Letters

Lloyd K Morgan General practitioner (retired), PO Box 150, Lorne, VIC 3232. lloydmorganATiprimus.com.au To the Editor: O’Leary et al1 are pessimistic about the value of antibiotic treatment for leptospirosis, based on an inconclusive Cochrane review2 and no proven mortality decrease. Yet we can be more optimistic, given the efficacy of prophylactic doxycycline (soldiers in Panama were 95% protected by 200 mg once-weekly3), the susceptibility of leptospira to various antibiotics in vitro (especially penicillin, but not erythromycin4), and the existence of a Herxheimer reaction with penicillin,5 which indicates in-vivo activity. The Cochrane review2 was of randomised controlled trials of confirmed cases. It included 75 patients given antibiotics and 75 given placebo. Penicillin (61 patients) and doxycycline were not compared. The time from symptom onset to starting antibiotics was stated in only two trials (9 and 2 days). Nevertheless, the review concluded that penicillin or doxycycline may do more good than harm. In the spirochetaemic phase of leptospirosis (Days 4–7), vasculitis causes multiorgan failure. Successful treatment with antibiotics seems likely if commenced within 2 days of symptom onset, before generalised vasculitis is irreversible. Unfortunately, early diagnosis and efficacy assessment is difficult because symptoms are protean and non-specific, no rapid laboratory test exists, the condition is mild and self-limited in most cases, and mortality varies from zero to 7%. A high index of suspicion is essential so that antibiotics can be commenced empirically. The consensus is that antibiotics should be commenced within 4 days. In one study, starting antibiotics within 7 days was associated with shorter illness, and if antibiotics were started within 2 days the shorter duration was highly significant (P = 0.006).6 Another trial showed penicillin commenced on Day 9 was beneficial, but antibiotics had been used before entry to the trial.2 Various penicillins and tetracyclines have seemed useful, but only oral doxycycline and intravenous benzylpenicillin are recommended. These are the first and second preferences, respectively, in Therapeutic guidelines antibiotic.7 In the case described by O’Leary et al,1 antibiotics were commenced on Day 3, but the penicillin dose was only half the recommended daily dose for leptospirosis. The vasculitis was probably terminal before the patient was transferred to Concord Hospital.

Lloyd K Morgan

Marianne E Jauncey,* Paul K Armstrong,† Emily L Morgan,‡ Jeremy M McAnulty§ NSW Public Health Officer, Public Health Training and Development Branch; † Medical Epidemiologist, § Director, Communicable Diseases Branch; NSW Health, North Sydney, NSW. ‡ General Practitioner, Ballina West Medical Centre, Ballina, NSW. Marianne.jaunceyATyahoo.com.au To the Editor: In 2003, severe acute respiratory syndrome (SARS) became the first pandemic of the 21st century. Despite spreading to 29 countries, a rapid and coordinated international effort led to its containment. Here, we examine Australia’s only laboratory-confirmed case, and the investigation of possible subsequent transmission. In June 2003, the World Health Organization (WHO) notified Australian health authorities of a 26-year-old tourist in whom SARS-coronavirus-specific antibodies had recently been detected. She was part of a retrospective serological survey of people who stayed at the Hotel Metropole, Hong Kong, on 21 February,1 the same time a SARS source case infected at least 14 other hotel guests.2 On 22 February, the 26-year-old tourist travelled to Australia and 4 days later developed myalgia, lethargy and cough. On 6 March, 6 days before the first WHO global alert on SARS, she saw a general practitioner (GP) in northern New South Wales, to whom she also reported nausea, vomiting, nocturnal fever and pronounced lethargy. On examination she was afebrile, pale, unwell, with a cough and clear chest on auscultation. She declined further investigations and hospital admission; her condition gradually improved, and she left Australia 6 days later. She reported close contact with only three people during her Australian visit — her partner, the GP, and the GP’s surgery nurse. None reported subsequent illness and all tested negative for SARS-coronavirus antibody by direct immunofluorescence, a highly sensitive and specific method.3 Australia was fortunate that the tourist was not particularly infectious. The Hotel Metropole case was identified as the source case for four national and international clusters of SARS.2 The resulting human and economic cost was substantial.4 Without specific treatments, basic public health measures proved the only effective means to contain SARS. These included rapid case detection and isolation, contact tracing, handwashing and the correct use of personal protective equipment.5 Many GP practices and some hospitals in Australia do not have isolation facilities or infection control resources to effectively contain diseases like SARS. In the event of local transmission of SARS, infection may well have occurred in Australian healthcare workers. In the wake of SARS and, more recently, avian influenza, GPs must develop infection control plans to protect their own health as well as that of their patients. These should include obtaining a history of travel to outbreak-affected areas, reserving an area for patient isolation, and using appropriate infection control precautions during such outbreaks. Clinicians in other healthcare settings also need to review current infection control practices. If Australia is to remain the “lucky country” with regard to communicable diseases, basic public health measures aimed at preventing transmission of infection in healthcare settings is essential.

