Volume 184 Issue 2

Further complications of the “obesity epidemic” The potential health burden to our community of escalating overweight and obesity is well documented and publicised. Attention has focused on the association with chronic diseases such as hypertension, diabetes, cardiovascular disease and all-cause mortality. The effects of obesity on reproductive function and outcomes have received less attention. The ability to conceive spontaneously is reduced by obesity. While many overweight women can conceive easily, they are over-represented among subfertile groups and those presenting with menstrual disorders.1 Overweight women, both with and without polycystic ovary syndrome, present with menstrual irregularity and anovulation more frequently than women with normal body mass index (BMI). The US Women’s Health Study concluded that even a slightly elevated BMI at age 18 was a risk factor for subsequent anovulatory infertility.2 Several studies have confirmed the association between obesity and reduced fertility.1,3 Elevated BMI is also associated with poorer outcomes from assisted reproduction.3 Obesity also affects pregnancy outcomes. The article in this issue by Callaway et al4 is an important and timely reminder of the high prevalence of obesity in women of reproductive age and the serious adverse effects of overweight during pregnancy. Risks are increased for both mother and baby. Maternal problems can result from pre-existing obesity-related illnesses such as hypertension and type 2 diabetes. The increased pregnancy-related risks of obesity include increased rates of miscarriage,1 gestational diabetes, pregnancy-induced hypertension, pre-eclampsia, thromboembolism, haemorrhage, caesarean section, sleep apnoea, wound infection and anaesthetic complications.5,6 These risks persist, even when adjusted for pre-existing illness. The offspring of overweight and obese women are more likely to require admission to neonatal intensive care and to have congenital abnormalities such as neural tube and cardiac defects. Birth-related injuries and fetal death in utero are also higher in this group, and babies are more likely to be macrosomic, placing them at risk of birth trauma and possible subsequent childhood (and, indeed, lifelong) obesity.5,7 What are the effects of weight loss on fertility and pregnancy outcomes? Weight loss alone often leads to improvement in conception rates. Clark et al,1 evaluating a 6-month diet and exercise program in overweight anovulatory women, found that participants in the program tended to lose weight and resume ovulation. Pregnancy rates, self-esteem and endocrine parameters improved, while rates of miscarriage fell. Seventy-eight per cent of the women conceived, with 67% achieving a live birth. Weight loss of dramatic proportions was not required — a relatively small weight loss (6–10 kg) could lead to resumption of spontaneous ovulation. The effects of weight loss on pregnancy outcomes have recently been reported by Dixon et al.8 Their prospective study sought to examine the effects of laparoscopic adjustable gastric banding (LAGB) in severe obesity. They concluded that “pregnancy outcomes after LAGB are consistent with general community outcomes rather than outcomes from severely obese women”. Callaway et al4 comment on the implications for health care delivery costs of obesity-related increases in maternal and neonatal morbidity. This problem will only worsen. The AusDiab study9 reported that the prevalence of obesity in 2003 was 2.5 times higher than in 1980. Moreover, obesity is occurring at a younger age, the problem increases with time, and women are becoming pregnant later in life.10 Solutions to such a complex problem will inevitably be multifaceted and costly. Callaway and colleagues recommend that maternal BMI should be recorded at the booking visit for all pregnancies. While this will assist in documenting the problem, any meaningful intervention must occur before presentation with an established pregnancy. Given the potential for adverse health outcomes for both mother and baby, and the potential lifelong effects of neonatal macrosomia, there is a pressing need for action well before conception. As part of general public health efforts to combat obesity, we strongly recommend pre-pregnancy counselling for all women, with every effort being made to intervene in the case of women who are overweight or obese. The majority of women are highly motivated to strive to have healthy babies, and the power of this commitment could well be used to achieve behavioural change that could have short-term (and potentially lifelong) benefits for both mothers and children.

Alison J Nankervis MB BS, MD, FRACP · Jennifer J Conn MB BS, MClinEd, FRACP · Rachael L Knight MB BS, MD, FRANZCOG

Clinical trials show partial meal replacement products to be safe, acceptable and effective when used as part of an overall low-energy diet Overweight (body mass index [BMI] > 25 kg/m2) and obesity (BMI > 30 kg/m2) are now major health concerns, being causally related to a number of metabolic disorders, and affecting at least one in two adult Australians.1 However, the long-term evidence on treatment of these conditions is disappointing. A strategy recommended in the recent clinical guidelines from the National Health and Medical Research Council is the use of low-energy meal replacement products.1 These have been marketed for many years, but have only recently been considered seriously in large clinical trials. If effective, this strategy offers promise as: it provides a discrete option for doctors dealing with a difficult condition; it is easy to administer and supervise; and it is relatively cheap. However, questions remain about the long-term outcomes and safety of meal replacement products, their effects in comparison with other strategies, and their acceptability to patients. What are meal replacements? Meal replacements are defined as “a single food or pre-packaged selection of foods that is sold as a replacement for one or more of the daily meals, but not as a total diet replacement”2 (Box 1). These replacements exert their effect through reducing portion size, and consequently energy intake.3 In patients with morbid obesity requiring large weight losses (BMI > 40 kg/m2), specially formulated very low calorie diet (VLCD) forms of meal replacement may be used in place of all meals. However, more commonly, partial meal replacements are used for one or two meals a day, with at least one usual meal consumed as part of an overall low energy diet. Here, I focus on the use of partial meal replacements, because of their wider potential clinical use. Why are partial meal replacements returning to favour? Traditionally, there has been concern about the use of any meal replacements, probably based on concerns about: the nutritional balance of some commercial mixes; potential “bounce back” weight gain on discontinuing use, when this use is unsupervised (as for any low-energy diet plan); and the fact that they may not teach users good long-term eating habits. These concerns have now been largely overcome by: advances in food technology, which allow more complete and better balanced nutrient mixes; a move towards better training of clinicians about weight control; and the fact that most reputable products are now part of a broader weight loss program, with accompanying nutritional education about non-replacement meals (Box 2). While different forms of meal replacements have been used for weight loss over many years, controlled research on the effectiveness of partial meal replacements is relatively recent. Several studies, reviews and meta-analyses now attest to the benefits of partial meal replacements. Their use commonly results in weight loss of around 9%–10% of total body weight in the short term (6–12 months), and 6%–8% in the long term (eg, 1–5 years), with no reported adverse effects when used as part of an overall low-energy diet plan.3-6 This compares favourably with a 3%–7% loss on some other types of diet plans,3-6 although at least one study showed similar short-term weight losses from meal replacements and a prescriptive, structured low-fat diet plan.7 The benefits of partial meal replacements are even more obvious when compared with no treatment. In a 5-year study, an average weight gain of over 1 kg per year occurred in control subjects, compared with a loss of 5.8 kg in men and 4.2 kg in women using partial meal replacements.8 It has been suggested that replacing two meals a day, while maintaining one other main meal, is most effective for initial weight loss, while replacing one meal a day (preferably a meal which is usually high energy, such as lunch or dinner) is enough for long-term maintenance.6 Quick effects from supervised short-term use might be expected to have the added benefit of increasing motivation for long-term lifestyle change. Several studies have also shown improvements in metabolic risk factors with use of partial meal replacement products, exceeding the changes achieved by dietary change alone (even structured low-energy diets).6,8 Partial meal replacements have particular benefits for patients with diabetes.9,10 The effects on glucose control occur within days, and last for as long as weight loss is maintained, enabling a reduction in diabetic medications, but there are also improvements in blood pressure, and serum cholesterol and triglyceride levels (probably more due to the weight loss than the meal replacement per se). Partial meal replacements appear to have an effect across a range of ages and in both sexes (although men generally have better results than women).8,11 They can be used with minimal supervision,11 but are probably most effective when closely supervised with regular follow-up.12 Most studies show greater patient satisfaction and lower drop-out rates with partial meal replacements than with other diets, possibly because use of meal replacements results in less hunger.13 Partial meal replacements also seem effective in people from low socioeconomic backgrounds,14 who are currently more likely to be overweight, and hence in greater need of weight loss treatments.1 Importantly, partial meal replacements are generally cheaper than other diet plans (Box 2), and certainly more so than non-diet meals. Meal replacements are not contraindicated in common weight-related diseases (eg, diabetes and heart disease), but food sensitivities, such as lactose intolerance or food allergies, need to be taken into account when choosing specific products. Which product should I recommend? Selection of a commercial meal replacement product in Australia is complicated by the food standards, product marketing, the different conditions under which the products can be mixed (eg, with milk or water), and confusion with VLCD foods, which are based on total meal replacements, and for which only draft standards exist. There are currently few products that satisfy all requirements for a meal replacement, although some are still promoted as such. For example, low-energy “weight loss” drinks and other (usually supermarket-supplied) products are sometimes labelled to imply they can be used as a meal replacement, despite not meeting minimum Food Standards Australia New Zealand (FSANZ) requirements (Box 1). Box 2 shows a cross section of popular products from different outlets in Australia that meet or approach the minimum standard for nutritionally balanced meal replacements. Partial meal replacements seem to be safe, acceptable to patients, and more effective over the long-term than most other diet-based weight loss techniques, although it is likely that best results will be achieved with the supervision of a clinician skilled in weight control.11 Because most individuals in modern societies consume too much energy in relation to expenditure, there now seems little reason not to prescribe properly constituted partial meal replacements for overweight patients for whom this treatment is appropriate, in line with the emerging realisation that one treatment does not necessarily fit all.15 In fact, with the trend to modern sedentary lifestyles and escalating levels of obesity, it is not difficult to imagine much of our population needing to use partial meal replacements judiciously at some time in the future for prevention or treatment of overweight and obesity. 1 Food Standards Australia and New Zealand requirements for commercial meal replacements2 Meal replacements (minimum requirements per meal) 12 g protein 850 kJ 25% of the recommended daily intake of 16 prescribed vitamins and minerals Very low calorie diets (VLCDs) (draft requirements) 1.7–3.3 MJ per day Omega-3 and omega-6 fatty acids 50 g carbohydrate per day 50 g protein per day Minimum and maximum levels for 24 prescribed vitamin and minerals 2 Characteristics of some examples of commercially available meal replacement products in Australia* KicStart VLCD (Pharmacy Health Solutions) Optifast VLCD (Novartis) Dr MacLeod’s (Orfam) Ultra Slim (Associated British Foods) Availability Pharmacies Pharmacies Doctors, clinics Supermarkets Presentation 24-sachet box 21-sachet box Single sachets Tin of powder Price per meal to patient $2.04 $2.33 $2.65 $1.00 Protein per serve† (g) 17.9 17.3 15.2 4 Carbohydrate per serve† (g) 9.8 15 19.2 20.5 Fat per serve† (g) 3.0 2.3 1.8 2.6 Omega-3 and -6 fatty acids Yes Not listed Not listed Not listed No. of vitamins and minerals 26 27 16 24 Fibre Yes Not listed Not listed Yes Total energy of prepared drink (kJ) 584 (water), 883 (skim milk) 638 (water) 640 (water) 875 (skim milk) Accompanying material on weight loss Yes Yes Yes No Qualifies as VLCD Yes Yes No No * Characteristics apply to the chocolate variety of each product. † Protein, carbohydrate and fat levels are for the dry powder. If directions are to mix with skim milk, levels of protein increase by approximately 7 g, carbohydrate by 10 g and fat by 0.2 g.

