Letters

To the Editor: It has been claimed that patients are missing out on the most effective current treatments if they are not given an opportunity to enrol in clinical trials. Such statements are misleading and have the potential both to create concern in those without access to trials and to reduce the likelihood of true informed consent for involvement in trials. Trials are, by definition, just that — trials. Treatment in the “innovative” arm(s) may result in worse outcomes. The finding that those involved in trials have a better outcome (eg, 5-year survival) may have numerous explanations. It is unlikely that the innovation is an adequate explanation for the finding — confounding factors such as selection bias, adherence to best current practice, and intensity of monitoring are more likely explanatory factors. Furthermore, it is important to focus on other outcomes of therapeutic endeavour, such as quality of life, and the impact of the illness on other family members. Patients who live some distance away from tertiary referral centres or trial centres may have a greater adverse effect from involvement in a trial than other patients who live close to such centres. Well designed trials are a crucial part of advancing medical therapeutics. However, the recent editorial by Cole1 and the article by Mitchell and colleagues2 in the Journal have been picked up by the news media as demonstrating that only through involvement in clinical trials can patients get best-quality care. It is not surprising that this is the way that the message has been received. The truth is importantly different. It is only through the conduct of clinical trials that best practice can be defined. However, patients anywhere in the country should be able to access current best-practice treatment even if they do not want to be involved in a clinical trial. Encouragement to participate in clinical trials should be based on arguments about the “greater good” and not about issues of quality of care. To use the latter as the basis for argument must be seen as coercion and as unethical.

Alex N Thomson

In reply: Thomson is correct in stating that patients involved in clinical trials have better 5-year survival rates when compared with patients not recruited into clinical trials. There may, as Thomson points out, be numerous possible explanations for this finding. Nonetheless, this improvement in survival is well documented and has been recognised for some time.1 Although it is becoming increasingly important to focus on other therapeutic outcomes, such as quality of life, it is incorrect to assume that involvement in clinical cancer trials equates to impairment of quality of life and an increase in adverse effects. In fact, the primary end-point of numerous clinical cancer trials is improved quality of life.2 We agree with Thomson when he states that patients anywhere in the country should be able to access current best-practice treatment. We agree that best-practice treatment can only be defined through the conduct of clinical trials. Hence, well designed clinical trials are necessary, and indeed crucial, to the advancement of cancer therapy. In the context of adolescents and young adults with cancer, the lower than expected improvement in survival may be explained, in part, by a low rate of participation in clinical trials.3 There is no doubt that participation in late-phase clinical trials provides a “benchmark” and ensures the provision of quality medical care. Rural and regional settings should not, a priori, be a barrier to trial participation. Adequate infrastructure and support should be available for such centres to participate. Greater cooperation between all adult and paediatric clinicians involved in the care of adolescents and young adults with cancer is essential to ensure that the inequity in survival is corrected.

Anne E Mitchell · Deborah L Scarcella · Gemma L Rigutto · David M Ashley · Vicky J Thursfield · Graham G Giles · Maree Sexton

John Orchard,* Caroline Finch† * Sports Physician, Sports Medicine Unit; † Director, NSW Injury Risk Management Research Centre, University of New South Wales, 111 Anzac Parade, Kensington, NSW 2033. johnorchardATmsn.com.au To the Editor: We agree with very few of the conclusions in the recent article by Mitton et al.1 It is fascinating that the authors single out elite athlete funding as being the only notable area of discretionary government spending that prevents more from being spent on healthcare. We suspect that the authors share the widely-held view within the healthcare professions that sport is an indulgence rather than a contributor to the good health of this nation. Sports medicine is the only recognised branch of medicine in Australia that is considered an “area” of medicine (all other recognised branches being considered “specialties”), a view held by both the Health Insurance Commission and the Australian Medical Association. Therefore, an Australian athlete who suffers a sports injury and is referred to a sports physician receives lower Medicare rebates for the visit than all other patients referred elsewhere in the system, and is unable to claim any Medicare rebate if he or she requires a magnetic resonance imaging scan for an injury, again the only such example in the Australian healthcare system.2 Injuries which occur as a result of traffic accidents, workplace accidents, falls, assaults and suicide attempts are all monitored by various government departments, with priority funding specifically directed towards their prevention. The federal government in Australia directs no funding towards sports injury monitoring or prevention3 and does not devote sufficient resources towards making the population more active.4 The article by Mitton et al ignores the concept of efficiency (in terms of prolonging life) within healthcare spending. Health promotion and prevention of illness and injury are far more efficient ways of prolonging life than treating existing disease (compare smoking cessation programs with coronary care units). Lack of sport and exercise is an increasingly prevalent risk factor for major diseases.4 The use of elite athletes as role models may or may not contribute to a more active population — we suspect the former. We also believe that the disrespect shown within the Australian healthcare system towards sports injuries (compared with other injuries and illnesses) is a major disincentive for Australians to become more active. This is a disincentive for which we will pay a high penalty in terms of decreased life expectancy and increased healthcare costs in the future.

John Orchard · Caroline Finch

Craig R Mitton,* H Dele Davies,† Cam Donaldson‡ * Assistant Professor, Department of Health Care and Epidemiology, University of British Columbia, 4480 Oak Street, E414 A, Vancouver, BC V6H3V4, Canada; † Professor, Pediatrics and Human Development, Michigan State University, USA; ‡ Professor, School of Population and Health Sciences and Business School, University of Newcastle, UK. cmittonATcw.bc.ca In reply: We thank Orchard and Finch for their letter about our article comparing spending on the Sydney Olympics to expenditure on healthcare for Australia, Canada and Britain.1 The reason we “singled out elite athlete funding” was simply to choose a high profile expenditure as an illustration that government does indeed make decisions about priorities with the limited societal resources available. While we would strongly agree, and in fact state, that “spending more on athletics may improve the health of the population”,1 the necessary public debate about how societal resources should be best spent is lacking. In our view, such a debate should be informed by the costs and wide-ranging benefits of government expenditure and be based on clearly articulated public values. Contrary to the claim that we “ignore the concept of efficiency”, it is precisely here, when costs and benefits of alternative claims on limited resources are explicitly compared (both within healthcare and across government sectors), that the notion of efficiency is addressed.2 Upstream investment in promotional activities may well be an appropriate way to spend health and non-health dollars — let’s just make these choices, and the underlying values, explicit.

Craig R Mitton · H Dele Davies · Cam Donaldson

Donald M Clark Obstetrician, PO Box 503, Mount Lawley, WA 6929. To the Editor: Giles et al1 have “poisoned the well” for future research by attacking the obstetricians who took the trouble to help them with their study on management of hepatitis B virus (HBV), hepatitis C virus (HCV) and HIV. Many of the discrepancies noted between current practice and the recommendations/guidelines are easy to explain: Failure to screen. Many obstetricians were told that it is discriminatory to screen for HIV and HCV without extensive pretest counselling. The advice is obsolete, but old habits die slowly. Failure to recommend caesarean section for women with HIV. Many obstetricians have never seen a case of HIV and would most certainly phone for advice if the situation arose. Failure to promote breastfeeding. Many obstetricians leave advice on breastfeeding to the midwives and paediatricians. However, the article does concede that mother-to-baby transmission is a theoretical risk, so patients are entitled to be informed. Failure to adhere to guidelines. Many obstetricians regard guidelines issued by the Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG) as just that — guidelines, not gospel.