Marianne E Jauncey · Paul K Armstrong · Emily L Morgan · Jeremy M McAnulty

Jennifer W Majoor,* Joseph E Ibrahim† * Associate Professor, Department of Psychiatry, Alfred Hospital, Prahran, VIC; † Monash University Professor of Aged Care Medicine, Peninsula Health, Frankston, VIC. J. MajoorATalfred.org.au To the Editor: We applaud the Journal’s new series to improve the standard of teaching within the medical profession.1,2 However, it seems ironic that a profession that relies so heavily on an experiential, apprentice-based model of learning should be running such a series. Since the early nineties, we have seen a paradigm shift with regard to improving the quality of healthcare. However, this recent managerial preoccupation with systems, processes and outcomes has largely ignored the relationship between effective teaching and patient care. Clinical service work is given priority over training and education activities, and it is likely that, if it weren’t for the clauses in our employment contracts, all training, conferences and educational activities would occur out of work hours. Although we have seen a number of structural interventions to promote ongoing education, such as the introduction of Continuing Medical Education programs, the idea that “any” education will do, and that “anyone” can teach, remains pervasive. The danger of promoting “teaching on the run” is to reinforce the view that teaching is not a specialised discipline that requires specific skills and training. It is astounding that no formal qualifications in education are required for teaching at the most senior level, whereas to be taken seriously as a researcher requires an MD or PhD. It is a rare gifted teacher who instinctively performs well without formal training. High-quality teaching requires formal training, just as high-quality research does. Do we allow anyone in medicine to simply do “research on the run”? Would we ever consider a series called “Research on the run”? In medicine, we recognise that people are drawn to particular specialties because of their different knowledge, skills, interests and temperaments. This is not always the case in teaching, and names on a tutorial roster are too often allocated without regard for the style or ability of the teacher. Lake points out that the majority of problems with teaching are related to the traditional culture of medical practice and health service delivery.2 Similarly, Quadrio has observed that “career advancement in medicine . . . depends primarily upon research productivity, less upon clinical work and teaching . . .”.3 In our view, medicine requires another paradigm shift towards competency assessment and promotion of our teachers in academic settings. Furthermore, the allocation of appropriate resources is paramount and is justified because of the likely spin-offs for improved quality of patient care. We look forward to the day when medical education is rewarded as a highly valued endeavour, rather than a burden for busy clinicians and academics. We eagerly await further instalments of this well intentioned series on teaching, and hope that it goes some way towards effecting a “Kuhnian revolution”.4 (US scientist Thomas Kuhn proposed that scientific knowledge proceeds according to popular paradigms that, every now and then, undergo “intellectually violent revolutions . . . in each of which one conceptual world view is replaced by another . . .”.)

