its genesis in childhood. Realistic management of this problem must involve strategies to decrease sedentary behaviour, particularly television and computer viewing in childhood, and also to promote physical activity and appropriate dietary intake. Another determinant of lifestyle disease in adulthood is upper-airway obstruction. Children who snore have been shown to have a neurocognitive disadvantage compared with their peers of the same age and socioeconomic group. The series concludes with an article on the care of children in Australian society. This reminds us about the social determinants of health, which are fundamental to our understanding of child growth and development.5 Academic paediatricians teach medical students to be a conduit for entitlements for their patients. Paediatricians need to become more involved in policy-making and advocacy. Parents of children with autism, as well as those with children with chronic disability, are beginning to demand this and they should be heeded. Finally, in addressing each of these important topics, the authors have sought to apply the best evidence available. Each article includes some evidence-based practice tips, with the level of evidence graded according to the National Health and Medical Research Council’s system for assessing evidence (Box 2). We hope you will enjoy this series and that it will provoke debate and discussion. 2 Designation of levels of evidence of the National Health and Medical Research Council6 Level I: Evidence obtained from a systematic review of all relevant randomised controlled trials. Level II: Evidence obtained from at least one properly designed randomised controlled trial. Level III-1: Evidence obtained from well-designed pseudorandomised controlled trials (alternate allocation or some other method). Level III-2: Evidence obtained from comparative studies (including systematic reviews of such studies) with concurrent controls and allocation not randomised, cohort studies, case-control studies, or interrupted time series with a control group. Level III-3: Evidence obtained from comparative studies with historical control, two or more single-arm studies, or interrupted time series without a parallel control group. Level IV: Evidence obtained from case series, either post-test or pretest/post-test.

Richard T L Couper MB ChB, FRACP · Richard L Henry MD, FRACP, DipClinEpid · Michael South DCH, FRACP, MD

Up to 20% of parents report a problem with infant crying or irritability in the first 3 months of life. Crying usually peaks at 6 weeks and abates by 12–16 weeks. For most irritable infants, there is no underlying medical cause. In a minority, the cause is cow’s milk and other food allergy. Only if frequent vomiting (about five times a day) occurs is gastro-oesophageal reflux a likely cause. It is important to assess the mother–infant relationship and maternal fatigue, anxiety and depression. Management of excessive crying includes: explaining babies’ normal crying and sleeping patterns; helping parents help their baby deal with discomfort and distress through a baby-centred approach; helping parents recognise when their baby is tired and apply a consistent approach to settling their baby; encouraging parents to accept help from friends and family, and to simplify household tasks. If they are unable to manage their baby’s crying, admission to a parenting centre (day stay or overnight stay) or local hospital should be arranged.

Harriet Hiscock FRACP, MD, GradDipEpi · Brigid Jordan BSW, PhD

Janine M Smith,* Edwin P E Kirk† * Senior Fellow in Clinical Genetics, Department of Clinical Genetics, The Children’s Hospital at Westmead, Westmead, NSW; † Clinical Geneticist, Department of Medical Genetics, Sydney Children’s Hospital, Randwick, NSW. kirkedATsesahs.nsw.gov.au To the Editor: The original understanding of cystic fibrosis (CF) as a well-defined, severe disorder has changed dramatically with the recent description of a wide range of clinical presentations. Correlations between genotype and phenotype have been reported, although the genotype–phenotype relationship is not a simple one.1 We report on a patient, now a 39-year-old woman, who had a single episode of distal intestinal obstruction (meconium ileus equivalent) at the age of 5 years, leading to a diagnosis of CF. She had a lower respiratory tract infection (caused by Klebsiella species) at the age of 10 years, but has otherwise been well, and is now asymptomatic, despite not being treated for CF since her teenage years. Her two pregnancies have been uncomplicated. She presented wishing to clarify the previous diagnosis of CF and to determine the health implications for her, if any. Her sweat chloride level was 93 mmol/L. Levels above 70 mmol/L are abnormal in adults, and this cutoff value reliably distinguishes people with CF from controls.2 Lung function testing and a chest x-ray were normal. Genetic testing revealed a genotype consistent with a diagnosis of CF. CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene on chromosome 7. The most common mutation is ΔF508, which produces misfolding of the CFTR protein. The polythymidine tract is a region in the CFTR gene that varies in size depending on the number of thymidine bases present — most commonly 5, 7 or 9. The 5T variant causes a reduction in functional CFTR protein, but is not of itself associated with classic CF. In this case, testing for 30 CFTR mutations showed heterozygosity for ΔF508. Testing for the poly-T polymorphism showed the presence of 9T and 5T alleles. As ΔF508 is essentially always found in cis (on the same chromosome) with 9T,3 we conclude that the patient’s genotype is ΔF508(9T)/5T. The symptoms a patient develops and their severity are thought to be related to the amount of functional CFTR protein produced. If this is above 10% of normal, an abnormal phenotype is unlikely. Levels < 10% are associated with congenital bilateral absence of the vas deferens (CBAVD), levels < 4.5% with progressive pulmonary disease, and levels < 1% with pancreatic exocrine deficiency.4 Homozygosity for ΔF508 is associated with a severe phenotype, whereas the genotype ΔF508(9T)/5T has been associated with a range of clinical phenotypes, including CBAVD, atypical CF, or no clinical features.5 Currently, our patient has no symptoms attributable to CF. She is presumably at increased risk of chronic lung disease, and has been advised to have her lung function monitored. Giving a long-term prognosis for individuals with mild variants of CF is challenging, and a normal outcome should be considered. In future, it may be possible to predict which patients with ΔF508(9T)/5T are likely to develop symptoms. CF and its variants need to be considered in an increasingly wide range of clinical presentations. Testing for CF mutations is available from a number of Australian laboratories (listed on the Human Genetics Society of Australasia website, www.hgsa.com.au) and should be conducted in the setting of appropriate genetic counselling.