Donald M Clark

Dale W Hanson,* Herbert R Sadlier,† Reinhold Muller‡ * Tom and Dorothy Cook Research Fellow, James Cook University; † Director, Emergency Department, Mackay Base Hospital, PO Box 5580, Mackay Mail Centre, Mackay, QLD 4741; ‡ Associate Professor, School of Public Health and Tropical Medicine, James Cook University, Townsville, QLD. dwhansonATmackay.matilda.net.au To the Editor: It has been argued that reduced levels of bulk billing have resulted in emergency department (ED) overcrowding due to an increase in non-emergency, primary care ED presentations.1 In the 2001–02 financial year, Queensland EDs experienced a 7.1% growth in caseload compared with 2000–01 (Mr D Searle, Surgical Access Team, Queensland Health, personal communication, Nov 2002). During the same period, there was a 1.5% decline in the proportion of general practice services bulk billed in Queensland. Before December 2000, no dedicated general practice bulk-billing clinics existed in Mackay. The opening of two bulk-billing clinics, one within 1 km of Mackay Base Hospital, provided an opportunity to assess the effect of the increased availability of bulk-billing services on ED presentations. The Mackay region had a full-time-equivalent GP : patient ratio of 1 : 1648 in 2002, compared with a Queensland average of 1 : 1143.2 In the September quarter of 2000, 58.4% of GP consultations were bulk billed in Mackay, compared with 85.7% in Brisbane (Ms D-A Kelly, Federal Member for Dawson, personal communication, Jun 2003). The Mackay Base Hospital ED provides 24-hour, 365-day emergency medical services to the Mackay region, and managed 34 558 presentations in the 1999–00 financial year, admitting 15% of its caseload. On the Australasian Triage Score (ATS) classification, 0.2% of presentations were category 1, 4% category 2, 20% category 3, 54% category 4, and 21% category 5. Since the bulk-billing clinics were established, there has been an average of 237 extra bulk-billing consultations per day, with a resultant 7.3% increase in the proportion of GP consultations bulk billed in the federal electorate of Dawson (Ms D-A Kelly, Federal Member for Dawson, personal communication, Jun 2003) (91% of the electorate lives in the Mackay region). However, ED presentations have remained stable, with a median 93 presentations per day (Box). Changes in the proportion of ATS 3, 4 and 5 presentations were observed (25%, 55% and 14%, respectively), but were associated with internal organisational changes (shifting surgical and orthopaedic dressing clinics out of the ED and into the outpatient department, and a review of triage policy), and cannot be reliably attributed to the influence of the bulk-billing clinics. In Mackay, the implementation of two bulk-billing GP clinics did not result in a measurable reduction in the absolute number of ED presentations. These results are consistent with previous studies that suggest that non-emergency, primary care ED presentations are not a major determinant of ED overcrowding.3 Effect of general practice bulk-billing presentations on average daily emergency department presentations, Dawson electorate, Queensland

Dale W Hanson · Herbert R Sadlier · Reinhold Muller

Ian F Knox President, Australasian College for Emergency Medicine, 34 Jeffcott Street, West Melbourne, VIC 3003. iknoxATgil.com.au Comment: The report by Hanson et al1 comes at an important time in the debate regarding emergency departments, especially at the onset of winter, a time of high demand and stretched resources. The authors describe the effect of the opening of two bulk-billing clinics on attendances at the emergency department (ED) of a provincial Queensland hospital. Despite the clinics seeing 2.5 times the number of patients seen at the emergency department each day, this resulted in no reduction in ED attendances. This should give pause for thought to those who maintain there is a simple and direct relation between the level of bulk billing of general practitioner services and ED workloads. The nature of the relation between GP services and ED attendances has never been clearly defined, but it is likely to be complex. Similarly, the nature of ED workloads is also complex, and more than just a matter of the total attendances.2 In the Journal last year, Cameron and Campbell cited the major causes of access block and overcrowding as being the reduction in hospital beds and aged care facilities, along with changes in workforce and community attitudes.3 In that issue, the Journal published a series of articles that essentially represented a national audit of responses to ED overcrowding. Only one article described the opening of a GP clinic as a response; the authors noted that this was unsuccessful in reducing access block.4 Thus, the findings of Hanson and colleagues are neither new nor surprising. Overcrowding is the single most important barrier to quality in ED care. It is a symptom of a serious and growing mismatch between demand and supply for acute healthcare services. Solutions require a whole-of-systems approach. Efforts to improve the flow of patients through acute-care hospital beds are needed, as are strategies to divert some current inpatient flow to community-based subacute services. There is an important role to be played by GPs in coordinating the management of patients with chronic and complex health problems, to reduce the demand for acute-care admissions to hospital, and in working in partnership with the acute-care sector in coordinating community-based subacute alternatives to hospital care. Such initiatives will only come about if state and Commonwealth governments and health departments work together.

Ian F Knox

Elizabeth J Comino Senior Research Fellow, School of Public Health and Community Medicine, University of New South Wales, Liverpool Hospital, Liverpool, NSW. E. CominoATunsw.edu.au To the Editor: The Australian Bureau of Statistics recently released details of asthma mortality for 2002. These figures indicate that asthma mortality has continued to decline in 2002 and that deaths in young people aged 5–34 years are at their lowest level since the early 1950s (Box). In this age group, the number of deaths fell from 43 in 2001 to 33 in 2002 (a 23.3% drop), and for all ages the number of deaths fell from 422 in 2001 to 397 in 2002 (a 5.9% drop). This suggests that the various asthma awareness activities, spearheaded by the National Asthma Council and other interest groups, have been successful in raising awareness of asthma and its management. Or does it? Emerging evidence suggests other changes in the epidemiology of asthma in Australia. Robertson recently reported a 26% decrease in the prevalence of asthma in Melbourne school children between 1993 and 2002, but increased reporting of rhinitis and eczema over the same period.1 The significance of these findings is difficult to interpret without measures of airway function. A second study supported these results and also observed a small decline in the prevalence of parent-reported asthma, but found little change in atopy or airway hyperresponsiveness.2 Age-adjusted hospital separation rates for asthma decreased by 31.1% in young people and 31.4% in all ages between 1989–90 and 1999–00.3 There is little evidence of improved management of asthma in the general practice setting. Data published from the BEACH (Bettering the Evaluation and Care of Health) survey of general practice activity indicates a significant reduction in rates of presentation for asthma among children but not adults, with no changes in indicators of severity over time.4 Our recent research in south-western Sydney, examining uptake of the “asthma 3+ visit plan”5,6 by general practitioners and their patients, is disappointing. It suggests reluctance on the part of both GPs and patients to participate in the plan. Clearly, there remains much that we do not understand about the natural history of asthma.7 We need to continue to monitor asthma through regular surveys and routine data collection in order to understand more about fluctuations in asthma prevalence, the relationship to changing child-rearing practices (such as use of childcare facilities) and the impact of management practices. Asthma mortality in Australians aged 5–34 years, 1920–2002* * Points on the graph represent 3-year “moving” averages — for example, the 2001 value is the average of 2000, 2001 and 2002 data; the 2000 value is the average of 1999, 2000 and 2001 data, etc. This technique is used to smooth annual fluctuations that occur in data of this kind.