Garry Egger BA, MPH, PhD

We recommend screening all infants whose mothers are HCV antibody-positive Perinatal transmission of hepatitis C virus (HCV) is the main source of newly diagnosed paediatric HCV infections in Australia.1 About 5% of infants born to women who are positive for both HCV antibody and HCV RNA during pregnancy will acquire HCV infection.2 The risk of transmission is increased by HIV coinfection during pregnancy. It is estimated that 1%–2% of women of childbearing age in Australia are infected with HCV.3 Assuming that 75% of these have chronic hepatitis and viraemia in the third trimester of pregnancy, we would expect about 75–100 new cases of vertically acquired childhood HCV infection in Australia per year. However, rates reported from national deidentified laboratory data4 and from the Australian Paediatric Surveillance Unit1 are much lower, suggesting that paediatric HCV infection may be underrecognised in Australia. We thus recommend a more standardised approach to identification and follow-up of infants exposed perinatally to HCV. Why identify infants with HCV infection? Although most HCV-infected children have good health for at least the first two decades of life, HCV-induced chronic liver disease and liver failure have both been reported in childhood.5,6 As it is not possible to predict which children will develop severe liver disease, long-term monitoring of HCV-infected children is needed.6 In addition, children identified as HCV-positive should be offered vaccination against both hepatitis A (after 2 years of age) and hepatitis B. Superinfection of HCV-infected individuals with hepatitis A virus increases the risk of fulminant hepatitis and death, while coinfection with HCV and hepatitis B virus is associated with a higher risk of cirrhosis and hepatocellular carcinoma.7 HCV-infected children with severe hepatic involvement should be offered antiviral therapy. A number of treatments (interferon-alfa, ribavirin and pegylated interferon) successfully eradicate HCV in 40%–80% of HCV-infected adults, depending on the HCV genotype. Although data about their efficacy in childhood are limited, these treatments have been used safely and effectively in children. Identifying Australian children with HCV infection could also allow them access to novel therapies and ongoing international multicentre randomised controlled trials.5 Why is HCV infection underdiagnosed in childhood? Children with HCV infection may not be identified for several reasons: They are unlikely to attract medical attention, as most have no symptoms or signs of liver disease, while a small proportion have mild hepatomegaly.1,5 Consequently, their identification relies on careful follow-up of offspring from at-risk pregnancies. Antenatal HCV screening practices vary widely around the country,8 and therefore many HCV-exposed infants are missed. The Royal Australian and New Zealand College of Obstetricians and Gynaecologists recommends universal antenatal screening for HCV.8 However, other national bodies recommend selective testing for HCV infection in pregnant woman with identifiable risk factors (eg, intravenous drug use, tattooing, body piercing, needle sharing, or receipt of blood products or invasive procedures overseas or before 1990 in Australia).8,9 Appropriate methods of testing HCV-exposed infants and children are not widely understood, and national guidelines for testing and follow-up of offspring of HCV-infected mothers8,9 are not detailed or widely known to child health care providers. In children aged under 18 months, persistence of maternal antibody complicates the interpretation of HCV antibody tests, while in infants aged under about 2 months qualitative HCV RNA polymerase chain reaction (PCR) testing is insensitive.10 How should we screen for vertically transmitted HCV infection? For diagnosing perinatal HCV infection, the most cost-effective strategy may be to screen offspring of HCV RNA-positive women. However, as HCV RNA levels can fluctuate in pregnancy, and as antenatal HCV screening practices vary, we recommend: Screening all infants born to women who are HCV antibody-positive, using HCV antibody and liver function tests, at 18 months of age or older. If results are negative, then the infant can be safely assumed not to have HCV infection. If antibody results are positive or liver function is abnormal, then the child should be referred to a paediatric gastroenterologist. Testing infants who are considered unlikely to attend for 18-month follow-up, using HCV RNA and liver function tests at 3 months of age, when they are more likely to be receiving local medical care. Those with positive HCV RNA results or abnormal liver function should be referred to a paediatric gastroenterologist. If both tests give negative results, we recommend repeating HCV antibody testing at age 18 months, as both viraemia and transaminitis can be intermittent in HCV infection. HCV RNA testing for the diagnosis of vertically transmitted HCV infection (in isolation) is not an approved item on the current Medicare Benefits Schedule11 and costs about $90 (ie, six times the cost of HCV antibody testing). Testing for HCV should be performed only after pre-test family counselling and with the consent of the infant’s parent(s) or guardians. There is an urgent need to disseminate clinical practice guidelines in Australia for the screening, diagnosis and management of children born to women with HCV infection during pregnancy. Ongoing collection of national data on HCV infection in children is needed to document the scale of this emerging disease in the paediatric population, and the groups of children at risk of infection. Identification and referral of HCV-infected children will allow early initiation of therapy and monitoring of outcomes.

Winita Hardikar PhD, FRACP · Elizabeth J Elliott MD, FRACP · Cheryl A Jones PhD, FRACP

Objective: To assess the prevalence and impact of overweight and obesity in an Australian obstetric population.Design, setting and participants: The Mater Mother’s Hospital (MMH), South Brisbane, is an urban tertiary referral maternity hospital. We reviewed data for the 18 401 women who were booked for antenatal care at the MMH, delivered between January 1998 and December 2002, and had a singleton pregnancy. Of those women, 14 230 had an estimated pre-pregnancy body mass index (BMI) noted in their record; 2978 women with BMI ≤ 20 kg/m2 were excluded from further study; the remaining 11 252 women were divided into four categories: “normal” (BMI 20.01–25 kg/m2), “overweight” (BMI 25.01–30 kg/m2), “obese” (BMI 30.01–40 kg/m2) and “morbidly obese” (BMI > 40 kg/m2).Main outcome measures: Prevalence of overweight and obesity in an obstetric population; maternal, peripartum and neonatal outcomes associated with raised BMI.Results: Of the 14 230 women, 6443 (45%) were of normal weight, and 4809 (34%) were overweight, obese or morbidly obese. Overweight, obese and morbidly obese women were at increased risk of adverse outcomes (figures represent adjusted odds ratio [AOR] [95% CI]): hypertensive disorders of pregnancy (overweight 1.74 [1.45–2.15], obese 3.00 [2.40–3.74], morbidly obese 4.87 [3.27–7.24]); gestational diabetes (overweight 1.78 [1.25–2.52], obese 2.95 [2.05–4.25], morbidly obese 7.44 [4.42–12.54]); hospital admission longer than 5 days (overweight 1.36 [1.13–1.63], obese 1.49 [1.21–1.86], morbidly obese 3.18 [2.19–4.61]); and caesarean section (overweight 1.50 [1.36–1.66], obese 2.02 [1.79–2.29], morbidly obese 2.54 [1.94–3.32]). Neonates born to obese and morbidly obese women had an increased risk of birth defects (obese 1.58 [1.02–2.46], morbidly obese 3.41 [1.67–6.94]); and hypoglycaemia (obese 2.57 [1.39–4.78], morbidly obese 7.14 [3.04–16.74]). Neonates born to morbidly obese women were at increased risk of admission to intensive care (2.77 [1.81–4.25]); premature delivery (< 34 weeks’ gestation) (2.13 [1.13–4.01]); and jaundice (1.44 [1.09–1.89]).Conclusions: Overweight and obesity are common in pregnant women. Increasing BMI is associated with maternal and neonatal outcomes that may increase the costs of obstetric care. To assist in planning health service delivery, we believe that BMI should be routinely recorded on perinatal data collection sheets.

Leonie K Callaway MB BS(Hons), FRACP · Allan M Chang PhD, FRANZCOG · H David McIntyre MB BS(Hons), FRACP · Johannes B Prins PhD, FRACP

Objective: To compare changes in autonomic nervous activity in healthy senior individuals while walking with and without a dog, and during routine activities at home and periods of interacting with the dog at home.Design: Controlled crossover study.Participants and setting: 13 healthy volunteers (3 men, 10 women; mean age, 67.5 years) who walked in a park adjacent to Gunma University, Japan, and 4 volunteers among these who underwent monitoring in their own homes.Interventions: Heart rate variability was monitored continuously by means of a palm-sized electrocardiographic monitor (which facilitated spectral analysis of the RR interval) while participants walked for 30 minutes (first with, then without, the study dog, or vice versa); three participants underwent this intervention on 3 consecutive days. Four participants underwent continuous monitoring for 6 hours in their own homes, including two 30-minute periods of free interaction with the study dog.Main outcome measures: High frequency (HF) power values of heart rate variability, which is a measure of parasympathetic neural activity.Results: During dog-walking, HF power increased significantly (P < 0.01); this increase was sustained throughout each dog walk, and was more pronounced during succeeding dog walks. At home, HF power was 1.87 times greater when the dog was present, and 1.57 times greater (P < 0.01) than in the walking experiment.Conclusions: Walking a dog has potentially greater health benefits as a buffer against stress in senior citizens than walking without a dog; and, independent of actually walking, merely patting and talking to a dog also raises parasympathetic neural activity. Power spectral analysis of heart rate variability shows promise as a non-invasive approach to quantifying clinicophysiological research on human health benefits possibly derived from interaction with companion animals.