Janine M Smith · Edwin P E Kirk

Emma J Glasson,* John Wray† * Research Fellow, University of Western Australia, Telethon Institute for Child Health Research, West Perth, WA, and WA Register for Autism Spectrum Disorders; † Paediatrician, State Child Development Centre, West Perth, WA, and WA Register for Autism Spectrum Disorders Emma. GlassonAThealth.wa.gov.au To the Editor: There is growing international awareness about the realities and difficulties of obtaining written informed consent from patients to compile and use data recorded in population-based registries. In some cases, such data could be of substantial benefit to the community, while posing relatively low risk of infringing patients’ privacy.1-3 The Canadian Stroke Registry achieved only a 39% participation rate from 4285 eligible patients when applying a policy of written informed consent to their data collection, resulting in significant representation bias.1 The issues and consequences are mirrored in our own endeavour, since 1999, to maintain a prospective register of people diagnosed with autism spectrum disorders in Western Australia.4 As protocol, diagnosing clinicians in Western Australia ask parents for written consent to allow their autistic child’s name, date of birth and postcode to be forwarded to the register. However, for many reasons, parents are not always asked and diagnostic information is not always forwarded. Missed cases are collected annually from the major diagnostic and service provision centres, but only the sex and year of birth are recorded for the child. Between January 1999 and December 2002, 757 new cases of autism were registered in WA, but only 35% of parents gave written consent to include identifying details. Forty-three per cent of the 757 cases were identified by cross-referencing to diagnostic centres. When clinicians remember to notify new cases to the register, 56% of parents give consent, either at the time of diagnosis, or by sending the forms directly to the register, indicating that clinicians are instrumental in encouraging patient participation. Sometimes clinicians send anonymous diagnostic information without giving parents information about the register, and sometimes parents forget to send permission forms to the register. Various characteristics of the child or the child’s family have a bearing on whether consent is given. For example, consent is received for only 31% of children living in rural areas, 25% of children with no intellectual disability, 23% of children not Australian-born, and 16% of children from families whose primary language is not English. Without consent for every case, the register cannot accurately reflect the age or geographic distribution of children with autism. If the register only collected information on consenting cases, there would be severe under-ascertainment and the output would be notably biased. Perhaps more importantly, unidentifiable records cannot be linked to other datasets. Other WA population databases include information on hospitalisations, genetic testing, genealogical links, midwife notifications, birth defects, pharmaceutical history, and people with cerebral palsy. Linkage to these datasets would enormously facilitate population-based autism research to investigate the aetiology, associations and natural progression of autism disorders. The WA autism register is an internationally unique population-based resource, but its application is limited without the inclusion of identifying information. This remains the reality at a time when the research community and affected families desperately seek information about the condition and solutions for their children.

Emma J Glasson · John Wray

Patrick G P Charles,* Michelle Ananda-Rajah,† Paul D R Johnson,‡ M Lindsay Grayson§ Infectious Diseases Physician, † Infectious Diseases Registrar, ‡ Deputy Director, § Director, Infectious Diseases, Austin Health, PO Box 5555, Heidelberg, VIC 3084. Patrick. CharlesATaustin.org.au To the Editor: We agree with Buising and colleagues1 that, in terms of predicting clinical outcomes, the Pneumonia Severity Index (PSI) developed by Fine and colleagues2 is heavily weighted towards age and pre-existing comorbidities. However, we disagree with both their proposed “solution” and the concept on which it appears to be based. Although the current Australian antibiotic guidelines suggest that admission to the intensive care unit should be considered mainly for patients with class V community-acquired pneumonia (CAP),3 a review of the data of Fine and colleagues suggests that patients in both class IV and class V are most likely to need this type of care. In the PSI’s validation cohort of 38 039 patients, 73% of those requiring intensive care fitted these classes.2 Thus, by simply modifying the current antibiotic guidelines to include patients with CAP in either class IV or V as being at greatest risk of needing intensive-care admission, the recommendations would be accurate. By comparison, Buising and colleagues advocate using the modified British Thoracic Society (BTS) rule, which was validated in only 244 patients.4 While this approach may have some future merit, we believe there are insufficient data to advocate its use at present. A comparison of the PSI and original BTS criteria found that PSI classes IV and V were more sensitive at predicting need for intensive-care admission.5 Secondly, we are concerned about the suggestion by Buising and colleagues that young patients with severe CAP who are not in PSI class V could have worse outcomes if they do not receive broad-spectrum antibiotics.1 This implies that severe CAP is more likely to be due to unusual or resistant pathogens. This is not supported by available evidence. Instead, early clinical consideration of the likely pathogens and the potential use of new diagnostic “point of care” tests (eg, pneumococcal and Legionella urinary antigen assays and analysis of throat swabs by polymerase chain reaction for respiratory viruses and “atypical” pathogens) are likely to be of greatest benefit in empirical antibiotic prescribing. Although CAP is a common admission diagnosis, there are very few published Australian studies defining its aetiology, optimal treatment and clinical outcomes. We are currently undertaking a large prospective study (the Australian Community-Acquired Pneumonia Study) at six major hospitals in three states to address these issues. Results should be available in late 2005.