Elizabeth J Comino

John R Gowardman,* Maria Brosnan,† Joy Whiting,‡ Peter Collignon§ * Intensive Care Physician, † Medical Student, ‡ Data Manager, Intensive Care Unit, § Director, Infectious Diseases Unit and Microbiology Department, The Canberra Hospital, PO Box 11, Woden, ACT 2607. peter.collignonATact.gov.au To the Editor: In most serious infections associated with intravascular devices, the device is a central venous catheter (CVC).1,2 Good clinical practice dictates that these devices should be removed when no longer needed.3 Our intensive care unit maintains a clinical practice of prompt removal of CVCs once they are no longer required. In addition, CVCs are to be removed before patients are discharged from the unit (for “general” patients) or within 24 hours (for cardiothoracic surgical patients). We conducted an audit to determine how often this practice was followed and whether it had unintended adverse clinical consequences (eg, need to reinsert a CVC). The audit was conducted over 8 weeks in 2001 and included 126 CVCs in 103 patients. Fifty-eight CVCs (46%) were removed by the predetermined time, and 68 (53%) were retained past this time (Box). The data demonstrated: Low removal rates, with 31% (23/74) of CVCs removed in general patients, but higher rates in cardiothoracic surgical patients (67%; 35/52). APACHE II scores, ventilation times and lengths of stay in the intensive care unit were similar in the group who had the CVC removed and the group who retained the CVC, implying that severity of illness was not a factor biasing retention. Among patients who had a CVC removed, none had another CVC reinserted; cannulation rates with short peripheral catheters were low and acceptable. Retention of the CVC past the predetermined time resulted in significant prolongation of CVC in-situ time (eg, general patients 7.0 v 3.2 days). The reason given for CVC retention in general patients was antibiotic administration for 37/40 (93%) (vancomycin, 6; β-lactams, 20; aminoglycosides, 9; and quinolones, 2), while total parenteral nutrition and poor peripheral access were factors in only seven (18%). In the 13 cardiothoracic surgical patients, the reason given was inotrope infusion in four (30%) and amiodarone infusion in four; no reason could be ascertained in the other five. Two issues emerge from this audit. Firstly, there did not appear to be good reasons for retaining many of these CVCs. Drug therapy was most often quoted, but many of these drugs (antibiotics and amiodarone) could have been safely administered via a short peripheral intravenous cannula, with markedly lower risk of infection.2-5 We believe that when a patient left the intensive care unit with a CVC, it most likely remained in place as a “convenience” factor for busy nursing and junior medical staff on the wards. However, this was at the cost of a significant increase in CVC in-situ times, increasing the risk of both mechanical and infectious complications. Secondly, implementation of predetermined CVC removal appears safe in our hospital. Although removal rates were lower than expected, nearly half of all CVCs inserted over the 8-week study period were removed as per “clinical practice”, without any need for CVC reinsertions. We have now further refined our clinical practice and introduced a formal written policy that: All CVCs should be removed and replaced with a suitable alternative before patient discharge from the intensive care unit, unless there is a specific indication for retention. Retention of a CVC should be based on simple guidelines, such as need for total parenteral nutrition, poor peripheral venous access, or use of drugs that require central access. We recommend implementation of this simple policy in other intensive care units. Characteristics of patients and central venous catheters (CVCs) in the audit General ICU patients Cardiothoracic patients CVC removed CVC retained P CVC removed CVC retained P Number of patients 20 40 30 13 Number of CVCs 23 51 35 17 APACHE II score (mean [SD]) 14 (3) 16 (6) 0.13 13 (4) 13 (2) 1.00 Length of ICU stay (d) (mean [SD]) 3.9 (5.4) 2.4 (3.5) 0.2 1 (0) 2.1 (3.7) 0.1 Ventilation time (h) (mean [SD]) 61 (86) 47 (51) 0.5 17 (3.5) 20 (15.6) 0.3 % Of patients ventilated* 60% 41% 100%‡ 100%‡ CVC in-situ time (d) (mean [SD]) 3.2 (3.2) 7.0 (5.6) 0.003 2.1 (0.25) 4.5 (3.8) 0.001 Number of peripheral IV catheters† (mean [SD]) 1.8 (1) 0.6 (0.6) < 0.001 0 0.07‡ Number of CVCs reinserted 0 na 0 na ICU = intensive care unit. IV = intravenous. na = not applicable. * Mechanically ventilated in the intensive care unit. † At 7-day follow up. ‡ Only one peripheral catheter was inserted in one patient.

John R Gowardman · Maria Brosnan · Joy Whiting · Peter Collignon

Jennifer H Barralet,* Neil R Parker† * Epidemiologist, Communicable Diseases Unit, † Public Health Physician, Darling Downs Public Health Unit, Queensland Health, GPO Box 48, Brisbane, QLD 4001. Neil_ParkerAThealth.qld.gov.au To the Editor: Queensland has a small but increasing number of Q fever notifications in children. This is of concern to public health services in the Darling Downs and south-west Queensland where most Q fever notifications originate (Box). Little is known about Q fever in children, especially in Australia, as the disease is primarily diagnosed in adults following occupational exposure to Coxiella burnetii. Here we report a case series examining clinical presentation, exposure to risk factors and disease outcomes in children. Twenty-one children aged 3–14 years notified with Q fever from the Darling Downs and south-west Queensland in 2001 and 2002 were followed up. In acute cases the febrile illness was similar to that in adults from the same region. The one child with chronic Q fever had no known acute illness and presented with osteomyelitis of the wrist. All the children recovered, although relapsing symptoms were reported in two children and three reported persisting fatigue for 3 months or more after diagnosis. All but one patient reported contact with cattle, sheep or goats (13 lived on a farm and 7 had visited a farm). The single exception reported contact with kangaroos and feral pigs through hunting. Prolonged exposure to animals or the farm environment was not necessary for infection. Twelve of the children had high risk exposure to C. burnetii (contact with animal births, newborn animals, or animal carcasses). With increasing age, exposure of children from rural properties approaches that of their parents as they participate in the same activities. An effective vaccine is available,1 but use in people younger than 15 years is not recommended because of the lack of safety and efficacy data. Although avoidance of high risk situations such as shearing, animal births or on-farm butchering will decrease the chance of infection, these measures may be impractical for rural children. Realising this, some practitioners choose to vaccinate younger children who assist with animal births and butchering. Increasing notifications in children may reflect increased awareness that Q fever is not confined to adults with occupational exposures. Increased awareness leading to recognition of infection would give children access to effective treatment and may contribute to prevention of chronic disease. However, much remains unknown about Q fever in children, including how often the infection is asymptomatic, the spectrum and outcome of disease, and if there are effective preventive strategies. As many rural children cannot avoid potential exposure to Q fever, our study highlights the need for a safe and effective vaccine for children. Q fever notifications in children aged 0–14 years, 1997–2002