Jennifer W Majoor · Joseph E Ibrahim

Fiona R Lake Associate Professor in Medicine and Medical Education, Faculty of Medicine and Dentistry, University of Western Australia, Nedlands, WA. flakeATcyllene.uwa.edu.au In reply: As noted by Majoor and Ibrahim, teaching and learning, as a mission, are not well regarded when compared with research. Not only that, but changes in healthcare are making it harder to teach. Shorter patient stays and more complex patients result in “survival” learning by junior staff, rather than in-depth learning.1,2 Experts in medical education will be increasingly important in teaching, guiding curricula, and assessing trainees.2 However, professional learning occurs while doctors immerse themselves in clinical practice. “On the run” teaching doesn’t mean substandard teaching, but relates to doing it while delivering patient care.3 Although there is room for improvement, many clinicians teach well. Most are keen to teach and would like to have formal training,4 and evidence suggests that, with support, they can improve.2,3 How much support? Short workshops have been shown to have an impact, as has the provision of a few simple educational ideas.5 By not supporting our clinicians/teachers in ways that could be very simply put into practice, we risk losing in-context learning and wasting an enormous resource. Along with focusing on the teacher, I believe we need an important shift in the way health services recognise (provide time for) and reward (see as important) the mission of teaching and supervision alongside their mission of excellence in delivery of care.

Fiona R Lake

Chin-Pin Yeo,* Melissa J Gillett,† Samuel D Vasikaran‡ * Chemical Pathologist, † Biochemistry Registrar, ‡ Head, Core Clinical Pathology and Biochemistry, Royal Perth Hospital, GPO Box X2213, Perth, WA 6847. gptycpATsgh.com.sg To the Editor: In about 2% to 5% of patients with subclinical hypothyroidism, the condition progresses to overt hypothyroidism each year.1 It is currently recommended that thyroid function tests should be repeated at 6- to 12-month intervals to monitor improvement or worsening in level of thyroid-stimulating hormone (TSH).1 Testing for thyroid peroxidase antibody (TPOAb) is also common practice in subclinical hypothyroidism, as it has been shown that individuals with raised TSH and TPOAb levels have a 40-fold increased risk of developing overt hypothyroidism.2,3 We audited the management of patients who had a result indicating subclinical hypothyroidism from our hospital laboratory, focusing on follow-up thyroid function and TPOAb tests. In December 2003, we retrospectively inspected clinical case notes of patients who had been reported in November 2002 with a TSH level of 4.1–9.9 mIU/L (normal reference interval, 0.4–4.0 mIU/L) and a free thyroxine (FT4) level within the reference range of 10–23 pmol/L (subclinical hypothyroidism). We also contacted the patients’ general practitioners (GPs) for further information when necessary. There were 72 patients with results suggesting subclinical hypothyroidism. Of these, we excluded 29 from other hospitals and three whose GPs were not able to be contacted. Of the remaining 43 patients, 18 had no previous history of thyroid disease (8 men and 10 women; age range, 24–90 years). Six patients were seen in the emergency department, four in the outpatient clinics, and eight in the wards. All the laboratory reports of subclinical hypothyroid results were accompanied by a comment advising repeat thyroid studies at a later date and thyroid antibody tests. However, only three of the 18 patients (17%) had TPOAb tested. Only seven of the 18 patients (39%) were followed up with repeat thyroid function tests, at intervals ranging from 3 days to 7 months. One patient, with a TSH level of 9.8 mIU/L, was started on thyroid replacement therapy. The GPs of 10 of the 11 patients who did not have follow-up testing were not informed of the initial TSH results. The low rate of follow-up of hospital patients with a first-time diagnosis of subclinical hypothyroidism is of concern. While the increase in TSH level in some of these patients may have been related to sick euthyroidism, this can only be confirmed by normalisation of TSH level on repeat testing. TPOAb testing can be deferred until confirmation of persistently raised TSH level. Better strategies, such as a computerised system for selective copying of results to GPs whenever relevant, and inclusion of treatment advice dependent on TPOAb status in the reports,4 may be needed to improve follow-up.