Patrick G P Charles · Michelle Ananda-Rajah · Paul D R Johnson · M Lindsay Grayson

Kirsty L Buising,* Karin A Thursky,† James F Black,‡ Graham V Brown§ * Clinical Research Fellow, † Physician, ‡ Head of Epidemiology, § Head, Victorian Infectious Diseases Service, Royal Melbourne Hospital, Grattan Street, Parkville, Melbourne, VIC 3050. Kirsty.buisingATmh.org.au In reply: We thank Charles and colleagues for their comments. The modified British Thoracic Society (mBTS) severity score for patients with community-acquired pneumonia (CAP) has been validated in more than one study (the largest involving 1068 patients from three countries1) and is recommended by the British and American thoracic societies. It predicts requirement for intensive care with comparable sensitivity to the Pneumonia Severity Index (PSI) score (using classes IV and V)2 (unpublished data), and is easy to use, requiring four variables rather than 21. The study cited by Charles and colleagues showing that the BTS severity score was less sensitive used an older version of the tool. We believe the mBTS score represents a reasonable, simple alternative tool to identify severe pneumonia, although neither score should replace clinical judgement. Caution is needed when relying on a scoring system that may give false reassurance about patients not recognised to be at risk. Early recognition of severe illness enables early intensive-care intervention, which is associated with better outcome.3 The major guidelines for management of CAP recognise the entity of severe pneumonia and recommend broader-spectrum antibiotic therapy.4-6 Whether the spectrum of pathogens in severe pneumonia differs from that in mild pneumonia is not yet clear, as data are conflicting.7,8 However, a percentage of patients with severe pneumonia will have more resistant or unusual pathogens. Inadequate antibiotic therapy for patients with severe pneumonia is associated with higher mortality. For intensive-care patients, where there is less perceived “room for error”, a strategy of broad empirical antibiotic therapy and early narrowing to directed therapy is usually promoted.

Kirsty L Buising · Karin A Thursky · James F Black · Graham V Brown

Nat Lenzo Head, Department of Nuclear Medicine, Royal Perth Hospital, Wellington Street, Perth WA 6000, and Co-ordinator, WA PET/Cyclotron Service, Sir Charles Gairdner Hospital, Nedlands, WA 6009 nat.lenzoAThealth.wa.gov.au To the Editor: I read with interest the article by Ware et al1 and the response from Davies.2 Let me first commend Ware and his colleagues on an excellent piece of investigative journalism. For the readers’ information, there are about 200 operational positron emission tomography (PET) scanners in the United States, and the United Kingdom has recently committed to 50–60 PET scanners within the next 5–10 years.3 This is based on the vast amount of published evidence with respect to the benefit of PET for the diagnosis, staging and monitoring of a range of malignancies and other disorders. Despite more than 15 000 publications3 and the fact that some countries reimburse for many indications not covered in Australia (eg, breast cancer restaging, dementia assessment), our authorities request “Australian data” before allowing expansion of the Medicare benefit for PET in Australia. The issuing of only eight Medicare licences (ie, about 1 per 2.5 million population) also impedes access to what may be the most important imaging development of the past 20 years. What was not mentioned by Ware et al is the grossly inadequate amount paid for PET services under the Medicare Benefits Scheme in Australia. Currently, the reimbursement for a fluorodeoxyglucose PET scan in the US is about US$2000/scan. In Australia, the Medicare Benefits Scheme pays about $900. This makes our reimbursement one of the cheapest in the world. So cheap that it makes no economic sense for private entities to provide PET services in this country (note: isotope cost, about $350/patient; cost of PET set-up, $2.5–5 million). So the Commonwealth has no need to worry — it already has done much to slow the growth of clinical PET in Australia. Before Davies replies that we need “Australian data”, cost-effectiveness data, etc, before allowing new technology expansion, I ask: are Australian data so much better than those from our colleagues overseas? And what is the level of evidence for much of what we currently do and get paid for in clinical practice? For example, what is the rationale behind the reimbursement, without limit, of regular computed tomography scanning in the follow-up of patients with treated lymphoma? I direct readers to the articles by Guppy et al4 and Dryver et al5 to see what little benefit there is in this practice. Of course, these are British and Canadian studies, so surely they cannot be taken seriously.