Jennifer H Barralet · Neil R Parker

Nicola Petrosillo,* Vincenzo Puro,† Giuseppe Ippolito‡ * Clinical Director, † Epidemiologist, ‡ Scientific Director, National Institute for Infectious Diseases “L. Spallanzani”, Rome, 00149, Italy. petrosilloATinmi.it To the Editor: In their article describing the Australian experience of border screening for severe acute respiratory syndrome (SARS), Samaan and coworkers add new insights about the low efficacy of this measure in identifying SARS cases at entry into a country.1 To our knowledge, this is the first report on this issue from a low-risk area for SARS.2 Indeed, as summarised by Samaan et al, other available data derive from countries where people with SARS, entering at the early stage of the epidemic, generated a sustained local transmission of SARS-associated coronavirus (SARS-CoV) disease. Among the reasons for a low sensitivity of entry screening, Samaan suggests that subjects may evade screening by making false declarations or by taking anti-pyretic drugs, or by simply being in the incubation period with no symptoms or only mild symptoms. To contribute to this debate, we report the experience of our Institute, which was designated as a referring centre for SARS by the Italian Ministry of Health. In Italy, where only four imported probable cases of SARS were identified and no local transmission occurred,3 entry screening was implemented at the two international airports of Milan and Rome. In particular, travellers and crews arriving from World Health Organization SARS-designated areas, directly or after transiting in other EU countries, were provided with health alert cards and screened for body temperature.4 Suspected SARS cases identified at Rome airport were to be referred to our institute. However, of the 72 subjects attending our admission unit for clinical evaluation for possible SARS, none was referred by the airport authorities. Among these patients was one of the four people with SARS arriving in Italy: an airline flight crew member coming from a SARS-designated area who passed both exit and entry screening, despite complaining of mild fever before his departure. He was admitted 6 days after arrival, at which time the clinical picture had evolved into full-blown SARS. He was discharged after 2 weeks. Among the measures recommended by WHO to reduce SARS-CoV spread, the identification of symptomatic subjects at border departure screening was the only measure with some evidence of efficacy, although this only reduced on-flight transmission.5 Conversely, evidence from several sources, including Samaan et al, showed that screening travellers (visual inspection and screening for fever) as they disembark identifies very few SARS cases and is of questionable value.1 We agree with the conclusions of Samaan et al that, in the light of a possible resurgence of SARS or similar diseases (avian flu), entry screening should, at least, be more focused, and needs further evaluation, including cost-effectiveness analysis.

Nicola Petrosillo · Vincenzo Puro · Giuseppe Ippolito

Julia E Fawcett,* Anthony P Shakeshaft,† Mark F Harris,‡ Alex Wodak,§ Richard P Mattick,¶ Robyn L Richmond** * PhD Candidate, † NHMRC Research Fellow, ¶ Director, National Drug and Alcohol Research Centre, University of New South Wales, Sydney, NSW 2052; ‡,** Professors, School of Public Health and Community Medicine, University of New South Wales, Sydney, NSW; § Director, Alcohol and Drug Service, St Vincent's Hospital, Sydney, NSW. A. ShakeshaftATunsw.edu.au To the Editor: Revised Australian Alcohol Guidelines1 were released in 2001. Although general practitioners (GPs) can be influential in initiating and supporting behaviour change to reduce levels of alcohol misuse among their patients,2,3 the extent to which their advice remains relevant and effective depends largely on the extent to which screening tools can be modified to take account of revised versions of such guidelines. The Alcohol Use Disorders Identification Test (AUDIT)4 is a clinical instrument used widely to screen patients for problematic alcohol use. The aims of our study were to examine the ability of AUDIT to classify general practice patients’ alcohol consumption into the categories specified in the revised Australian guidelines, and to identify any additional information needed for such classification. Patients aged at least 16 years attending a general practice surgery in western Sydney were asked by receptionists to complete a health-related survey by means of a hand-held computer while waiting for their consultation. Items covered a number of domains, including demographics, the AUDIT, and two additional questions about consumption of specified quantities of alcohol. The use of computers ensured patients were only asked questions relevant to them. Risk of harm in the long term: Respondents’ average number of standard drinks per week was calculated from the first two AUDIT questions, using a previously devised method.5 Risk of harm in the short term: AUDIT question 3 is not specific enough to distinguish short-term risk of harm, so additional, sex-specific questions on how many occasions in the previous 30 days the patient had consumed “7–10” and “11 or more” (men) or “5–6” and “7 or more” (women) standard drinks were asked. Of the 115 patients who completed the survey, 62% were female; their mean age was 42 years; 10% were unemployed; 34% had had tertiary education; 65% were married or in a de facto relationship; and 80% were born in Australia. Their alcohol consumption patterns are shown in the Box. AUDIT is a reliable and valid instrument, and is widely used as a clinical tool. However, as national guidelines are updated, clinical tools such as AUDIT need to remain consistent with them. Ideally, revisions would build on the benefits of existing tools rather than rendering them obsolete. For example, a major advantage of AUDIT is that it measures a number of drinking dimensions within the one, brief, validated instrument. This multidimensionality could be preserved while promoting AUDIT’s consistency with new guidelines by adding two items, with high face validity, to more accurately assess risk of harm in the short term. Incorp-orating the two additional consumption items we used in this study with AUDIT allows drinkers to be classified according to the guidelines as “low-risk”, “risky” or “high-risk” both in the long term and short term, with minimal additional response time. Alcohol consumption patterns in one general practice in western Sydney, as defined by the recently revised Australian Alcohol Guidelines1 Characteristic Males (%) Females (%) Total (%) Abstinent 18.2 29.6 25.2 Long-term harm Low-risk 68.2 67.6 67.8 Risky 11.4 1.4 5.2 High-risk 2.3 1.4 1.7 Short-term harm Low-risk 61.4 52.1 55.7 Risky 9.1 8.5 8.7 High-risk 11.4 9.9 10.4 Bold text represents categories that cannot be distinguished using AUDIT alone.

Julia E Fawcett · Anthony P Shakeshaft · Mark F Harris · Alex Wodak · Richard P Mattick · Robyn L Richmond

Michael Thomsen,* Luis Vitetta,† Avni Sali,‡ Matthias Schmidt§ * Research Associate, † Deputy Head, and Director of Research, ‡ Head, Graduate School of Integrative Medicine, Swinburne University, 9 Frederick Street, Hawthorn, VIC 3122; § Research Head of Toxicology, Society of Nutritional Medicine and Dietetics, Harsewinkel, Germany. LVitettaATmedicine.swin.edu.au To the Editor: We wish to comment on the case report by Lontos and colleagues on the proposed causal relationship between the herb black cohosh (Cimicifuga racemosa) and acute hepatic failure.1 One other case has been reported in Australia,2 and the evidence linking black cohosh to liver toxicity was weak and contested.3 The medication in the case report presented by Lontos and colleagues1 included a herb (ground ivy) containing a known liver toxin (pulegone). Pulegone is considered a strong hepatotoxin and should not be dismissed, even though it was reported that there was less pulegone in ground ivy than in pennyroyal. The authors do not indicate the daily dose of the pulegone ingested. The Therapeutic Goods Administration (TGA) made only qualitative analyses of three of the five herbs in the mixture. In our opinion the most suspect ingredient was ground ivy, and it was not assayed. The argument that the TGA could not find a standard for pulegone or ground ivy is untenable given the level of expertise and the capacity of the TGA and its laboratories. Was the supply company asked to provide analytical evidence of the contents of the herbal extracts? Ground ivy is not known to be hepatotoxic, but it is possible that the extract could have contained ground ivy with pennyroyal, which might explain the hepatoxicity of the mixture. Although uncertain without thoroughly investigating all ingredients in the herbal mixture, this alternative is a possibility. Without thorough investigation of herbal preparations, adverse events attributed to certain herbs remain dubious at best. Black cohosh has a very good safety record. There is a large body of clinical evidence and research which suggests that this herb has no hepatotoxic effects. Indeed, a German manufacturer has sold more than 350 million daily doses of black cohosh preparations worldwide since the pharmacovigilance system was introduced, and no comparable cases have been reported until these two reports in Australia. An Ames test (salmonella microsomal assay) showed no in-vitro evidence of mutagenic potential of an extract of black cohosh,4 and no chemical or organ toxicities were observed in Wistar rats given up to 5000 mg of a Cimicifuga racemosa extract granulate per kilogram body weight for 26 weeks.5 What may also be of concern is that the TGA may not have the full capabilities to test ingredients used in Australian herbal products. That substitution of herbs with potentially toxic herbs may be a common event, and that neither the TGA nor the manufacturers may have the expertise to prevent deleterious contaminants, is of even greater concern.