Masahiko Motooka MMS · Nell L Kennedy PhD · Hiroto Koike MD, PhD · Tomoyuki Yokoyama MD, PhD

Objectives: To examine whether children’s television viewing may be a useful indicator of risk of obesity-promoting versus healthy eating behaviours, low-level physical activity (PA) and overweight or obesity among children of primary school entry and exit ages.Design: Cross-sectional study, stratified by area-level socioeconomic status.Participants and setting: 1560 children (613 aged 5–6 years [50% boys], and 947 aged 10–12 years [46% boys]) from 24 primary schools in Melbourne, Australia, randomly selected proportionate to school size between 1 November 2002 and 30 December 2003 .Main outcome measures: Parents’ reports of the time their child spends watching television, their participation in organised physical activities (PA), and their food intake; each child’s measured height and weight and their PA levels as assessed by accelerometry for one week.Results: After adjusting for the age and sex of child, the parents’ level of education, clustering by school, and all other health behaviour variables, children who watched television for > 2 h/day were significantly more likely than children who watched television for ≤ 2 h/day to: to have one or more serves/day of high energy drinks (adjusted odds ratio [AOR], 2.31; 95% CI, 1.61–3.32), and to have one or more serves/day of savoury snacks (AOR, 1.50; 95% CI, 1.04–2.17). They were also less likely to have two or more serves/day of fruit (AOR, 0.58; 95% CI, 0.46–0.74), or to participate in any organised PA (AOR, 0.52; 95% CI, 0.34–0.80).Conclusions: Health practitioners in the primary care setting may find that asking whether a child watches television for more than 2 hours daily can be a useful indicator of a child’s risk of poor diet and low physical activity level.

Jo Salmon PhD · Karen J Campbell MPH, PhD · David A Crawford PhD

Objective: To identify risk factors for dementia in an elderly Australian cohort.Design and setting: A longitudinal cohort study conducted in Dubbo, NSW.Participants: 2805 men and women aged 60 years and older living in the community and initially free of cognitive impairment, first assessed in 1988 and followed for 16 years.Main outcome measure: Admission to hospital or nursing home with any kind of dementia.Results: There were 115 cases of dementia in 1233 men (9.3/100) and 170 cases in 1572 women (10.8/100). In a proportional hazards model for dementia, any intake of alcohol predicted a 34% lower risk, and daily gardening a 36% lower risk. Daily walking predicted a 38% lower risk of dementia in men, but there was no significant prediction in women. The lowest tertile of peak expiratory flow predicted an 84% higher risk of dementia, the upper tertile of depression score predicted a 50% higher risk.Conclusion: While excess alcohol intake is to be avoided, it appears safe and reasonable to recommend the continuation of moderate alcohol intake in those already imbibing, as well as the maintenance of physical activity, especially daily gardening, in the hope of reducing the incidence of dementia in future years.

Leon A Simons MD FRACP · Judith Simons MACS · John McCallum DPhil · Yechiel Friedlander PhD

To provide physical activity recommendations for people with cardiovascular disease, an Expert Working Group of the National Heart Foundation of Australia in late 2004 reviewed the evidence since the US Surgeon General’s Report: physical activity and health in 1996. The Expert Working Group recommends that: people with established clinically stable cardiovascular disease should aim, over time, to achieve 30 minutes or more of moderate intensity physical activity on most, if not all, days of the week; less intense and even shorter bouts of activity with more rest periods may suffice for those with advanced cardiovascular disease; and regular low-to-moderate level resistance activity, initially under the supervision of an exercise professional, is encouraged. Benefits from regular moderate physical activity for people with cardiovascular disease include augmented physiological functioning, lessening of cardiovascular symptoms, enhanced quality of life, improved coronary risk profile, superior muscle fitness and, for survivors of acute myocardial infarction, lower mortality. The greatest potential for benefit is in those people who were least active before beginning regular physical activity, and this benefit may be achieved even at relatively low levels of physical activity. Medical practitioners should routinely provide brief, appropriate advice on physical activity to people with well-compensated, clinically stable cardiovascular disease.

Tom G Briffa PhD · Andrew Maiorana PhD · Noella J Sheerin RN, BAppSc · Anthony G Stubbs · Brian F Oldenburg PhD · Neville L Sammel DDU, FRACP, FACC · Roger M Allan FRACP, FCSANZ, FACC

Many claims about nutrition and weight loss stem from small, short-term studies, incorrect interpretations or distortions of evidence. Our knowledge of what people eat is poor; difficulties include accurate assessment of consumption, the complex composition of foods and individual variations in nutrient bioavailability. When advice appears to be ineffective, poor compliance is a likely explanation. There is no simple solution to obesity, and no fast way to create the energy deficit required for sustainable loss of fat — weight loss requires long-term commitment to permanently change eating and exercise habits. Valid advice is to reduce overall energy intake, include more vegetables, fruits and wholegrain products and fewer foods high in saturated fat, sugar and salt. While mindful of the need to encourage individuals to make changes, the medical profession needs to lead the charge to advocate for changes to our obesogenic environment.

Rosemary A Stanton OAM, PhD

Men seek help and use health services less frequently than women do. Men’s help-seeking practices and health service use are complex issues involving biological, psychological and sociological considerations. Most discussion on men’s help-seeking positions them as reluctant consumers or “behaving badly” with respect to their health. Few studies have explored whether health service providers are equipped to deal with men’s health issues appropriately. The current health system appears not to be tailored to meet the health needs of men. Better collaboration is required across disciplines, to further investigate men’s health using both qualitative and quantitative research methods.