Nat Lenzo

Robert E Ware,* Hilton W Francis,† Kenneth E Read‡ * Nuclear Medicine Physician, 49 Augusta Road, Lenah Valley, TAS 7008; † Rheumatologist, Hobart; ‡ Barrister, Malthouse Chambers, Hobart. robwareATtrump.net.au To the Editor: In light of our article examining the Australian Government’s review of positron emission tomography (PET),1 it is interesting to note that the accompanying official response is attributed to the Department of Health and Ageing (DOHA).2 When asked to clarify its role in the review of PET, DOHA had previously persuaded the Commonwealth Ombudsman that it had contributed only secretarial support to the process. With no accountability for policy decisions or the review itself, is it any wonder that DOHA’s response does not address the hard evidence that the politicians are “misusing” evidence-based medicine. The comment that “one of the concerns that has been raised about the PET reviews is that the government did not follow the views of individuals who were involved in the process” does not relate to our text. We are aware that individual opinion is considered very low-level evidence. Our argument is that the supporting committee made a decision that PET was safe, clinically effective and potentially cost-effective on the basis of the evidence it reviewed. The Medical Services Advisory Committee (MSAC) itself did not review any evidence, so, by changing the decision of its supporting committee, MSAC’s own opinion was substituted without any sound scientific basis. Therefore, the decision at a ministerial and government level to restrict Medicare funding for PET is purely a political decision, and must not be misrepresented as “evidence-based”. Indeed, the evidence suggests that the policy decision to restrict Medicare funding for PET prejudiced the objective analysis of the evidence by MSAC. The suggestion that “the government is funding the collection of data by service providers to improve the evidence base related to the use of PET in a wider range of indications” is misleading. To improve the level of evidence for PET would require, in the words of the permanent medical adviser to MSAC, “very large randomised trials, which are probably not feasible”. The current data collection is not a randomised trial. For many of the indications being examined, the validity of the PET findings and consequent management changes will not be assessed. There is no plan to evaluate cost-effectiveness. Therefore, the process is not going to improve the level of evidence for subsequent decision-making. Perhaps this is the outcome envisaged for 2006! The problem with the PET review was a fundamental disregard for the promised standards. The ongoing problem is that MSAC is not an appropriately legislated body (unlike the Pharmaceutical Benefits Advisory Committee). MSAC is secretive and its process and decision-making are difficult and costly to penetrate. Unless the structure, process and accountability of MSAC are changed, history is likely to repeat itself. The official response to our article only serves to heighten our concerns.

Robert E Ware · Hilton W Francis · Kenneth E Read

Kevin L Forbes Head, Years 3 and 4 MB BS Program, University of Queensland, Mayne Medical School, Herston, QLD 4006. k.forbesATuq.edu.au To the Editor: In response to the recent column on medical education,1 I would like to point out that many of the medical schools in Australia have broadened the content of their curricula to reflect the expected demands of professional practice and to satisfy the objectives of the accrediting body.2 Medical schools involved in curriculum change have tended to favour a broad education that emphasised learning across four domains (basic and clinical sciences, clinical skills, population health and ethics, and professional development). Another principle influencing changes to curricula was the need to ensure that the students were competent to enter supervised practice as an intern and be equipped with the desire to pursue life-long learning. Remarkably, medical schools have tended to deliver similar curricula in response to these and other issues (eg, emphasis on communication skills, critique and clinical application of evidence, exposure to rural health issues). Medical educators see a need to prepare medical students to cope with continuing changes in healthcare. Some of us would argue that many of the principles of such ongoing learning are fundamental to problem-based learning programs, and expect that graduates of such programs will be able to adapt to new continuing professional development programs. However, there is as yet no hard evidence that incorporating self-directed and problem-based learning techniques into medical curricula has any beneficial effect. Although it is not yet possible to measure the long-term effects of the changes in medical curricula, in the short term objective measures are encouraging. Today’s Australian medical school graduates function well as interns and residents.3 However, many in the profession are concerned about the level of knowledge of current graduates, particularly (but not exclusively) about anatomy. Although knowledge of anatomy needed by doctors varies considerably between disciplines, the basic sciences, including anatomy, do need to be included in college training programs. Clearly, the profession needs to measure the outcome of changes to medical school curricula.4 Ideally, as you say in your column, the outcome measures would be generally agreed by the profession.1 A debate in the Journal about the most appropriate outcome measures for medical schools would ensure that the concerns of many medical practitioners could be considered. Meanwhile, those involved in medical education need to develop and publish the outcomes that are measured in the medical schools.