Michael Thomsen · Luis Vitetta · Avni Sali · Matthias Schmidt

Fiona J Cumming,* Larry Kelly† * Director, Office of Complementary Medicines; † Acting Director, TGA Laboratories; Therapeutic Goods Administration, PO Box 100, Woden, ACT 2606. fiona.cummingAThealth.gov.au Comment: Thomsen and colleagues have pointed to what they believe were uncertainties in the case described by Lontos et al, associating the use of a herbal preparation containing black cohosh with acute liver failure.1 They assert that on the basis of these uncertainties, and other evidence, black cohosh was unlikely to have been the cause of the liver failure. There are indeed uncertainties about the cause of the illness. The first, and quite critical one, is that we cannot be certain that the patient was given the same herbal materials as those supplied to the Therapeutic Goods Administration (TGA) for analysis. The pharmacist who dispensed the herbal formula for the patient provided the TGA with samples for analysis of each of the five individual extracts in the formula. Documentary evidence supporting the correct identity of the five herbs was supplied in the form of certificates of analysis from the manufacturers of the individual herbal extracts. However, it was not possible to ascertain whether the exact batch of the exact formulation taken by the patient was that which was tested by the TGA. While the title of the article by Lontos et al suggests a “problem” with black cohosh, the body of the article makes clear that the causative agent(s) are unknown,1 which is in agreement with the letter by Thomsen et al.1 Thomsen and colleagues claim that the TGA did not test the ground ivy extract supplied by Lontos et al, and said that this was because the TGA did not have a standard for pulegone or ground ivy. This is not the case, and the letter by Lontos et al1 does not state that either. The reason the TGA did not test initially for pulegone was because it is a minor constituent of the essential oil of ground ivy. We did not expect there to be any significant levels of this compound. In fact, we have subsequently confirmed that pulegone was not detectable (limit of detection 5 ppm) in the sample of ground ivy extract provided by Lontos et al. Thomsen and colleagues refer to the good safety record of black cohosh in Australia and internationally, and claim there has been only one other case in Australia where black cohosh was linked to liver toxicity. Some caution is needed in drawing broad conclusions about the safety of herbal medicines. Most countries do not have adverse reaction reporting systems which include herbal remedies. In Australia, where we have a well-developed reporting system, there have been several reports of liver problems in patients taking various preparations containing black cohosh. However, causality has not been established beyond doubt in these cases. The TGA has state-of-the-art testing facilities and a team of internationally recognised scientific staff. The formulation supplied to the patient was extemporaneously dispensed by a pharmacist. Such medicines are not subject to the regulatory controls of the TGA and would not normally be included in the TGA’s testing program. However, the TGA offered to test the herbal formulation supplied by the pharmacist to assist the clinical team. The results of the TGA’s testing confirmed the absence of undeclared pharmaceuticals in the samples of herbal extracts provided. In view of these uncertainties, it is not possible to conclusively identify the cause of the patient’s liver failure. On the evidence available it cannot be concluded that black cohosh was a cause. It is simply not possible to rule in or rule out black cohosh, or indeed any of the other herbal extracts in the formulation taken by the patient, as a cause. Where practitioners suspect a complementary medicine is involved in an adverse reaction, providing the exact product and batch taken by the patient is essential if laboratory testing is to help in confirming causality.

Fiona J Cumming · Larry Kelly

Leon A Flicker,* Samuel D Vasikaran,† Jenny Thomas,‡ John G Acres,§ Paul E Norman,¶ Konrad Jamrozik,** Nicola T Lautenschlager,†† Peter J Leedman,‡‡ Osvaldo P Almeida§§ * Professor of Geriatric Medicine, ‡ Research Nurse, School of Medicine and Pharmacology, § Research Fellow, School of Medicine and Pharmacology and School of Psychiatry and Clinical Neurosciences, ¶ Associate Professor of Surgery, †† Senior Lecturer in Psychiatry of Old Age, ‡‡ Professor of Medicine, §§ Professor of Psychiatry of Old Age; University of Western Australia, Royal Perth Hospital, Box X2213, Perth, WA 6000. † Head, Department of Core Clinical Pathology and Biochemistry, Royal Perth Hospital, Perth, WA. ** Professor of Primary Care Epidemiology, Imperial College London, London, UK. leonflicATcyllene.uwa.edu.au To the Editor: Elevated levels of homocysteine (Hcy) have recently been associated with increased risk of vascular events1 and dementia.2 The clearance of Hcy is dependent on three vitamins — folate, B6, and B12. Vitamin B12 deficiency has been described in older people for over 40 years,3 and may have wide-ranging effects through this vitamin’s influence on Hcy. The aims of this study were to examine serum B12 and folate status, and their relationships with plasma Hcy concentrations, in community-dwelling healthy older people living in Perth. Older men and women were recruited from two different sources: 299 men aged 75 years and over were recruited from a large population-based study of screening for abdominal aortic aneurysm,4 where 70% of those invited joined the project; and we recruited 273 community-dwelling women aged 70 years and over through advertisements. Exclusion criteria for both groups included significant cognitive impairment, severe physical illness and current use of B-group vitamin supplements. The Human Research Ethics Committee at the University of Western Australia approved the study, and all participants provided informed consent. Fasting total plasma Hcy, serum B12 and folate concentrations were measured in all participants, and serum creatinine concentration was measured in the men only to calculate glomerular filtration rate (cGFR). For analyses, the variable plasma Hcy was heavily skewed to the right and natural logarithmic transformation was used. Pearson’s product moment correlations were calculated for univariate analyses of continuous variables. Descriptive statistics are presented in Box 1. Fourteen per cent and 1% of the men, and 6% and 1% of the women, were deficient in B12 and folate, respectively. Hcy concentrations above upper reference limits (15 μmol/L for men and 13 μmol/L for women) were found in 24% of both men and women. There were significant (P < 0.001) positive correlations between age and log Hcy concentration for men (r = 0.23; 95% CI, 0.12–0.33) and women (r = 0.25; 95% CI, 0.13–0.36), inverse correlations between B12 and log Hcy concentrations for men (r = – 0.25; 95% CI, – 0.14 to – 0.35) and women (r = – 0.30; 95% CI, – 0.19 to – 0.41), and inverse correlations between folate and Hcy concentrations for men (r = – 0.43; 95% CI, – 0.33 to – 0.52) and women (r = – 0.28; 95% CI, – 0.16 to – 0.39). Plots of log Hcy against B12 and folate concentrations for all participants are presented in Box 2. Under multiple regression, the association of B12 and folate concentrations with log Hcy concentration remained after adjustment for age and cGFR in men only; beta values (SE) were: – 0.00060 (0.00011) for B12 concentration; – 0.0155 (0.0017) for folate concentration; – 0.0029 (0.0008) for cGFR; and 0.012 (0.005) for age. In this sample there were high prevalences of B12 deficiency and hyperhomocysteinaemia. Although the prevalence of folate deficiency was substantially lower, there were still moderate inverse associations between serum folate and Hcy concentrations. Unfortunately, vitamin B12 deficiency of this kind may not be universally corrected with small doses of oral supplements,5 and this has intensified concerns about precipitating neurological complications by population-based folate supplementation.6 There is a need for intervention studies of B-group supplements to evaluate whether the risks associated with hyperhomocysteinaemia can be ameliorated. 1: Demographic characteristics, serum B12 and folate, and plasma homocysteine in 299 older men and 273 older women Men Women Mean (SD) Range Mean (SD) Range Age (years) 78.9 (2.8) 68–86 74.8 (4.4) 70–92 Weight (kg) 78.4 (1.2) 50.6–119.5 69.3 (1.3) 39.0–120.0 Height (cm) 171 (6.5) 150–197 159 (6.7) 132–176 Body mass index (kg/m2) 26.6 (3.5) 16–37 27.4 (5.3) 17–52 Ever smoked 66% 41% Ever drank alcohol 95% 66% Serum folate (nmol/L) 24.3 (7.6) 5.5–45.3 (RI, 7–34) 25.3 (7.6) 3.9–45.2 (RI, 7–34) Serum B12 (pmol/L) 254.5 (116.7) 57–890 (RI, 140–646) 313.5 (158.7) 59–1270 (RI, 140–646) Plasma Hcy (μmol/L) 13.50 (5.3) 6.7–70.5 (RI, 6.0–15.0) 11.46 (6.8) 3.8–96 (RI, 5.0–13.0) Glomerular filtration rate (mL/min) 78.3 (16.3) 35.8–142.4 SD = standard deviation. Hcy = homocysteine. RI = reference interval. 2: Plot of serum B12 and folate concentration against log homocysteine concentration (with regression line for B12) in 299 older men and 273 older women