James A Smith · Annette Braunack-Mayer PhD · Gary Wittert MB BS, FRACP

An infant, born at 35 weeks’ gestation to a woman who sniffed petrol, had a cord blood lead level eight times the accepted limit. Treatment with oral dimercaptosuccinic acid promptly reduced his blood lead levels. To our knowledge, this is the first reported case of congenital lead poisoning secondary to maternal petrol sniffing. We suggest that at-risk pregnancies should be identified, cord blood lead levels tested, and chelation therapy and developmental follow-up offered to affected infants. Clinical recordA 27-year-old Indigenous woman, who had sniffed petrol since childhood, presented for antenatal care during her first pregnancy. At the age of 14 years, she had severe lead encephalopathy that led to chronic neurological deficits, including permanent ataxia and memory impairment. Her serum lead levels at 8 and 35 weeks’ gestation were raised at 1.48 and 2.21 μmol/L, respectively (recommended level, ≤ 0.48 μmol/L1). At 35 weeks’ gestation, she went into spontaneous labour and gave birth vaginally to a boy. The infant’s Apgar score was 9 at both 1 and 5 minutes, and birth weight was 2280 g. He was admitted to the special care nursery because of prematurity, and required nasogastric tube feeding because of poor sucking and general sleepiness. On Day 6, the infant developed temperature instability and diarrhoea, with associated dehydration and metabolic acidosis (Box 1). He was treated with 48 hours of intravenous antibiotics and intravenous fluids. No pathogen was grown from blood cultures, urine or stool. Cord blood lead levels were available on Day 10 and were raised at 3.98 μmol/L. No signs of lead encephalopathy were found on examination: muscle tone and reflexes were normal, and there were no signs of seizure activity. Treatment was begun with oral succimer (dimercaptosuccinic acid [DMSA]) on Day 11, at a dose of 10 mg/kg three times daily for 5 days, followed by 10 mg/kg twice daily for 14 days. No adverse effects of chelation therapy (such as vomiting, diarrhoea, fever, rash, or elevated serum transaminase levels) were noted. The infant’s blood lead levels decreased with succimer treatment (Box 2), liver function results remained in the reference range, and his alertness and feeding improved by the 5th day of treatment. At 28 days of age, the infant was feeding well on formula and weighed 3160 g. He was discharged into foster care, and succimer therapy was ceased on Day 35. His growth and development were monitored. At the age of 12 months, he had global developmental delay, with an overall Denver Developmental level of 6–7 months.2 His blood lead levels at 4, 6 and 9 months of age were at least twice the upper acceptable limit (Box 2), although not at the level at which chelation therapy is recommended (> 2.16 μmol/L).3 DiscussionLead exposure in early childhood has long been known to have significant adverse effects on cognitive development.4,5 The National Health and Medical Research Council recommends that lead levels for all Australians be less than 0.48 μmol/L (10 μg/dL).1 However, intellectual impairment is seen in children with lower blood lead levels, and there may be no safe lower limit.6 Chelation therapy is recommended for any child with blood lead levels of 2.16 μmol/L and over.3 Although chelation therapy in early childhood lowers blood levels, recent studies have not shown significant improvement in cognitive and behavioural measurements compared with untreated children.3,4,7 There are a few case reports of neonatal lead intoxication that occurred from maternal exposure to lead through pica, home renovation, or use of contaminated herbal medications.8-10 Petrol sniffing is a form of substance misuse that is widespread in some Indigenous communities in Australia, and is associated with elevated serum lead levels.11 Changing the available petrol to an unleaded form should theoretically lessen the burden of lead toxicity in petrol sniffers. However, the aromatic hydrocarbons in both forms of petrol still cause considerable acute neurotoxicity,12 and petrol sniffers appear to prefer leaded petrol.13 Infants born to women who sniff petrol are more likely to have a birth weight < 2500 g than the infants of non-sniffers, and to require admission to a neonatal nursery for care, although this may be related to other associated lifestyle factors such as smoking and alcohol use.14 Lead freely crosses the placenta and is found in cord blood, amniotic fluid and fetal tissues.8 Cord blood lead levels are often higher than maternal blood levels,8,10 which might indicate preferential placental transfer,8 or be related to the higher neonatal haematocrit.9 In our patient, the cord blood lead level (3.98 μmol/L) was higher than levels in maternal blood collected 2 days before delivery (2.21 μmol/L). Reported effects of congenital lead exposure include intrauterine growth restriction, long-term cognitive problems, and radiographic abnormalities, such as increased bone density at the metaphyses.8,9 Acute neurotoxicity manifested as encephalopathy and peripheral neuropathy has also been described.10 Chelating agents used in the management of lead poisoning include intravenous sodium calcium edetate (CaNa2EDTA) and oral succimer (DMSA).3 Oral succimer is as effective as parenteral CaNa2EDTA.15 It has been previously reported that oral DMSA therapy has not been effective in the chelation of lead in newborns,10 although it is a proven and safe therapy in older children and adults.4,15 In our infant patient, blood lead level decreased spontaneously by 11% (0.45 μmol/L) during the first 10 days of life. After chelation therapy began, serum lead levels fell by 55% in 9 days. No drug-related side effects were noted in the infant.16 This infant did not show clinical signs of acute encephalopathy. His feeding and alertness improved after the start of chelation, but it is uncertain if this was due to falling lead levels or to the normal maturation of the premature infant. After the completion of therapy, serial blood lead levels showed a slow decline, but remained above the recommended level. This was most likely due to a slow release of bound lead from bone,8 but could also have resulted from ongoing exposure to environmental lead. As in similar cases, the infant had global developmental delay at 12 months of age despite chelation therapy.10 Factors other than lead, including malnutrition, recurrent infections and socioeconomic deprivation, might also have contributed to a poor developmental outcome. Petrol sniffing is a significant problem in some Indigenous communities, and it is likely that more infants will be born with lead exposure. Ideally, women who sniff petrol should be identified early in pregnancy. Interventions that might reduce the burden of fetal lead exposure include stopping further petrol sniffing, and giving calcium supplements to the mother to reduce bone resorption, as mobilisation of lead from maternal bone stores is a significant source of fetal lead exposure.17 Chelation agents are contraindicated in pregnancy, and are used only if maternal lead poisoning is life-threatening.8 Cord blood lead levels should be tested in at-risk infants, and chelation therapy given if levels are levels are over 2.16 μmol/L.3 Affected children are at high risk of neurodevelopmental delay. Follow-up and formal developmental assessment is made difficult in remote Indigenous communities by communication barriers, social and economic deprivation, and geographic isolation. Every effort should be made to offer early intervention services, as well as measures to optimise nutrition and general health. 1 Laboratory results for a neonate with lead poisoning and suspected sepsis Reference range* Day 4 Day 5 10:00 13:00 19:35 07:30 Serum levels Sodium (mmol/L) 133–146 140 140 141.6 140 Potassium (mmol/L) 4.6–6.7 4.9 4.5 4.7 4.8 Urea (mmol/L) 1.1–9.1 3.1 2.8 1.3 Creatinine (μmol/L) 56–146 65 65 43 HCO3 (mmol/L) 18–25 12.5 12.8 14.5 21.3 Venous pH 7.35–7.45 7.17 7.19 7.26 7.35 Base excess (mmol/L) − 4 to + 3 − 17.6 − 17.3 − 14.7 − 3.8 Haemoglobin (g/L) 150–170 179 Blood counts (× 109/L)† White cells 5.0–21.0 7.7 Neutrophils 1.5–10.0 1.6 Platelets 150–350 217 * For preterm infant. † Blood film appeared normal for a preterm infant, with no basophilic stippling of red blood cells. 2 Serial blood lead levels in an infant with lead poisoning * Chelation treatment with dimercaptosuccinic acid was given from Days 11 to 29 at a dose of 10 mg/kg, initially three times daily, reducing to twice daily from Day 16. † Maximum acceptable blood level of lead = 0.48 μmol/L. ‡ Urine lead level was raised at 0.82 μmol/L (maximum acceptable level = 0.02 μmol/L).

Suzanna T Powell FRACP · Srinivas Bolisetty FRACP · Gavin R Wheaton FRACP

Clinical record A 65-year-old beef-cattle farmer with a 9-year history of sarcoidosis presented with a 2-year history of depressed mood with cognitive decline, weight loss and vomiting. Treatment with three antidepressant medications had proved ineffectual. After bronchoscopic diagnosis, his sarcoidosis had been treated for the ensuing 9 years with prednisolone (initially 30 mg/day and slowly reduced to 2 mg/day). At the time of initial diagnosis, three sputum samples had stained positive for acid-fast bacilli, and the patient was placed on conventional antituberculous therapy. This was ceased after 3 months, following negative mycobacterial cultures of sputa and bronchoscopic specimens. His family history was unremarkable. On examination, the patient appeared cachectic and older than his stated age. He was vague, with slow speech. Bedside cognitive testing revealed severe memory impairment, with moderate impairment in attention, visuo-constructional ability and executive function. The result of a mini-mental state examination (MMSE) was 17/30. Neurological examination revealed ataxia, brisk tendon reflexes, bilateral habituating palmomental reflexes and proximal weakness. There were no other physical abnormalities. Magnetic resonance imaging (MRI) scans of the brain showed ventricular enlargement, supratentorial white-matter hyperintensities, and extensive leptomeningeal enhancement in the posterior fossa, brain stem and basal cisterns, with extension along the cranial nerves (Figure 1). The MRI results were reported as consistent with neurosarcoidosis. A SPECT (single-photon emission computed tomography) scan, undertaken to differentiate possible causes of dementia, demonstrated global hypoperfusion (Figure 2). Cerebrospinal fluid (CSF) analysis revealed a raised protein level (3.02 g/L; reference range, 0.15–0.45 g/L) and an opening pressure within the normal range. Cryptococcal antigen was detected in the CSF at a titre of 1 : 4. Although India-ink staining for Cryptococcus was negative, Cryptococcus neoformans var. neoformans was isolated on culture. Serum cultures were negative for fungae. Notably, no malignant cells or bacteria (including acid-fast bacilli) were identified from stained smears. Mycobacterial cultures showed no growth after 8 weeks. A number of measurements showed that the patient’s sarcoidosis was stable: serum angiotensin-converting enzyme and 24-hour urine calcium levels were normal; respiratory function testing showed moderate air flow obstruction and gas transfer, with no change from previous measurements; and a chest x-ray (Figure 3) showed no new changes. The patient was diagnosed with cryptococcal meningitis and secondary hydrocephalus. He was initially given antifungal therapy for 4 weeks (intravenous amphotericin B 40 mg a day and oral 5-flucytosine 1.5 g four times a day, followed by intravenous ambisome 200 mg a day when he developed renal impairment with toxic accumulation of 5-flucytosine). Twelve months’ oral fluconazole therapy (400 mg a day) was planned, and a ventriculoperitoneal shunt was inserted. The patient’s mental state had improved when he was re-examined 2 weeks after commencement of therapy (MMSE result, 23/30), and cryptococcal antigen titres fell to levels below detection. The patient’s longer-term course was complicated by worsening confusion, with chronic subdural haematoma and bilateral posterior cranial fossa infarcts seen on MRI scans done at intervals of several weeks. To ensure that inadequately treated cryptococcosis was not contributing to his cognitive decline, treatment with amphotericin B and 5-flucytosine was reinstituted for 3 weeks. Three months after discharge, the patient was well, with moderate cognitive impairment. Sarcoidosis is a multisystem granulomatous inflammatory disorder of unknown cause. It affects the lungs in 90% of affected people and the nervous system in 5%–15%. About 5% of people with sarcoidosis have clinically evident neurological involvement (neurosarcoidosis).1 It most commonly presents as a cranial neuropathy, although other presentations — such as aseptic meningitis; mass lesions in the pituitary, hypothalamus, and other brain regions; spinal and peripheral neuropathy; and epilepsy — may occur. Hydrocephalus is uncommon, but can occur secondary to basal obstruction and may present with a progressive dementing syndrome.2 Neuroimaging may reveal focal lesions or periventricular and leptomeningeal enhancement, but results are often non-specific and do not correlate with disease activity.3 Tests on cerebrospinal fluid (CSF) may show an increased white cell count and/or raised protein and angiotensin-converting enzyme levels, but the CSF is normal in up to a third of patients.4 Steroids are the mainstay of treatment for neurosarcoidosis, but recalcitrant illness may require treatment with cytotoxic drugs and irradiation.5 Given the protean nature of presentation of neurosarcoidosis, it is very difficult to diagnose in patients without a history of systemic sarcoidosis. Furthermore, it may be restricted to the central nervous system in some patients.6 Additionally, in patients with known systemic sarcoidosis, the risk is that any new neurological condition will be attributed to the systemic disease without a new diagnosis being sought.2 Lessons from practice Chronic meningitis may present with atypical depression and/or dementia. Sarcoidosis is associated with an increased risk of infection with Cryptococcus neoformans, independent of immunosuppression. Cryptococcal meningitis is a treatable and reversible cause of dementia. An association has been postulated between systemic sarcoidosis and infection via inhalation of Cryptococcus neoformans, a dimorphic fungus found in soil. While it is well recognised that cryptococcosis is seen in patients with reduced cell-mediated immunity (such as those with AIDS), patients with sarcoidosis may also have an increased risk of infection independent of immunosuppressive therapy. Up to half of patients with sarcoidosis manifest alterations in cell-mediated immunity.7 The annual incidence of cryptococcal meningitis in Victoria is 4.9 cases per million population, which is lower than the national incidence of 6.6 per million.8 It typically presents with meningism and fever, but may masquerade as Alzheimer’s disease or vascular dementia,9,10 and is often complicated by elevated intracranial pressure or hydrocephalus.11 Typical CSF findings are lymphocytic pleocytosis, elevated protein levels, reduced glucose levels, and, commonly, an increased opening pressure. Cryptococcal meningitis is initially treated with amphotericin B, with or without flucytosine, followed by prolonged oral fluconazole.12 While there are data to support the exclusive use of fluconazole, complicated cases with severe presentations, such as that described in the case presented here, should be treated with amphotericin B and flucytosine.13 Cognitive impairment secondary to communicating hydrocephalus in cases of cryptococcal meningitis often responds to treatment with ventriculoperitoneal shunting.11 The differentiation of cryptococcosis from neurosarcoidosis in a patient with known sarcoidosis is difficult, as there is significant clinical overlap between the two disorders. CSF examination in both may show a raised cell count and protein level, and magnetic resonance imaging (as in our patient) may demonstrate non-specific leptomeningeal enhancement and hydrocephalus. In the setting of suspected neurosarcoidosis in patients with cognitive impairment and clinical or neuroradiological suggestion of meningeal involvement, the exclusion of cryptococcal disease through CSF analysis and culture is mandatory. Cryptococcal meningitis is among a range of inflammatory, infectious, metabolic and neoplastic/paraneoplastic conditions that can closely mimic the presentation and course of more established dementing disorders, and which can be diagnosed or excluded by a careful combination of clinical assessment and choice of investigations. Although it often presents with symptoms of meningism, it may progress indolently and lead to cognitive impairment (resulting from hydrocephalus) in more than half of individuals.14 It should be considered as a cause of reversible dementia10 in at-risk individuals — including patients with a history of sarcoidosis — and when its presence is suggested by clinical presentation and/or findings on neuroimaging. 1 Magnetic resonance imaging scans Sagittal view (left), view through posterior fossa (middle), and axial view through hemispheres (right). Sagittal and axial views show ventricular enlargement and global cortical loss; posterior fossa view shows enhancement of the leptomeninges in the basal cisterns as bright white structures. 2 Axial slices of SPECT (single-photon emission computed tomography) scan Scan shows global hypoperfusion. Areas in the cortical rim appear yellow/green (low perfusion) rather than red/white (high perfusion). Ventriculomegaly is visible as enlarged, non-perfusing blue spaces containing cerebrospinal fluid. 3 Chest x-ray Hilar adenopathy characteristic of sarcoidosis was present, but there was no change from previous films.