Kevin L Forbes

Paul G McMenamin Associate Dean (Teaching and Learning), Faculty of Medicine and Dentistry, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009. mcmenaminATanhb.uwa.edu.au To the Editor: In the lead-up to the description of events at a recent Royal Australasian College of Surgeons (RACS) conference,1 it appears that you do not fully agree with the changes in medical education in Australia and overseas in recent years. Firstly, it should be pointed out that problem-based learning has not “all but displaced didactic teaching”1 in Australian medical schools. Many schools have hybrid courses and a wide variety of teaching methods are used. Secondly, including outcomes such as “communication skills and compassion!”1 in the curricula can hardly be less than desirable. The desired outcomes of medical schools are driven by Australian Medical Council guidelines on the requirements for the safe and competent practice of clinical medicine by a generalised doctor in the intern setting before specialist training. Individual surgeons, the RACS, and their United Kingdom counterparts2 have lamented the decline in medical students’ anatomical knowledge for generations, even when students were taught 500–700 hours or more of anatomy.3 There is nothing new in this call-cry. A generalised doctor prepared for internship does not require much of the knowledge that some are lamenting has been lost from medical curricula. The “old” curricula were crowded with excessive amounts of topographical anatomy that was of questionable relevance and seldom taught within a clinical or medical context. The optimal time and context for students to learn detailed topographical anatomy is surely when the knowledge is most relevant and valuable. This is surely during basic and advanced surgical training programs, both administered through the RACS. There is good evidence that detailed teaching of topographical anatomy in targeted postgraduate surgical training courses is of measurable benefit and greatly appreciated.4,5 Indeed, is it really very suprising that, for example, urological and gynaecological surgeons have a greater interest in the nine branches of the anterior division of the internal iliac artery and the detailed relations of the ureter in the pelvis than 18-year-old first-year or second-year medical students? It is now the responsibility of surgeons and anatomists to deliver postgraduate programs that address the desired outcomes for RACS training (and the UK equivalent2). We at the University of Western Australia have launched a Graduate Diploma in Surgical Anatomy. A similar course has been in place in Melbourne for some years. Other states can only be encouraged to follow.

Paul G McMenamin

Martin B Van Der Weyden Editor, The Medical Journal of Australia, Locked Bag 3030, Strawberry Hills, NSW 2012. medjaustATampco.com.au In reply: McMenamin reiterates the importance of the educational components of current medical curricula: problem-based and self-directed learning, along with the enhancement of students’ capacities for communication and compassion. Forbes agrees and advances that these changes are to prepare future doctors for life-long learning. There are two issues at the centre of this discourse — what do medical students think of the curricular changes, and are these changes informed by scientific evidence? Anecdotal reports suggest that some medical students in the United Kingdom1 and Australia2 have concerns “that basic science does not get the priority that it once did”. Similar concerns have been raised in the popular press.3 Furthermore, UK academics fear that the dilution of basic sciences in current curricula may, in the long term, adversely affect medical graduates entering into research.1 Forbes concedes that the evidence underpinning these changes to medical education is wanting. And herein lies the rub. Despite continued calls for educational research that matters4,5 (and perhaps in keeping with opinions as to how difficult performing such research might be),6,7 the medical education community has yet to report solid evidence to support the intentions of these resource-intensive changes.8 The profession, hardened by the evidence-based movement, expects no less. This, I believe, was an undercurrent of the audience disquiet at the plenary session of the meeting of the Royal Australasian College of Surgeons in May this year. As to McMenamin’s robust defence of the pruning of anatomy in medical curricula, this debate is more than 2 centuries old. An 18th-century guide to the training of apothecaries (the forerunners of general practitioners) stated that “he” should be “tolerably well acquainted” with Latin, be competent in “his” own language and “acquainted with botany chemistry, and pharmacy; and have studied anatomy and physiology”. But “the minutiae of anatomy are not necessary”9 [my italics].

Martin B Van Der Weyden

Lionel L Wilson Principal, Qual-Med, 34B Kangaloon Road, Bowral, NSW 2576. Lwilson10ATbigpond.com To the Editor: Nisselle’s recent editorial on managing medical indemnity raises important issues.1 I would like to comment on some points. The quality movement, in the form of a system of hospital accreditation, actually began via the New South Wales Branch of the Australian Medical Association in the late 1960s. However, credentialling and the delineation of clinical privileges for medical staff are far from the norm that Nisselle claims. In fact, although some hospitals claim to be credentialling medical staff, in most instances this is little more than an exercise in tokenism and is quite incapable of contributing either to quality or to minimising risk. Nisselle also refers to the “safety movement”. While recognising current common usage, to talk of safety as separate from quality in healthcare is tautological. It is not credible to visualise a hospital that claims to provide quality care but tolerates unsafe practices of any description. Similarly, unsafe practices in a facility mean that quality care is not being achieved. In attempting to untangle the semantic problems occasioned by the term “risk management”, Nisselle merely compounds the problem that bedevils this subject. Of course, he is far from alone, and the medical literature further aggravates this confusion. I suggest the following definitions in the hope of introducing some clarity: Quality management: The management of all these issues, as Nisselle points out, is a big task. While the term “clinical governance” is currently in vogue, it means little, I believe, to most doctors. Managing quality is a complex task (as illustrated by Nisselle’s appropriate elephant analogy). So why not call it what it is? Managing quality is largely about avoiding patient harm. Risk management: The same definition should be used whether we are talking about an insurance company or a medical service. It is the minimisation of financial loss. In the case of healthcare, the risk is malpractice litigation directed at both doctors and hospitals. The techniques of risk management are very similar to those of quality management, and risk management is an intrinsic component of quality management.2 Risk management in healthcare is not simply about reducing error, any more than is quality management. It is this focus that leads to so much confusion. Quality assurance: This is the deliberate activity of ensuring that what was done and achieved is what should have been done and should have been achieved. It is another facet of the broader activity of quality management. The management of quality and avoidance of the risk of litigation is difficult enough. It would help if we did not all use the terminology to mean whatever we want it to mean.