Leon A Flicker · Samuel D Vasikaran · Jenny Thomas · John G Acres · Paul E Norman · Konrad Jamrozik · Nicola T Lautenschlager · Peter J Leedman · Osvaldo P Almeida

Malcolm H Parker Associate Professor of Medical Ethics, School of Medicine, University of Queensland, Herston Road, Herston, QLD 4006. m.parkerATuq.edu.au To the Editor: Gerber1 appears sympathetic to the following reasons for rejecting damages in cases of wrongful birth, quoted from the High Court minority in Cattanach v Melchior,2 and judges in similar cases: doctors do not owe a duty of care that protects the economic interests of patients; the birth of a healthy child should not be regarded as a legal harm, because the birth of a healthy child is a good thing, the cost of rearing a child does not exceed the value of parenthood, and parents ought not to enjoy the advantages of parenthood without the concomitant responsibilities; awarding damages would indicate to the child that he or she was unwanted; and doctors should not be liable for most of the costs of rearing a child, because parents have a choice of rearing the child or surrendering it for adoption. As to the first point, why should doctors be exempt from any loss that results from their negligence? Depicting this duty as one of “protecting economic interests” distorts the nature of the duty of care, which requires the duty holder to avoid foreseeable damage, which includes economic loss consequent on the negligence. Regarding the second point, balancing the costs of rearing the child against the value and advantages of parenthood is conceptually misleading. The implication is that the value of parenthood should render the costs of rearing the child relatively trivial. A more coherent interpretation is that, because the costs of rearing the child and the value of parenthood are incommensurable, the natural love for the child and the value of parenting that follow the birth ought not discount the damage. This interpretation also informs responses to the third and fourth points. Not wanting another child, and not wanting the particular child once it exists, are distinct concepts. The idea that Jordan Melchior was not wanted at the time his parents took steps to avoid further pregnancies is incoherent. Wanting to avoid further pregnancies and wanting to nurture the child who is born are perfectly consistent positions, whether the case involves forgotten contraception or negligent sterilisation. Finally, the idea that, because they have the choice to keep or surrender the child, the parents should bear the costs if they keep it suggests that, once born, the particular child can be regarded as a commodity — something that the general position against awarding damages for wrongful birth repeatedly disavows. One of the judges quoted by Gerber claimed that such children would come to think of themselves as unwanted, and that this was “obscene”. The same judge’s glib claim that the parents can choose to keep or surrender the child strikes me as the obscenity.

Malcolm H Parker

Paul Gerber Honorary Reader in Legal Medicine, University of Queensland, Brisbane, QLD. In reply: Parker’s letter does little more than repeat the arguments that found favour with the majority in the High Court. He approaches the issues raised by this controversial litigation from an ethical perspective. Alas, the parents’ claim for the cost of raising a healthy child, conceived as a result of the alleged negligence of the defendant gynaecologist, raises the legal issue of restitution: does the law of tort recognise this head of damages as a “loss” for which parents may be compensated? Courts have, in the past, answered this question by reference to general principles based upon legal values. In the Melchior case,1 the majority departed from that hallowed principle. So be it. Does that make Jordan Melchior a “commodity”, having a commercial value? Yes! The plaintiffs faced the choice of either keeping their son, or mitigating their “loss” by placing him for adoption. They chose the former. Priestley JA had, in an earlier case, put the issue succinctly: “After that decision was made, the defendant was not legally responsible for the parents’ financial cost of rearing the child”2 (this was restated by Kirby J in the Melchior case1). Parker may not like it, but the law of tort has — up till now — shown more caution in awarding damages for what is called pure economic loss (ie, loss affecting purely financial interests) than it has in relation to conduct that causes damage to person or property. Before the Melchior case, that distinction had been firmly embedded in the law of tort and formed the basis of established rules governing liability for damages.3 That distinction has now been blurred by placing a financial value on the parent–child relationship.