Siddhartha Deb MB BS · Mark Walterfang FRANZCP · Daniel Varghese MB BS, BMedSci · Bruce Tomlinson FRACP · Dennis Velakoulis FRANZCP · Damon P Eisen MD, FRACP

Frank H Beard,* Jeremy M McAnulty,† John W Tapsall,‡ Angelo M Zaia§ * Senior Medical Officer, Communicable Diseases Unit, Queensland Health, 147-163 Charlotte Street, Brisbane, QLD 4001; † Director, Communicable Diseases Branch, NSW Health, Sydney, NSW; ‡ Senior Specialist in Microbiology, SEALS, Prince of Wales Hospital, Sydney, NSW; § Molecular Biologist, University of Melbourne, VIC. Frank_BeardAThealth.qld.gov.au To the Editor: We report two cases of serogroup B meningococcal disease, caused by genotypically indistinguishable organisms, where transmission is likely to have occurred on a school bus. To our knowledge, transmission of meningococcal disease on a bus has been reported only once before.1 In June 2005, two cases of serogroup B meningococcal disease in teenagers from the same school were reported to the Northern Sydney Public Health Unit. Patient 1 had symptoms of fever, headache, vomiting, and an erythematous rash. Two days after onset of this patient’s symptoms, Patient 2 also developed fever, headache and vomiting. In both cases, diagnosis of meningococcal disease was confirmed by polymerase chain reaction (PCR) testing of cerebrospinal fluid (CSF). CSF cell counts were consistent with bacterial meningitis, but blood and CSF culture were negative, despite lack of prior antibiotic administration. The patients were in different school years. No obvious links, such as common classes, sporting teams, or mutual friends, could be found. However, they reported travelling on the same buses to and from school each day. These buses carry up to 78 students (53 seated and 25 standing) from the patients’ school and other nearby schools. The patients reported that the buses were usually crowded. Chemoprophylaxis was provided 8–9 days after symptom onset in Patient 2 to 132 students who claimed to have travelled on these buses during the exposure period. The two patients recovered fully and returned to school. No subsequent cases of meningococcal disease have occurred at the school. In the absence of meningococcal isolates, porA/porB genotyping2,3 was conducted on the meningococcal DNA contained in the CSF samples, and yielded identical sequences. While genotyping is not routinely conducted, porA/porB sequence nomenclature can be equated with serotype/subserotype (phenotypic expression of porA/porB). All 38 serogroup B isolates to date in NSW in 2005 have had serotyping/subserotyping performed, with no other cases having a serotype/subserotype equivalent to that of the two cases reported here. This supports the school bus as the most likely setting of transmission, given the lack of mutual friends and activities identified between the two cases. Asymptomatic nasopharyngeal carriage of meningococci is common, with about 10% of individuals being carriers at any one time.4 While crowding and close contact increase transmission of meningococci, factors leading to invasive disease are poorly understood.5 Antibiotic chemoprophylaxis is given to close contacts to eradicate nasopharyngeal carriage and limit disease spread.5 However, the absence of further cases among the 132 fellow travellers in this setting does not provide evidence of effectiveness of the chemoprophylaxis, given that the secondary attack rate, even in close household contacts, has been estimated at 2–4 per 1000 people.6 Current Australian guidelines recommend that, in school-based outbreaks, chemoprophylaxis be considered for a wider group than solely close contacts of a household nature.7 This report provides evidence to support chemoprophylaxis in similar circumstances, where linked cases are identified in school bus co-travellers, and no other, more specific natural grouping makes epidemiological sense.

Frank H Beard · Jeremy M McAnulty · John W Tapsall · Angelo M Zaia

David B Preen,* Belinda E S Bailey,† Alan Wright‡ * Research Associate, School of Population Health, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009; † State Manager, Royal Australian College of General Practitioners — Western Australian Faculty, Perth, WA; ‡ Hospital Liaison General Practitioner, Department of General Medicine, Fremantle Hospital and Health Services, Perth, WA. davidpATsph.uwa.edu.au To the Editor: The care of patients at the time of hospital discharge and on returning home is often neglected, and has implications for those needing multidisciplinary care. Research has shown that discharge planning can produce better health outcomes, facilitate the patient’s and the general practitioner’s involvement with discharge care, and improve communication between hospital and general practice services.1-3 To encourage GPs to be involved in discharge care planning for patients with chronic diseases, there are Enhanced Primary Care (EPC)-specific Medicare Benefits Schedule (MBS) Items for contributing as a team member to EPC discharge care planning (Item 728), and for review at 3 months post-discharge (Item 724).4 However, the fact that < 1% of claims for EPC care plans are for discharge-related items has been attributed to barriers to GPs’ involvement in discharge planning, or their unwillingness or inability to initiate such a process rather than simply participate.5 Further, little evidence exists that, given the opportunity, GPs are willing to be involved as a team member in this process. In a recent study of ours investigating EPC discharge care planning for chronically ill patients,3 we required GPs to comprehensively review and comment (in writing) on discharge plans developed by the hospital. GPs also performed a follow-up consultation within 7 days of discharge and completed a questionnaire. We found that 90.1% of 91 GPs in the intervention arm of the study willingly contributed to discharge care planning for their patients, indicating that, when offered input into planning discharge and post-discharge care, GPs are willing to fulfil such a role. Further, this finding, in addition to the high questionnaire response rate of trial GPs (80.6%), indicates the importance of this issue to GPs and the belief that GPs are not sufficiently included in discharge processes. Additional results from a follow-up survey, at 28 days post-discharge, of those GPs who participated in discharge planning (n = 91, 70.3% response) showed that only 42% of GPs claimed the MBS Item 728 ($39.80 in 2002, at the time of the study). Results from a subsequent survey (n = 91, 45.1% response) suggested that even fewer (about 15% of respondents) claimed reimbursement for a 3-month care plan review (Item 724, $98.20), although we do not have data on the number of 3-month reviews performed. The reasons given for not claiming these Items included poor understanding of the Item and claiming procedures, and a belief that excessive administration was required to claim the increasing number of MBS items. In the light of sanctions for administrative claiming errors, this may explain the low claim counts for these Items. However, the most common response was that input into the discharge care plan was, in their opinion, not sufficient to justify reimbursement, even with the extra time required for care plan review and post-discharge follow-up. This suggests that GPs do not simply view EPC discharge care planning as a revenue raising exercise, but rather as quality patient care. Further, it may indicate an undervaluation by some GPs of their role in hospital-driven processes. Considering the evidence in support of discharge care planning for improving quality of care, focus should be directed towards ways of encouraging this process, other than simply providing a financial incentive.