Lionel L Wilson

Paul Nisselle Senior Advisor, Risk Management, Medical Defence Association of Victoria, PO Box 1059, Carlton, VIC 3053. nisselpATozemail.com.au In reply: Wilson highlights the confusing taxonomy of quality/risk in healthcare. My editorial distinguished prudential risk management (ensuring insurer solvency) from clinical risk management (reducing medical error).1 The term “clinical governance” combines quality improvement (ie, getting it right more often) and risk management (ie, getting it wrong less often). Wilson writes that “Managing quality is largely about avoiding patient harm”. But quality management is as much about finding more effective ways of doing things as it is about finding safer ones. Quality and safety are separate, albeit overlapping, concepts. Similarly, risk management is more than just “minimisation of financial loss”. Reducing the rate of head injuries by using seat belts has a human benefit, not just a financial one. One trade-off for the “Abbott reforms” to medical indemnity is a demand by government for a real commitment by both medical indemnity insurers and those insured to clinical risk management. Although we may disagree on the language, Wilson and I are in heated agreement on the need for a concerted, systemic approach to quality management. The medical indemnity insurers have a role to play that goes beyond just remaining solvent and keeping indemnity costs down!

Paul Nisselle

Kevin B Orr Surgeon, 3/22 Belgrave Street, Kogarah, NSW 2217. stgeorgedermATbigpond.com To the Editor: I report the case of an unexpected complication of a common cardiothoracic procedure which deserves the attention of the general medical community. An 82-year-old general practitioner required coronary artery bypass surgery. Although retired, he was fit enough to continue visiting patients in a number of nursing homes, and occasionally assisted at operations. His condition after the surgery was good for a few days, but deteriorated, with the development of dyspnoea, shortly before he was due to be transferred to a rehabilitation unit. Whether it was realised that his haemoblobin level had fallen from 150 g/L to 90 g/L over the days before surgery is not known. A blood count several days after surgery revealed a haemoglobin level of 100 g/L. This low level was attributed to insufficient transfusion during surgery. The patient was given two units of blood, which raised the haemoglobin level to 120 g/L. Although a repeat test on the day he was discharged to a rehabilitation unit showed the level was again 100 g/L, this result was not seen by a clinician before the transfer. On arrival at the rehabilitation unit, the patient was unable to complete the scheduled activities. He was breathless, returned to his room, almost fainted and had to be helped back into bed. Later that night, he had massive melaena and died. For some weeks leading up to the bypass surgery, the patient had suffered from dyspepsia and was “living on” antacid. He mentioned this to his general practitioner, who did not initiate any investigations or treatment. On the patient’s admission to hospital, the medical officer prescribed omeprazole, presumably in response to the history of dyspepsia. Whether this doctor was aware of a preoperative drop in haemoglobin level is not known. The most likely cause of this man’s death was a bleeding duodenal ulcer exacerbated by coagulation defects associated with major surgery (no autopsy was performed). Bleeding was initially slow but culminated in a fatal haemorrhage. The lesson from this case is that any suggestion of a serious concurrent illness should be thoroughly investigated before major surgery. In this case, a simple gastroscopy before the bypass surgery might have been lifesaving.

Kevin B Orr

During a diverse career as pharmacist, research synthetic chemist, pharmacologist and medical practitioner, George Eckert was always a charismatic teacher across this diverse knowledge base. He strongly influenced generations of students, doctors, dentists, and pharmacists through coaching, tutoring, mentoring, lecturing and published research. George was born in Sydney on 24 October 1931. He was educated at Sydney Boys’ High School, and studied pharmacy at the University of Sydney, graduating in 1951. After spectacular success as a pharmacy academic at the University of Sydney and private tutor to over 1000 students from 1953 to 1965, George changed direction and studied medicine, graduating with honours in 1968. He trained in the Department of Clinical Pharmacology at St Vincent’s Hospital, then, from 1974 to 1980, directed the first NSW Health Commission-funded Clinical Pharmacology unit at Sydney Hospital. In 1984, he transferred to St George Hospital, Kogarah, where he stayed until his retirement in 1992. During this time, he was responsible for changing methods of prescribing and managing drugs in hospitals and for instituting quality-assurance and risk-management procedures that are now benchmark best-quality practice worldwide in all areas of medical practice and healthcare delivery. He influenced the flow of information about drugs, believing that those who prescribed, administered and dispensed them, and the people who received them, were all entitled to more information about their use and effects than they were getting. He engaged in what he called “counter-detailing”: giving practitioners a view of drugs independent of that supplied by pharmaceutical companies, and often at odds with it. He was fearless and selfless in the public interest, passing up lucrative offers from pharmaceutical companies that were widely available to clinical pharmacologists and other medical specialists in that period. George had the many gifts and true modesty of a polymath. He had a creative intellect, bringing together his diverse education and life-long learning. The examiners for his Doctor of Medicine thesis wrote: “This thesis is to be highly commended, as it is so novel. It is so far ahead of the prevailing orthodoxy conceptually that it is not likely to be widely understood or appreciated until there is a broadening of pharmaceutical and pharmacological training.” He had an encyclopaedic knowledge of history (ancient and modern), music, opera, film, chess and cricket, and shared these interests with friends of all ages. George’s greatest gift was his capacity for friendship with a wide range of people in his diverse life roles. He saw the world as one moulded by human strengths and weaknesses, and shared his insights with kindness, compassion and humour. Towards the end of his life, suffering from prostate cancer, he faced his illness with stoicism, dignity and courage, and died at home among family and friends on 17 May 2004. Allan J McLean, Lisa L Demos, Constantine G Berbatis