Chin-Pin Yeo · Melissa J Gillett · Samuel D Vasikaran

Adam P Morton* * Endocrinologist, Mater Hospital, South Brisbane, QLD 4101. AmortonATmater.org.au To the Editor: I appreciated the recent comprehensive review of androgen deficiency and replacement therapy in men by Handelsman and Zajac.1 I ask their opinion of the importance of obstructive sleep apnoea as a cause of secondary hypogonadism, and also of the safety of androgen replacement in men with hypogonadism who have obstructive sleep apnoea but are intolerant of continuous positive airway pressure (CPAP) treatment. In my practice, obstructive sleep apnoea is one of the most common associations, if not indeed causes, of hypogonadotropic hypogonadism. Several studies have shown that obstructive sleep apnoea is associated with secondary hypogonadism, which is partly or completely reversed by both CPAP treatment and uvulopalatopharyngoplasty.2-4 Secondary hypogonadism is also a feature of several conditions in which there is a high prevalence of obstructive sleep apnoea, including chronic spinal cord injury and cardiac failure. Of concern, studies have shown that androgen replacement may precipitate or worsen obstructive sleep apnoea.5,6 Similarly, a study of women with endogenous androgen excess caused by polycystic ovary syndrome found they were 30 times more likely to suffer from sleep-disordered breathing than control women.7 A single case report describes resolution of obstructive sleep apnoea in a non-obese woman after removal of a benign testosterone-producing ovarian tumour.8 Thus, I would value Handelsman and Zajac’s comments as to whether they consider obstructive sleep apnoea to be an important cause of secondary hypogonadism, and whether symptoms of this condition should be sought before initiating androgen replacement therapy.

Adam P Morton

David J Handelsman,* Jeffrey D Zajac† * Director, ANZAC Research Institute, Concord Hospital, Hospital Road, Concord, NSW 2139; † Head, Department of Medicine, Austin Hospital, Melbourne, VIC. djhATanzac.edu.au In reply: We thank Morton for his thoughtful comment that, in addition to monitoring for obstructive sleep apnoea precipitated by testosterone therapy, it may be worthwhile screening for this condition before starting treatment. Symptoms to be sought include daytime sleepiness and partner reports of loud and irregular snoring, especially among overweight men with large collar size. Obstructive sleep apnoea rises steeply in prevalence with age and causes mild hypogonadotropic hypogonadism, which is rectified by effective continuous positive airway pressure (CPAP) treatment.1 Obesity, depression, cardiovascular disease and other conditions that become more common with age have similar effects. Together, they contribute to the lower blood testosterone levels found in unselected older men, in whom testosterone remains an unproven treatment.2 This condition differs from classical hypogonadotropic hypogonadism caused by hypothalamic or pituitary disorders, which routinely requires lifelong testosterone replacement, and (occurring in a younger population) is rarely associated with obstructive sleep apnoea. The prevalence of obstructive sleep apnoea precipitated by testosterone treatment remains unclear. A case precipitated by injectable testosterone has been reported,3 while testosterone has potential adverse effects on sleep in older men.4 Clinical experience suggests that, among younger hypogonadal men, obstructive sleep apnoea is a rare idiosyncratic reaction to testosterone, which, like polycythaemia, may be particularly related to supraphysiological blood testosterone levels. However, the prevalence may be higher among older men. Hence, we agree that pretreatment screening is wise (rather than proven) for older men starting testosterone treatment, but is not routinely necessary for young men with classical hypogonadism.

David J Handelsman · Jeffrey D Zajac

A Rod MacQueen Clinical Director, Drug and Alcohol Services, Mid Western Area Health Service, Bloomfield Hospital, Forest Road, Orange, NSW 2800 rod.macqueenATmwahs.nsw.gov.au To the Editor: The article by Martyres et al on drug-seeking behaviour by young heroin users,1 leading to the deaths of 202 people over 5 years, leads to an inescapable conclusion. Too often, the medical profession is part of the problem rather than the solution, and as a result young people die. Here is an issue where the admonition primum non nocere should be foremost in our practice. After working with drug users and prescribing methadone for 22 years in a variety of settings, my experience is that drug users use drugs! Whether it is logical, safe or appropriate, or not, this group seeks drugs to modify or modulate their state of being. They often have serious medical and mental health issues, but have sadly decided on their preferred treatment without much knowledge of the diagnosis or of alternative interventions. They are often very skilled in obtaining drugs. So, we must perform our role equally well. Doctors are not drug dealers. Our duty is not to promote or support intoxication, or even relaxed happiness if that increases the risk of misadventure. It is to promote and support health. It is difficult to see how a prescription for 50 benzodiazepines to a young person (or even an older person) can ever be construed as healthcare. To do it again next day, next week, on and on, is almost unbelievable, yet the data indicate that is exactly what is happening.1 Even publicans have rules prohibiting serving intoxicated patrons. That one was “offering the customer what he asked for”, a common excuse for this sort of prescribing practice, would not be a suitable defence in the Coroner’s Court if insulin, digitalis, or even vitamin A, had been prescribed on request. But appeals to good practice and commonsense, along with current regulatory strategies, are apparently not sufficient to protect this vulnerable group. Kamien points out that data from the HIC could be used to provide immediate information to doctors about whether a patient is a “doctor shopper”.2 The data are already collected and could easily be made available if the will existed. Potential prescribers could at least gain accurate and timely information on which to base their decisions. There would be less excuse for “convenience store” prescribing, and more chance of ethical behaviour. At present these data remain largely useless in preventing avoidable deaths. But, surely, learning nothing from the deaths of 202 young Australians is not an option?