David B Preen · Belinda E S Bailey · Alan Wright

Alan R Clough,* Bart J Currie,† Maymuna W Yunupingu,‡ Katherine M Conigrave§ * Postdoctoral Fellow, Institute of Advanced Studies, Menzies School of Health Research, Charles Darwin University, PO Box 1479, Nhulunbuy, NT 0881; † Professor, and Head, Tropical and Emerging Infectious Diseases Division, Menzies School of Health Research, Charles Darwin University, and Northern Territory Clinical School, Flinders University, Royal Darwin Hospital, Darwin, NT; ‡ Senior Aboriginal Health Worker, NT Department of Health and Community Services, Yirrkala, NT; § Specialist in Drug Health Services, Royal Prince Alfred Hospital and University of Sydney, Sydney, NSW. Alan. CloughATbigpond.com To the Editor: We are concerned that the Northern Territory’s regulations on kava have not succeeded in controlling its availability in Arnhem Land (the north-eastern region of the NT). Under the Kava Management Act 1998 (NT), one wholesaler is licensed to supply kava (Piper methysticum Forst. f.) to four licensed retailers in Arnhem Land Aboriginal communities.1 “Kava Management Plans” in “Kava Licence Areas” permit retailers to supply 600–800 g per week of kava powder to each purchaser1 — more than double the known harmful consumption levels (240–440 g per week).2 Legal kava supplied will reach 26 tonnes in 2005 (worth $3.6 million), with a persistent illegal trade adding 8 tonnes, worth perhaps $2 million (Box). Two proposed additional retail licences1 will increase kava’s availability. Kava’s social and economic effects remain an ongoing concern. The region’s community-controlled health service attributes to kava abuse an accelerated decline in participation in traditional ceremonies and mortuary rites in some localities. Kava is the psychoactive substance with greatest impact on the financial resources of communities and individuals in Arnhem Land.2 Kava’s health effects include seizures and extreme weight loss in heavy users (up to 20% of body mass), similar to that seen in anorexia nervosa.4 Extreme weight loss, evident during the 1980s, has re-emerged in the region’s kava users (M W Yunupingu, unpublished observations). Raised total and low-density lipoprotein (LDL) cholesterol levels4 add to unresolved concerns that heavy kava use may be a risk factor for cardiovascular disease and sudden cardiac deaths. Potential immunosuppressive effects are suggested by relative lymphocytopenia in heavy kava users4 and by increased risk of melioidosis.5 Raised levels of liver enzymes (alkaline phosphatase and γ-glutamyltransferase), which reverse after ceasing moderate kava use, should be monitored because of fatal hepatotoxicity documented in users of manufactured kava products available as natural therapies.6 Given the scarcity of substance misuse treatment services in the region, with no effective treatments for kava misuse, controlling supply is the only practical measure to reduce kava-related harms. Tighter controls on kava supply are urgently required while licensees implement promised demand-reduction and harm-minimisation strategies.1 We recommend that: no further retail licences be granted until kava supply is reduced; retail licensees supply no more than 440 g per week to individual kava consumers; quantities permitted to be imported by the wholesaler and supplied to retailers be limited; kava selling prices be reviewed in the light of trade-offs between higher prices to reduce demand and minimal financial drains on communities; rigorous enforcement be continued to eliminate illegal kava dealing; and the Kava Management Act be reviewed to facilitate these changes. History of kava use and retail value ($ million) on the legal and black markets in Arnhem Land, Northern Territory, since 1982, extrapolated to the end of 2005* * Data on kava supplied were obtained from d'Abbs (for 1982–1993);3 were estimated from population surveys of kava use (for 1994–1997); were estimated from kava seized by Police and Licensing Inspectors (for illegal use, 1998–2005) (seizures were estimated to account for 14% of the illegal kava supplied, based on correlation with population surveys in 1999 and 2000); and were based on the licensed wholesaler’s monthly figures, extrapolated to the end of 2005 (for legal use from May 2002). Retail value was calculated from data on kava supplied and regulated values of $100 per kg (1990–1993), $140 per kg (2002–2004) and $150 per kg (2005), or a black market value of $250 per kg.2 † Approval required from Minister for communities to supply kava. pa = per annum.

Alan R Clough · Bart J Currie · Maymuna W Yunupingu · Katherine M Conigrave

John W Orchard Visiting Fellow, South Sydney Sports Medicine, University of New South Wales, 111 Anzac Parade, Kensington, NSW 2033. johnorchardATmsn.com.au To the Editor: I congratulate Harris et al1 on conducting a survey that identified aspects of specialty training that are difficult for female doctors and doctors with partners and/or children. However, there are some omissions in their article, which, although small, illustrate further ways in which “specialty” training is unfriendly to the aforementioned groups. The authors purported to survey all medical graduates registered in 2002 “with a clinical college training program”. It appears that registrars on the Australasian College of Sports Physicians (ACSP) training program were not included. This training program has been in place since 1992, has been recognised by the Health Insurance Commission since 1999, and is most definitely a “clinical college training program”. Although similar in structure, there are two major differences between the sports physician training program and most other “specialty” training programs; namely, that the training is almost entirely non-hospital based and that the resulting qualification (the FACSP) is not recognised as a “specialty” in Australia. In 2002, I believe that the Australasian College of Sexual Health Physicians was in a similar position to the ACSP, administering a “non-specialty” clinical college training program (which is now under the auspices of the Royal Australasian College of Physicians). The recognised specialties in Australia, with the major exception of general practice, almost all conduct most of their training in hospitals. Not only are these hospital-based positions relatively “female-unfriendly” and “parent-unfriendly”, they don’t adequately train specialists for the majority of doctor–patient interactions, which do not actually take place in hospitals. They also contribute to the reality that our “health” system is focused on treatment of disease rather than prevention.2 Areas such as women’s and men’s health, travel medicine and dietary medicine also exist within our health system.3 Ideally, if we want a health system that is better at actually promoting health, these areas should also have formally recognised training programs. The conservatism of both the Australian Government and the medical profession is reflected in the process for recognising new specialties, which has severely discouraged community-based specialties from being developed. The “choice” of specialty training that Harris et al examined in their study was limited by what was officially sanctioned in 2002. If it were accepted that there should be more recognised specialty postgraduate training positions in community-based fields of medicine, then not only would our medical system start to address its deficiencies in health promotion, but there would be far more attractive training opportunities for doctors who don’t wish to pursue full-time hospital-based positions.

John W Orchard

Ami Schattner,* Noa Ben-Baruch† * Associate Professor of Medicine, † Head, Breast Cancer Unit, Hebrew University Hadassah Medical School, Kaplan Medical Centre, Bilu Junction, Rehovot, 76100, Israel. amiMDATclalit.org.il To the Editor: We describe a patient with malignant ascites and bacterial peritonitis, with no apparent intra-abdominal source of infection. A 56-year-old woman with advanced breast cancer was admitted to hospital with a 10-day history of diffuse abdominal pain, umbilical tenderness, and increasing abdominal girth. Breast cancer had been diagnosed 13 years before admission (T2 N0 M0) and treated with radical mastectomy and adjuvant chemotherapy. Five years before admission, disease had recurred at the chest wall, and 2 years before, liver metastases were found. Chemotherapy had failed, and her only current treatment comprised capecitabine and analgesics. On admission, the patient had tachycardia (110 beats per min), tachypnoea (26 breaths per min), blood pressure of 115/80 mmHg, and no fever or signs of sepsis. Examination showed evidence of local recurrence around the left mastectomy scar, and marked ascites with discoloration, warmth, tenderness and a diffuse infiltration over the umbilicus. There were no signs of peritoneal irritation, nor leg oedema. Blood test results were in the normal range, except for mild leukocytosis (10.6 × 109 cells/L; reference range [RR], 3.8–9.8 × 109 cells/L), with left shift (86% neutrophils, and 6% lymphocytes; RR, up to 67% neutrophils, and at least 32% lymphocytes). X-ray did not show abdominal free air. Abdominal computed tomography revealed ascites, retroperitoneal lymph nodes, omental and umbilical infiltration, and the known liver metastases without signs of portal hypertension. Peritoneal tap removed 2800 mL of fluid. Examination of the fluid revealed a white blood cell count of 2 × 109 cells/L (80% neutrophils), glucose concentration of 790 g/L, and albumin concentration of 22 g/L (serum–ascites albumin gradient, 0.7; a gradient < 1.1 indicates that the patient does not have portal hypertension). Gram stain of the ascitic fluid revealed gram-positive cocci, and culture identified Staphylococcus aureus. Cytological examination showed sheets of atypical enlarged epithelial cells highly suggestive of malignancy. Therapy was begun with parenteral cloxacillin and ciprofloxacin, but the patient died shortly after. This patient’s condition is unlikely to have been spontaneous (“primary”) bacterial peritonitis, which usually occurs in patients with liver cirrhosis, portal hypertension and ascites with high serum–ascites albumin gradient,1 and occasionally in patients with malignant ascites.2 However, in our patient, infection may have originated from the umbilical metastasis. The umbilicus has a direct connection with the intra-abdominal cavity and is also connected to a number of intra-abdominal organs via embryological remnants, such as the umbilical vein and the urachus. Both routes may be involved in the spread of malignant tumour to the umbilicus,3 but spread may also be in the opposite direction, causing peritonitis. This diagnosis may be missed by physicians who may not notice anything new in a patient with longstanding malignant ascites, and may fail to consider bacterial peritonitis, a treatable condition.

Ami Schattner · Noa Ben-Baruch

John C Bridgman,* William F Heddle† * Cardiology Registrar, † Cardiologist, Flinders Medical Centre, Flinders Drive, Bedford Park, SA 5042. cameronbridgmanAThotmail.com To the Editor: A 50-year-old morbidly obese woman (weight, 183 kg; body mass index, 70 kg/m2) presented after 1 month of worsening dyspnoea. Risk factors for cardiovascular disease included hypertension, smoking and previous heavy alcohol consumption. She had left ventricular failure (thought to be due to diastolic dysfunction) and atrial fibrillation with rapid ventricular response. There was no evidence of infection or pulmonary embolism. A transthoracic echocardiogram showed normal systolic function, although the images were poor. Measurement of arterial blood gases showed a compensated respiratory acidosis (Paco2, 58 mmHg; Pao2, 76 mmHg; pH, 7.39; bicarbonate, 34 mmol/L; base excess, 8 mmol/L). Administration of intravenous digoxin, frusemide and heparin led to some symptomatic improvement. Cardiac monitoring showed atrial fibrillation, with ventricular rates of 120–170 beats/minute despite the digoxin treatment. Overnight, 70 pauses in heartbeat of up to 7 seconds were recorded (Box). The constellation of the nocturnal rhythm disturbance, hypercapnia and obesity suggested sleep disordered breathing as a unifying diagnosis. Further questioning revealed symptoms indicative of obstructive sleep apnoea. Polysomnography, performed that night, showed a respiratory disturbance index (number of apnoeic or hypopnoeic episodes per hour) of 130 (normal value, < 15). The longest apnoeic episode was recorded at 34 seconds. The average minimum oxygen saturation was 84% during non-REM (rapid eye movement) sleep and 64% during REM sleep. The lowest saturations reached during non-REM and REM sleep were 64% and 61%, respectively. These results suggested severe obstructive sleep apnoea.1 The following night, her condition improved with application via mask of continuous positive airway pressure (CPAP) at a level of 12 cm H2O using room air. Cardiac monitoring continued to show atrial fibrillation with high ventricular rates, but no pauses in heartbeat occurred. This allowed treatment with atenolol and digoxin to control the ventricular rate. At 6-week review, the patient was complying with home CPAP therapy and felt well. An electrocardiogram confirmed spontaneous reversion to sinus rhythm at 70 beats/minute. There is increasing evidence to suggest a link between obstructive sleep apnoea and atrial fibrillation.2 Obstructive sleep apnoea is also a risk factor for hypertension, coronary artery disease and heart failure, all of which are known to precipitate atrial fibrillation.3,4 Transient heartblock has been found in 10% of patients with obstructive sleep apnoea. Pauses of up to 2 seconds are a predictable physiological response to inspiratory airflow obstruction and hypoxia. These pauses are exacerbated by negative chronotropes. Studies have shown that bradycardia can be effectively abolished with mask CPAP therapy.5 The dramatic response to CPAP therapy in this patient suggests that sleep apnoea caused the significant nocturnal ventricular pauses and had a role in the aetiology of the atrial fibrillation. Overnight cardiac monitor trace, showing atrial fibrillation and a 7-second pause