Allan J McLean · Lisa L Demos · Constantine G Berbatis

Marcus (“Marc”) Faunce was born in Sydney on 5 December 1922, and died in the early hours of 14 June 2004 in Canberra, after a protracted struggle with renal cancer. After qualifying in medicine from the University of Adelaide in 1946, Marc served in the Australian Army Medical Corps in post-war Japan and trained at the British Postgraduate Medical School at Hammersmith. He became Senior Registrar at Sydney Hospital in 1949 and married Marjorie Morison in 1951, obtaining his membership of the Royal Australasian College of Physicians (RACP) in the same year. From 1954 to 1956 he did research at the Brompton Chest Hospital in London, becoming a Member of the Royal College of Physicians (RCP) (London) in 1955. Two years later, Marc and Marjorie moved back to Australia and settled in Canberra. Marc established himself as a consultant physician and salaried specialist with the Commonwealth antituberculosis campaign. He was elected a Fellow of the RACP in 1965 and of the RCP (London) in 1968. During his 35 years of full-time practice, Marc was much loved by his patients and admired by colleagues and students as a great general physician with a special interest in respiratory medicine. He co-founded the Canberra Medical Society in 1959. He served on the ACT Medical Board (1963–1974) and was Senior Physician Consultant to the Royal Australian Air Force Medical Directorate (1976–1980), with the rank of Group Captain. For these services he was made an Officer of the Order of the British Empire in 1969 and a Member of the Order of Australia (Military Division) in 1981. Marc was a staunch advocate for a medical school in Canberra. He served on the Board of Management of the Royal Canberra Hospital (RCH) from 1967 to 1974. He fought against the demolition of the RCH, situated adjacent to Lake Burley Griffin. The battle to save the hospital ultimately failed, and its units were progressively transferred to the Woden Valley Hospital (now the Canberra Hospital) from 1991 until its eventual closure in 1993, when Marc was given the honorary accolade of Emeritus Consultant to the RCH. It was a source of great satisfaction to Marc that his son, Thomas, was appointed Senior Lecturer and Chair of Personal and Professional Development at the new Medical School established at the Australian National University in 2004. Marc was renowned for his stringent adherence to medical confidentiality, being individually selected to be honorary personal physician to five prime ministers and six governors-general, for which services he was made a Commander of the Royal Victorian Order in 1995. He was a voracious and eclectic reader. Though distrusting spiritual conceptions, he heavily annotated many copies of the New Testament. His favoured social introduction was “Just sit down and let me tell you the story of my life”. Marc is survived by his sons Thomas and Marcus and daughter Charlotte.

Bryan S Furnass

The health of refugees. Public health perspectives from crisis to settlement. Pascale Allotey (Editor). Melbourne: Oxford University Press, 2003 (xxiv + 232 pp). ISBN 0 19 551593 5. The health of refugees has generally been regarded as the health of people in “camps” in far-off places like Pakistan, Iran, Sudan, or Kenya. However, this book looks at refugee health from an Australian community perspective. We are brought very quickly from the view of the refugee as “the other”, “the stranger”, “the queue jumper” or “the legitimate refugee” and “the asylum seeker” to see them as people who live in our community, but are often excluded as legitimate members of it. By focusing on this minority within Australia from a public health perspective, our national responsibilities in helping to solve this global health problem are brought into sharp contrast. The book begins with a very good overview of the general health problems faced by those forced to migrate, and moves rapidly to focus on the specific health needs faced by refugee and asylum seekers in Australia. We begin to see this marginalised group as a vibrant resource to be nurtured, rather than one to be further excluded, persecuted and denigrated. This book provides us with timely and detailed health data which could be used to develop a rational refugee health policy. We are also given new data on the long-term effects of forced migration on the many children, accompanied and unaccompanied, who become caught up in these situations. We are asked to play a creative and healing role in this trauma cycle rather than exacerbating the damage. The tension between specialised service funding models and the ability for broader integrated mainstream services to adequately meet the health needs of minority groups is dealt with in the book. There are no easy answers offered, but it focuses on the need for building reasonable and auditable capacity into mainstream services, and so offer hope that better-integrated and more grassroots, community-based healthcare will be developed in the future. The building of cooperative approaches with advocacy groups, volunteers, asylum seekers and refugees, to work with mainstream health services to assess their capacity to respond to individual health needs and to work out creative solutions, stands well with current thinking worldwide on building integrated health partnerships. This book presents many excellent vignettes that make it fascinating and powerful reading. It also provides well-researched references gleaned from those who have built up expertise in refugee and asylum seeker health over recent years in Australia. Based on the information in this book we could, as a nation, develop a refugee healthcare policy to be proud of, and we could show leadership in our region and provide an example to other nations. This book provides food for thought on our public health policies on many levels and is highly recommended as a very practical manual for action. It is an excellent book for anyone with an interest in health, social justice and human rights. Rohan VoraEx-convenor, Brisbane Refugee and Asylum Seeker Health Network Registrar in Palliative Medicine, Brisbane, QLD