Paul Gerber

Bronwyn A L Crawford,* Channa Perera† * Endocrinologist and Clinical Senior Lecturer, Royal Prince Alfred Hospital and the University of Sydney, Sydney, NSW 2050; † Endocrinologist, Orange Base Hospital, Orange. brcrawfoATmail.usyd.edu.au To the Editor: Prolonged hypoglycaemia in patients taking a sulfonylurea may be refractory to intravenous glucose treatment with fatal consequences, as described by Veitch and Clifton-Bligh.1 Although these authors briefly mention the use of octreotide, we believe that an additional point in the “Lessons from practice” should have been: Octreotide may be an effective therapy in refractory sulfonylurea-induced hypoglycaemia. We describe the first two patients in whom we used this therapy. A 76-year-old man with type 2 diabetes was admitted after an acute myocardial infarction and cardiac arrest. He was successfully resuscitated and underwent emergency bypass surgery. His diabetes was controlled with gliclazide 80 mg twice a day. After surgery, he developed cardiac failure, renal impairment (serum creatinine level, 0.22 mmol/L) and frequent hypoglycaemic episodes. The gliclazide was stopped but, despite good oral dietary intake, hypoglycaemia worsened and failed to respond to vigorous intravenous glucose therapy. He suffered a hypoglycaemic seizure (blood sugar level, 0.8 mmol/L). Over the next day, he received more than 300 g of glucose in the form of a 10% glucose intravenous infusion, but, despite this, went into hypoglycaemic coma. Blood results were: insulin, 472 pmol/L (reference range [RR], 15–60 pmol/L); C-peptide, 7616 pmol/L (RR, 300–800 pmol/L); and gliclazide, 9.4 mg/L (steady state average, 2.5 mg/L). He was given an intravenous infusion (30 ng/kg per minute) of octreotide.2 Within an hour, his blood sugar level rose to 7.9 mmol/L and continued to rise. Dextrose and octreotide infusions were ceased within 13 hours, with no further episodes of hypoglycaemia. He was discharged home 2 days later. A 75-year-old man with type 2 diabetes was taking glibenclamide 2.5 mg each morning. He was transferred from a rural hospital with acute on chronic renal failure (serum creatinine level, 0.4 mmol/L), as well as recurrent hypoglycaemia. The glibenclamide was stopped, but blood sugar levels remained low, and he became comatose despite boluses of 50% dextrose and a continuous infusion of 10% dextrose. The high volume of intravenous fluid precipitated cardiac failure and pulmonary oedema, requiring inotropic support. Blood results were: blood sugar, 1.5 mmol/L; insulin, 1250 pmol/L; C-peptide, 20 949 pmol/L. As an alternative to the high-dose, continuous infusion of octreotide used in our first patient, we administered a single subcutaneous injection of octreotide 50 μg. One hour later, the patient’s blood sugar level had risen to 9.0 mmol/L. He had no further episodes of hypoglycaemia. Eight hours later, insulin and C-peptide levels had fallen markedly (insulin, 153 pmol/L; C-peptide, 5654 pmol/L). He made a full recovery. Octreotide is a somatostatin analogue that inhibits the secretion of a number of neuropeptides, including insulin. It is a safe and effective therapy for sulfonylurea-induced hypoglycaemia when initial therapy with oral or intravenous glucose fails.2-5 It is particularly useful in elderly patients with renal or cardiac complications, in whom fluid overload may be a limiting factor in intravenous dextrose therapy. Octreotide may also break the vicious circle that can occur in sulfonylurea-induced hypoglycaemia in which repeated dextrose boluses further stimulate insulin release.

Bronwyn A L Crawford · Channa Perera

Peter C Veitch,* Rory J Clifton-Bligh† *Specialist in Geriatric Medicine, Department of Aged Care and Rehabilitation Medicine; † Registrar in Endocrinology, Department of Endocrinology, Royal North Shore Hospital, Clinic 1, Level 3, Pacific Highway, St Leonards, NSW 2065. rcliftonATmed.usyd.edu.au In reply: Crawford and Perera highlight a very important point with respect to hospital-based treatment of sulfonylurea-induced hypoglycaemia. Whereas, in our article,1 we wished to emphasise the importance of recognising and preventing this condition in primary care settings, we agree that octreotide is an effective therapy in treating this condition. Octreotide inhibits the specific effect of sulfonylureas (glucose-stimulated β-cell insulin release) and prevents rebound hypoglycaemia, which, in this situation, may occur with the use of glucose.2 Case reports, including those elegantly presented and referenced by Crawford and Perera, clearly illustrate the safety and efficacy of octreotide in treating sulfonylurea toxicity when initial therapy with glucose fails. Octreotide may be administered either intravenously or subcutaneously, and its effect is maintained after a short course of therapy. At our own institution, we have now adopted guidelines for the treatment of refractory sulfonylurea-induced hypoglycaemia, which include the administration of octreotide (50 μg subcutaneously) every 8 hours for up to three doses, although, as Crawford and Perera note, some patients will have a sustained response after a single dose.

Peter C Veitch · Rory J Clifton-Bligh

Malvinder S Parmar Medical Director (Internal Medicine), Timmins and District Hospital, Suite 108, 707 Ross Ave East, Timmins, ON P4N 8R1, Canada. atbeatATntl.sympatico.ca To the Editor: I wish to add another cause of exogenous hyperthyroidism to those mentioned in the comprehensive review on hyper- and hypothyroidism by Topliss and Eastman.1 Inadvertent ingestion of animal thyroid (“hamburger” thyrotoxicosis), although rare, is worth mentioning. Meat may be inadvertently contaminated with thyroid tissue through the process of “gullet trimming” during butchering. While this process has been prohibited in most countries since the recognition of outbreaks of hamburger thyrotoxicosis,2,3 it may still occur when farm animals or wild game are prepared for consumption by farmers, hunters or local butchers unaware of the prohibition. I recently reported a case of a woman living on a farm in Canada who had five episodes of transient hyperthyroidism over a decade.4 These were initially diagnosed as episodes of “silent thyroiditis”, but were later attributed to consumption of meat patties contaminated with thyroid tissue, as the local butcher was not aware of the prohibition on gullet trimming. A history of eating wild game or locally prepared meat should be considered before a diagnosis of silent thyroiditis is made. Thyroid uptake of radioiodine is low in both conditions, but serum thyroglobulin level is raised in thyroiditis and decreased during the hyperthyroid phase of exogenous hyperthyroidism.

Malvinder S Parmar

Ngaire T Jones Medical Practitioner, Beaconsfield, WA. ngairejATbigpond.com To the Editor: The recent article on thyroid disorders by Topliss and Eastman notes that “around the world, iodine deficiency still remains the predominant cause of hypothyroidism” and furthermore that “mild iodine deficiency is re-emerging in Australia”.1 Indeed, the Journal has recently published at least two articles suggesting that the iodine status of the Australian population needs to be further explored.2,3 My question therefore is: when treating a patient who has results indicating clinical or subclinical hypothyroidism, would it be relevant and important to test for iodine deficiency (by 24-hour urine collection)? This seems analogous to undertaking iron studies in a patient with a falling haemoglobin level. In the same way that iron deficiency can exist and produce symptoms, even in the absence of anaemia, may not iodine deficiency affect health and well-being? Without the elemental “building blocks” of iron and iodine, the relevant systems are put into overdrive to no avail. It seems simple to test routinely for this possibility, correct any deficiency and then recheck thyroid function. There may be more “clinically significant iodine deficiency” than we realise. As it will no doubt be some time until further studies in the Australian population shed more light on this, is it not relevant meanwhile to at least check for this possibility in individual patients?