John C Bridgman · William F Heddle

John D Paull Anaesthestist, Launceston General Hospital, PO Box 200, Exeter, TAS 7275. jdpaullATintas.net.au To the Editor: A black day for the MJA, I thought, on seeing the title of the article by Crotty, “More students and less patients: the squeeze on medical teaching resources”.1 I hesitate, but only briefly, to wave the Fowler brothers’ classic work at you. The revised 3rd edition, by the brothers’ proxy, R W Burchfield, notes that “Regrettable, but prevalent among some standard as well as many non-standard speakers, is the use of less with an unprotected plural noun”.2 He goes on to give examples, among which your article title could well appear, and concludes, “The incorrect use is very widespread and seems likely to be ineradicable, however regrettable that may be”. The author of the Editorial is not discussing an amorphous pile of patients. He is writing about a countable number of people, of which, regrettably, fewer are willing to participate in the education of those they expect to look after them in later life.

John D Paull

Helen Randall Senior Assistant Editor The Medical Journal of Australia In reply: We plead guilty, but knowingly so. When this article was being proofread, there was much discussion about this “regrettable” use of less, but in this instance a catchy title was preferred to following Burchfield’s prescription.1 We take comfort from The Cambridge Australian English style guide, which notes that “using fewer rather than less is . . . a stylistic matter rather than one of correct grammar”.2

Helen Randall

Richard B Hays,* Ian Wronski,† Jan Veitch,‡ Tamara McCloskey§ * Foundation Dean, † Pro-Vice-Chancellor, ‡ Lecturer in Medical Education, § Project Officer, Faculty of Medicine, Health and Molecular Sciences, James Cook University, Townsville, QLD 4811. richard.haysATjcu.edu.au To the Editor: The School of Medicine at James Cook University (JCU) was established in 1999, based on a case that the workforce needs of northern Australia needed to be addressed.1 The model was based in part on other regional medical schools in the United States, Canada and Europe, which had demonstrated that local student recruitment and training could produce graduates who prefer to work in either local or similar regional and rural areas.2 The 6-year undergraduate curriculum at JCU has achieved considerable success in recruiting students from rural backgrounds3 and in developing and delivering a rural curriculum.4 The first cohort of students graduated at the end of 2005, and the intended locations of their internship are now known. JCU students were treated like graduates of other schools by the intern allocation systems within each state. Of 58 graduating students, 51 (88%) have chosen to remain within Queensland, with 29 (50%) in the three North Queensland intern training hospitals, occupying a majority of available intern places in the region. Twelve (21%) will work in other regional hospitals in Queensland and 10 (17%) in a hospital in Brisbane. Seven will work interstate. Furthermore, most of the 37 students of North Queensland origin are staying in North Queensland or adjacent regional centres (only two are leaving Queensland); and about half of the Brisbane-origin and interstate-origin students are staying in Queensland. Hence, while some local students have chosen to move away, some from other states have chosen to stay close to where they moved to study. Forty-two students (72%) responded to a brief survey exploring their decisions. The most popular reasons for choosing the location of their internship were proximity to family and friends, and trying somewhere different from where they had received their training. All but five respondents indicated that they were “likely” or “very likely” to work somewhere in North Queensland in the future, depending on the availability of postgraduate training opportunities. This outcome suggests that the intended workforce mission of the school may be achievable through a combination of selection and curriculum strategies. A longitudinal cohort study is in progress to address longer-term graduate career choice outcomes.

Richard B Hays · Ian Wronski · Jan Veitch · Tamara McCloskey

Robert G Batey Professor of Medicine, Faculty of Health, University of Newcastle, Locked Bag 119, Wallsend, NSW 2287. Robert. BateyAThnehealth.nsw.gov.au To the Editor: The article by Sanson-Fisher and Lynagh on problem-based learning (PBL)1 is very timely, raising important questions about the popularity and efficacy of this method. My “traditional” education included lectures involving 600 students, as well as small-group sessions on the wards and in tutorial rooms. The sessions focused on real patients. Problem-based sessions often deal with videos, at best, and, at worst, paper case histories and laboratory data. I believe the differences between PBL and the standard “curriculum” have been overstated. The quality of the teacher is a critical factor that is understated by proponents of PBL. An excellent teacher can captivate large groups with highly relevant and exciting deliveries, and there is nothing to suggest that such teaching is less effective, stimulating or encouraging than PBL-based teaching. The authors challenge the proponents of PBL to provide evidence that their methodology works. It is also time for those who teach PBL curricula to ask whether this approach is cost-effective. With the knowledge base of medical science increasing exponentially, it is hard to understand how students, without some guidance, can be expected to take on board the complexities of some of the problems that they are faced with. Taking a humane approach and communicating well with patients are commendable goals, but not if they are pursued to the point where patients fail to receive a correct diagnosis and appropriate treatment. Good teaching is provided by good teachers rather than by a particular teaching approach. The PBL system is just as fallible as any other system. I applaud the authors for raising this matter and for asking the questions they asked. I look forward to seeing answers provided in the months to years ahead.

Robert G Batey

Graham D Tracy Emeritus Professor of Surgery, University of New South Wales, PO Box 720, Port Macquarie, NSW 2444. gtracyATbigpond.net.au To the Editor: The two excellent articles in the MJA on an issue important for medical education provided too few strategies for improvement.1,2 First, there is a need for a fundamental attitude change concerning the role of student “doctors”. As long as they are viewed as inexperienced novices, intruding on hapless “guinea pigs”, barriers will always be found to reduce access. Patients should be informed that interview and examination by a student doctor adds much to the discussion of their problem, with real clinical advantage for their care program. Student doctors are usually grateful for the privilege, and should be encouraged to be part of the team, and assured of the value of discussion with nurses, residents and other team members. No additional funding should be needed for such activity. Secondly, as surgical patients are admitted on the day of operation, students should attend the preadmission clinics to help with fuller evaluation. Most teachers would welcome student doctors in their rooms, but this requires planning. It works best when there is a separate examining room for students and patients seeking the added benefit of re-examination. Thirdly, although it is difficult to conduct symptom analysis for someone without symptoms, much value can be obtained from rehearsing specific interrogation and physical examination of all systems in normal people; for example, family and friends. It is not surprising that a few students in exams cannot feel pulses, when they have never tried to feel their own! Fourthly, with modest financial compensation, an army of people with abnormal signs, not in need of treatment, could be recruited for clinical teaching. This task could be assigned to a teaching coordinator, with skills in social interaction, and would need the cooperation of clinical staff.

Graham D Tracy

To the Editor: Goldney and Fisher recently reported data on medication use in an Australian community sample and estimated the financial savings that could be made if the number of prescribed medications was reduced.1 However, the assumption that the average number of medications per patient could be reduced ignores the large body of evidence that has accumulated over recent years demonstrating under-use of beneficial medicines. Under-prescribing has been identified in the management of a broad range of chronic conditions, including heart failure, ischaemic heart disease, hypertension, atrial fibrillation, asthma, osteoporosis, pain, and depression.2,3 It has been suggested that under-use of beneficial therapies may be an even bigger problem than over-prescribing, especially in older patients.4,5 As Goldney and Fisher did not collect any clinical information about their study subjects, no conclusions can be drawn about whether medications were more frequently over-prescribed or under-prescribed. Focusing solely on reducing the number of medications prescribed may be misguided and may result in poorer health outcomes. A broader view of prescribing is required, recognising that problems result from both over- and under-prescribing, as well as inappropriate dose selection and monitoring.5

Rohan A Elliott

Robert D Goldney,* Laura J Fisher† * Professor of Psychiatry, † Research Officer, The Adelaide Clinic, Suite 13, 33 Park Terrace, Gilberton, SA 5081. robert.goldneyATadelaide.edu.au In reply: We agree that, because of our research methodology, we could not necessarily assume that any medication prescription was inappropriate, and we noted that on two occasions. However, our economic analysis addressed only those people using six or more prescribed medications (mean, 7.8), and we reported multiple use of same-class medications, and, at times, use of two different preparations of the same medication. Therefore, we believe our estimate of potential cost savings to be conservative. Nevertheless, we accept that our hypothesis needs more formal testing using clinical data.

Robert D Goldney · Laura J Fisher

CorrectionRe: “Is the Australian hospital system adequately prepared for terrorism?”, by Jeffrey V Rosenfeld, Mark Fitzgerald, Thomas Kossmann, et al, in the 5/19 December issue of the Journal (Med J Aust 2005; 183: 567-570). One of the coauthors’ names was incorrectly listed in the print issue as “Andrew Joseph”. His correct name is “Anthony Joseph”. The html and pdf versions were correct when published.