Rohan Vora

A new PSA era? US experts say that the prostate-specific antigen (PSA) era as we know it is probably over when it comes to the detection of prostate cancer. Stamey and colleagues reviewed 20 years' worth of data (from 1983 to 2003), finding a declining relationship between serum PSA level and the largest prostate cancers, from 44% in 1983–1988 to 2% in 1999–2003. Higher PSA levels reflect an overall greater prostatic volume rather than the presence of prostate cancer per se. Two decades ago, the prostatic tumours diagnosed were generally large, generating PSA levels that were high enough to provide an accurate measure of cancer severity; this is no longer the case today. However, these experts say PSA testing will become an enduring marker of the degree and rate of progression of benign prostatic hypertrophy. It will also continue to be useful as a marker of failure to cure after therapy for prostate cancer. J Urol 2004; 172: 1297-1301 Rofecoxib withdrawal Rofecoxib (Vioxx), a selective NSAID, has been voluntarily withdrawn from the market, worldwide, due to concern that long-term use may put patients at increased risk for serious cardiovascular events. According to the US Food and Drug Administration (www.fda.gov), the manufacturer’s decision was based on new data from the Adenomatous Polyp Prevention on Vioxx (APPROVe) trial, which had been designed to determine whether 25 mg rofecoxib was effective in preventing the recurrence of colon polyps. APPROVe was stopped two months earlier than planned when, compared with placebo, continuous use of rofecoxib for 18 months or more was associated with an increased risk of serious events such as myocardial infarction and stroke. www.cmaj.ca/news/30_09_04.shtml Once and for all? A single dose of dexamethasone has a place in the management of mild croup in most, if not all, children, say Canadian researchers. In their multicentre, double-blind, randomised controlled trial involving 720 children with mild croup, they compared a single dose of dexamethasone (0.6 mg per kg of body weight) with placebo. Dexamethasone use resulted in quicker resolution of the symptoms of croup, as well as less lost sleep, and, in the first 24 hours, less parental stress. However, the researchers did advise cautious use of dexamethasone in children with recent exposure to varicella or pre-existing immunodeficiency. N Engl J Med 2004; 351: 1306-1313 Sniffing out malignancy UK researchers have successfully trained six dogs, of varying breeds and ages, to sniff out cancer. Using operant conditioning, they trained the dogs to distinguish between urine from patients with bladder cancer and urine from "controls" who were either healthy or had diseases other than bladder cancer. As a group, the dogs correctly detected three times as many cases as would have been expected by chance alone. It is thought that the dogs learned to detect a characteristic combination of odours — an "odour signature" — in urine from bladder cancer patients. BMJ 2004; 329: 712-714 The dysglycaemic iceberg Patients with diabetes make up only the tip of a much larger "dysglycaemic iceberg". Now, glycosylated haemoglobin (HbA1c) has been shown to be a progressive risk factor for cardiovascular disease not only in people with diabetes but also in people without it.1 In a UK study, which followed a cohort of more than 10 000 adult men and women with and without diabetes for six years, each one-percent increase in HbA1c above a normal level of 5% led to about a 20% relative increase in the incidence of cardiovascular events.2 Further, most of these events occurred in people whose HbA1c level fell between 5% and 6.9%. 1. Ann Intern Med 2004; 141: 475-476 2. Ann Intern Med 2004; 141: 413-420 Maybe baby The promise of fertility restored via re-implantation of cryopreserved ovarian tissue has been fulfilled, with the report of the first live-birth using this technique. Five ovarian biopsy samples were taken from the left ovary of a 25-year-old woman before treatment for stage IV Hodgkin’s lymphoma. The patient was cured of lymphoma but rendered infertile. Five years later, a team of Belgian physicians and researchers re-implanted the freeze-thawed ovarian tissue into the patient’s peritoneum. The result (within two years): a take-home baby. Hopefully, the re-introduced tissue will not harbour any seeds of malignant cells overlooked by current screening methods. The technique described offers hope to women wanting to extend their reproductive lives, as well as to women undergoing cancer treatment. Lancet 2004; 364: 1405-1410 Dr Ann Gregory, MJA