Ngaire T Jones

Duncan J Topliss,* Creswell J Eastman† * Director, Endocrinology and Diabetes, Alfred Hospital, Commercial Road, Melbourne, VIC 3004; † Director, Institute of Clinical Pathology and Medical Research, Westmead Hospital, Sydney, NSW. Duncan.toplissATmed.monash.edu.au In reply: Jones asks if iodine excretion should be measured routinely in all patients with hypothyroidism in Australia as part of the initial assessment. We do not advocate this for the following reasons. Urinary iodine estimations are unreliable for assessing individual patients, as urinary iodine levels can vary considerably from day to day with iodine intake. These measurements should be reserved for population studies to provide an overall assessment of iodine nutrition in that population. In Australia, it is probable that virtually all cases of primary hypothyroidism are caused by chronic autoimmune lymphocytic thyroiditis, ablative therapy for Graves’ disease, or inadequate thyroxine replacement therapy in these conditions, as is the case in the United States and the United Kingdom.1-3 This contention is supported by data from the Busselton (Western Australia) survey on thyroid peroxidase antibody levels,4 which suggest that these antibodies will be of great diagnostic assistance, in contrast to the dubious clinical value of individual measurement of iodine excretion. In support of this view, in a large survey of the US population, where iodine intake has probably fallen similarly but not to the same degree as in Australia, there was no association between low urinary iodine levels and increased serum levels of thyroid stimulating hormone (TSH).5 In that study, the significant association between raised TSH and female sex disappeared after controlling for the presence of thyroid peroxidase antibodies, while the prevalence of clinical hypothyroidism was strongly correlated with positive results for these antibodies. In Australia, current information indicates that iodine deficiency, where it exists, is mild. The prevalence and regional variation are currently the subject of the National Iodine Nutrition Survey, which is surveying iodine excretion and thyroid size in primary school children. There is no evidence that this mild deficiency is associated with an increased prevalence of hypothyroidism. Jones’s suggestion that iodine deficiency impairs health by a mechanism other than impairment of thyroid function is not supported by any scientific evidence. Any consideration of advocating routine assessment of iodine status should await the results of the ongoing national study. However, iodine nutrition would appear to be best addressed as a public health issue, by promoting use of iodised salt and ensuring adequate iodine nutrition in pregnant and breastfeeding women and their infants.

Duncan J Topliss · Creswell J Eastman

David S Elder Occupational Physician, 517 St Kilda Road, Melbourne, VIC 3004. delderATbigpond.net.au To the Editor: In Bogduk’s review of the management of low back pain,1 he cited several international guidelines but did not address the effect of returning the patient to work. Disappointingly, return to work was mentioned only as an outcome of multidisciplinary therapy, with no mention at all of a planned and purposeful return to work in the suggested approach. This is surprising, given the literature available2,3 and the significant adverse effects of being out of work.4 Further, the algorithm in Box 3 (general practice management of chronic low back pain) appears to have a never-ending loop: I am cautious of the adverse effects that the reductionist model can have,5 and it appears possible in this algorithm to be forever stuck in the investigative loop. An additional pathway from this loop to intensive therapy would allow progression in some cases. The inclusion of a return to work in management of low back pain has been extensively analysed in the Australian setting and shown to significantly reduce disability.6 This advice should be included in any clinical update on management of low back pain.

David S Elder

John Salmon,* Anna Hilyard† * Pain Management Specialist, Bethesda Hospital, 25 Queen Mary Drive, Claremont, WA 6010; † Director, Achieve Pain Control Group, Perth, WA. salmon8ATbigpond.com To the Editor: Bogduk’s article on management of chronic low back pain1 was disappointingly retrogressive as a guide for general practitioners. Compartmentalising back pain management as monotherapy, multidisciplinary therapy or “reductionism”, and favouring the last, reinforces the medical model which has singularly failed to stem the epidemic of low back pain disability affecting the developed world. The biopsychosocial model of chronic spinal pain is now widely accepted and rationally emphasises the multi- or interdisciplinary model of management.2,3 Bogduk’s preference for the reductionist approach may be reasonable in a specialised centre and as a basis for research, but must justify its practical relevance in the face of the following: Available data on the reductionism approach are meagre, conflicting and mainly derived from pain-clinic populations likely to differ from patients presenting to GPs. Diagnostic joint and disc injection procedures and radiofrequency treatment performed to the required standard are available in only a very few centres. Radiofrequency lesioning of the nerve supply to symptomatic joints has been shown to provide pain relief limited to 9–18 months.4 Repeat lesioning may be less effective and is impracticable in the long term. At best, these treatments could be considered palliative. Of course, patients can only benefit from accurate diagnosis and reduction of pain from identified peripheral generators. Unfortunately, for most people with chronic back pain, it is not that simple. Usually there are multiple pathologies and pain generators, multisegmental dysfunction, disrupted motor control and interacting peripheral and central neural sensitisation mechanisms. And that is just the “bio” of the biopsychosocial model. There is then the interplay with the individual’s psychological and social environment. It is often a challenge to communicate the diagnosis effectively in the face of conflicting input from other health providers, the media and patient preconceptions. Just “plonking” “the diagnosis” before a patient and dangling a seductive “techno fix” that does not deliver in the long term is precisely what renders patients with chronic pain increasingly bewildered, dysfunctional and desperate to try one passive treatment after another. The biopsychosocial model provides a basis for management in both general and specialist practice. Appropriate interventions to reduce pain-generator input are embedded in a cognitive behavioural management matrix that imbues patients with accurate, relevant knowledge of their conditions and commonsense self-management techniques to maintain appropriate activity levels, goal setting and psychological positivity. For a time-challenged GP, collaboration with an activation- and exercise-oriented physiotherapist can be effective. The GP’s role is to provide the “white coat authority” so vital in recruiting patient confidence.

John Salmon · Anna Hilyard

Nikolai Bogduk Director, Department of Clinical Research, Royal Newcastle Hospital, Newcastle, NSW 2300. mgillamATmail.newcastle.edu.au In reply: There is a difference between wishful thinking and evidence. Elder advocates a focus on return to work. Elsewhere, I have described how this should be pursued.1 However, the evidence supports success only in the context of acute and subacute pain. I was commissioned to write on low back pain. In that context, evidence is lacking. Even Waddell, whom Elder cites,2 conspicuously avoided the issue of chronic low back pain; his evidence pertains only to acute low back pain. Salmon and Hilyard promote the biopsychosocial model. Indeed, this model is now widely accepted. Even our own studies have shown how successful it can be to recognise and treat patients’ fears and mistaken beliefs.3 However, the evidence of success is limited to acute and subacute low back pain. The predictions of the biopsychosocial model have not been fulfilled in the context of chronic low back pain. Although better than no therapy, behavioural therapy is not more effective than other therapies, and does not “reduce pain generator input”, as Salmon and Hilyard contend. Insurers, who pay for this treatment, do not share their enthusiasm for it.4 Salmon and Hilyard also repeat the commonly held view that patients have multiple pain generators. There is no actual evidence for this assertion, while the available evidence indicates the opposite. When investigated comprehensively, fewer than 10% of patients have more than one simultaneous pain generator.5 Further, Salmon and Hilyard consider that complete relief of pain for 9–18 months amounts to palliative therapy. Yet the opposite is true. Not relieving pain by behavioural therapy is palliative. They also deprecate radiofrequency neurotomy with the accusation that it “may be less effective” when repeated, but fail to cite the literature showing that this is not the case. They are correct in stating that reductionist procedures performed to the required standard are available in only a few centres. However, this does not invalidate these procedures; it reflects only a political and ideological problem in healthcare delivery. They also fail to reveal that in many places where these procedures are available, they are not performed according to best-practice standards. It is not the procedures, but misguided and unscrupulous practitioners, who render patients bewildered and dysfunctional.

Nikolai Bogduk