Jeffrey V Rosenfeld FRACS, FRCS(Edin), FACS · Mark Fitzgerald FACEM · Thomas Kossmann MD, FRACS · Gim Tan FACEM · Michele Gardner RN, GD, FRCNA · Andrew Pearce FACEM · Anthony Joseph FACEM · Shmuel Shapira MD, MPH

CorrectionRe: “The use of cusum analysis in the early detection and management of hospital bed occupancy crises”, the research article by Claire M Burns, Cameron J Bennett, Colin T Myers and Michael Ward, in the 19 September issue of the Journal (Med J Aust 2005; 183: 291-294). The first row of data in Box 1 should have read No. of samples (referring to the number of days in each 6-month study period, with one set of measurements being made each day), rather than No. of patients. The html and pdf versions were correct when published.

Claire M Burns RN, BNursing · Cameron J Bennett MB BS, FRACP · Colin T Myers MB ChB, FACEM · Michael Ward MB BS, FRACP

Carel van Gend died of bowel cancer at his home on the Clarence River, in northern New South Wales, on 18 June 2005, after 27 years as a Consultant Physician to Grafton Base Hospital. Carel was born in South Africa on 24 March 1933. He distinguished himself at Rondebosch Boys’ High School for winning the mile — but in the slowest winning time on record. He graduated from Cape Town University in 1957, at a high point in that medical school’s fame. Among his anecdotes he recalls being instructed in donning surgical gloves by Christiaan Barnard, and notes that the link between dietary cholesterol and heart disease was clarified through Cape Town’s racially segregated Groote Schuur Hospital. Rejecting the prevailing racism, Carel spent his first decade working in black African hospitals. Two years after graduation, he was the sole doctor at a remote hospital in Northern Rhodesia. Five years there saw his marriage to Margaret Moffat and the births of two children. Over the next 14 years, he held hospital positions in South Africa, England, Scotland, Malawi, Canada and New Zealand. In 1978, Carel moved to Grafton, New South Wales, where he worked as a private and hospital physician and obtained his Fellowship of the Royal Australasian College of Physicians. He initiated a bowel-cancer screening campaign with support from the local Rotary Club and raised funds for the Life Education van. He also served on the NSW Medical Board’s Area of Need Panel from 1999 to 2005, assessing overseas-trained doctors for hospital positions and giving valuable advice to those who would be working in country hospitals similar to his own. His down-to-earth approach to medical problems ensured that those recommended for registration would be adequately prepared for those jobs. In his leisure time, Carel was a keen squash player, amateur actor, Rotary Club member, and president of the local arts festival. He dabbled in breeding exotic cattle, and for several years guided his own “Cattlemen’s Study Tour” of Central Africa. Carel will be deeply missed by colleagues, friends, and family around the world. He is survived by Margaret and their three children, Marie, David and Anne.

David van Gend MB BS, FRACGP, DipPallMed

The last well person. How to stay well despite the health-care system. Nortin M Hadler. Montreal: McGill-Queen’s University Press, 2004 (viii + 313 pp) ISBN 0 7735 2795 8. Somewhat paradoxically, reading this book left me disturbed and critical, despite my wholehearted agreement with most of the imperatives presented in this critical analysis of modern medical practice. The basic message is accurate and important: too many with minor ailments who enter the health care system are convicted of being ill when in fact they are healthy. Well people, Hadler suggests, are those individuals yet to be investigated by a doctor! The health care system is, he argues, poorly evidence-based in far too many areas. Over-diagnosis and the reflexive resort to the prescription pad, rather than reassuring dialogue, is endemic. There is much truth in this of course, but he “doth protest too much, methinks”. For example, Hadler’s views on modern cardiological practices fail to avoid the bias and selective reporting of data he so strongly criticises in others. Individuals with suspected angina are advised to enter into a contract with their doctor that will exclude both angiography and bypass surgery as diagnostic or therapeutic options. In warning patients that much of what a doctor recommends may be of questionable benefit, he fails to educate the lay reader of the possible advantages of early diagnosis and intervention in a person who indeed still feels “well”. Hadler tells us that the book is written for those who are well but nonetheless tempted to stray into a doctor’s office from which they will undoubtedly emerge medicalised. In fact, the contented well are unlikely to pick up this volume while the worried well are unlikely to be persuaded that their concerns are baseless. No, this book is one for students and practitioners of clinical medicine. It is laudably academic in discussing most of the topics covered, with an extensive bibliography and no less than 56 pages of annotated critiques of the studies that, when analysed accurately, support the author’s contentions. Being challenged to re-analyse investigative and therapeutic approaches that are entrenched but by no means evidence-based is, of course, no bad thing, nor hardly revolutionary. Hadler’s challenge to improve statistical analysis to provide outcomes that are undoubtedly clinically relevant is welcomed. Meta-analyses and the Cochrane library have not served our patients well, he argues, wanting us to better define real rather than relative risk. A rheumatologist, Hadler is perhaps at his best when discussing the myriad dubious approaches to the management of musculoskeletal discomfort, turning many patients into invalids entangled in a nightmare of medico-legal wrangling. Such patients, he argues, will receive more help from their therapist than their pharmacist. It is modern medicine’s emphasis on investigations and pharmacy that is driving many patients, who want to ventilate their problems, into the offices of unscientific “alternative” practitioners. Hadler is on shakier ground when he argues that most of us have genes that program us to live for 85 years (plus or minus a few), and will do just that whether or not we treat high cholesterol or moderate hypertension. He doubts the ability of human strategies to have us live longer (a brave assumption given the remarkable increases in longevity achieved even in the post-antibiotic era), and opines that we have made too much of the obesity epidemic in modern societies. He argues that our approach to the diagnosis and management of prostate cancer is often too aggressive, but fails to call for better decision-making that may well save the lives of many who currently die in much discomfort from this malignancy. I’m glad I read this book and have no hesitation in recommending it. We have a long journey ahead of us before we consistently avoid the pitfalls forthrightly identified by Hadler. Doing so will give us our best chance of having many more people remain chronically well because of rather than despite the health care system. John M DwyerEmeritus Professor of Medicine, Sydney, NSW

John M Dwyer

SIDS: dummies reduce risk Sleeping with a dummy (pacifier) is linked with a reduced risk for sudden infant death syndrome (SIDS), according to US researchers. In a case-control study, they examined the use of a dummy the night before death in 185 SIDS cases and 312 non-SIDS infant deaths. Not only was there a 90% reduction in risk for SIDS in infants who had used a dummy during their last sleep — use of a dummy also seemed to reduce the influence of other known risk factors in the sleep environment, such as sleep position and co-sleeping with a mother who smoked. The researchers say that promoting the use of a dummy when an infant is sleeping may be an effective public health measure in further reducing the incidence of SIDS. BMJ Online First, 9 Dec 2005 World first finds favour A Lancet editorial says that the French team that recently performed the world’s first partial facial transplant had taken a cautious and justifiable first step in exploring the potential of facial transplantation.1 A team of nearly 50 people and 8 surgeons used the nose, lips and chin from a brain-dead living donor to repair the face of a 38-year old woman who had been mauled by a dog.2 The woman had been unable to eat, talk or breathe without difficulty. According to press reports, the patient was unlikely to benefit substantially from standard restorative surgery and had been prepared psychologically for the operation and its aftermath. Recognising key concerns, among them, the use of a potentially life-threatening procedure to treat a disfigurement, the Lancet said “. . . the time comes when enough is known to do an experiment and when an experiment may be the only way to answer the questions that remain”. 1. Lancet 2005; 366: 1984 2. BMJ 2005; 331: 1349-1350, 1359 Botox for tennis elbow? Botulinum toxin injection has shown some promise as a short-term treatment option for some patients with tennis elbow, according to Hong Kong researchers. They conducted a small randomised trial in 60 patients with lateral epicondylitis, comparing the effects of giving a single injection of 60 units of botulinum toxin type A (Dysport) with a normal saline placebo injection. Over a 3-month period, botulinum toxin led to greater pain relief than placebo; however, adverse effects of digit paresis and weakness of finger extension were noted. Although botulinum toxin has now been used in various pain syndromes, its exact mechanism for relieving pain remains unknown. Ann Intern Med 2005; 143: 793-797 Holiday fare In the movie Heartbreak Ridge, Clint Eastwood exhorted marines under his command to “adapt, improvise and overcome” when faced with a challenging situation. Clint would be proud of Canadian doctors Keegan and Bannister. Faced with a case of bilaterally impacted “cement-like” ear wax while holidaying on a rural island, they found no syringe readily available. A resident engineer referred them to his grandson, who kindly provided a super-duper water pistol. With the patient dressed in swimming shorts and holding a Tupperware container in lieu of a kidney basin (see Figure), the water cannon (operated by an emergency physician) cleared both ears of the offending wax in seemingly record time and without damage to the ear. Keegan and Bannister are calling for a trial. However, “despite what bush-mad physicians may get up to on their private islands”, CMAJ (and the MJA) do not endorse this use of a water pistol. Do not try this at home (or in Australia). However, by all means, enjoy your vacation! CMAJ 2005; 173: 1496-1497 Death by cannabis? Driving under the influence of cannabis increases the risk of having a fatal car crash, say French researchers. In a case-control study, they examined the use of cannabis in 6766 at-fault drivers in fatal crashes and 3006 not-at-fault drivers involved in fatal crashes. Cannabis users were about three times as likely to be responsible for a fatal car crash as drivers who didn’t use cannabis. Further, a dose effect was evident, suggesting that cannabis use may actually cause crashes. BMJ Online First, 1 Dec 2005 Antipsychotic agents and the elderly: more bad news Recently, the US Food and Drug Administration and Health Canada advised that atypical antipsychotic agents, such as risperidone and olanzapine, may lead to increased mortality among elderly patients with severe dementia.1 Now, US researchers have suggested that older, conventional antipsychotic agents may be just as dangerous, if not more so, in any elderly patient.2 They conducted a retrospective cohort study of 22 890 patients, 65 years of age or older, who had begun receiving either type of agent for any indication. Conventional agents were linked to a higher short-term risk of death than atypical agents — the greatest risk was within the first 40 days of use and with higher doses. 1. Med J Aust 2005; 183: 216 2. N Engl J Med 2005; 353: 2335-2341

Ann Gregory