A Rod MacQueen

John M Hart General practitioner, Swan Medical Centre, 280 Great Eastern Highway, Midland, WA 6056 swanmedATiinet.net.au To the Editor: I write to share my concerns about the “doctor shoppers” in our community.1 The large medical group in which I practice has long been tormented by the demands of a constant stream of drug addicts, and I feel that we have now lost a very useful tool for dealing with these patients. I refer to the loss of access to the “Doctor Shopping Hotline”. This has resulted in increased aggravation for both staff and doctors. The problem is compounded by our practice being open at weekends and public holidays, when these patients arrive with the familiar story of not being able to get their benzodiazepines and opiates because their own doctors are not available. The Health Insurance Commission recently notified me about a patient who had attended our surgery, and many others, during a 3-month period last year. During this time, he saw more than 30 doctors and was prescribed more than 300 Pharmaceutical Benefits Scheme (PBS) items (6000 benzodiazepines and more than 2000 opiates [Panadeine Forte]). I strongly feel that the hotline should be reinstated — for the benefit of the doctors and the patients, and to help reduce a totally unwarranted drain on the PBS.

John M Hart

Jeff Whalan Managing Director, Health Insurance Commission, PO Box 1001, Tuggeranong, ACT 2901 medicare.enqAThic.gov.au In reply: I note the concerns expressed by Hart in relation to the discontinuation of the Doctor Shopping Hotline, and his call for the reinstatement of such a service. The Doctor Shopping Project, which was funded to the end of June 2002, focused on a limited selection of nervous system medications. It has been replaced by the Prescription Shopping Project, which is much broader in scope, as it encompasses all medicines on the Pharmaceutical Benefits Scheme (PBS). The new project aims to reduce the number of patients obtaining PBS medicines in excess of therapeutic need, and provides the opportunity for more informed prescribing across all categories of PBS medicine. The Health Insurance Commission (HIC) recognises the value of an information service for medical practitioners under the Prescription Shopping Project. An independent researcher has been engaged to explore the reactions and attitudes of medical practitioners and consumers to implementing such an information service. The research also aims to gain insight into medical practitioners’ intentions of using such a service, and their expectations of the scope and delivery of the service. Findings were presented to the HIC in early July 2004. The HIC will now convene a forum of relevant peak bodies to consider the scope and delivery of an information service in light of the findings. The HIC looks forward to working with the profession to establish an information service for medical practitioners under the Prescription Shopping Project.

Jeff Whalan

Paul Prociv Honorary Research Consultant, School of Molecular and Microbial Sciences, University of Queensland, Brisbane, QLD 4072. p.procivATmailbox.uq.edu.au To the Editor: In their brief review of water and public health, Leder et al1 uncritically attributed the Palm Island “epidemic” of 19792 to algal toxicity, commenting that it was the only recorded manifestation of this phenomenon in Australia. The original report described a hepatitis-like illness (associated in many with dehydration and bloody diarrhoea) in 138 children and 10 adults of Aboriginal and Torres Strait Islander descent living on Great Palm Island, northeast of Townsville, Queensland.2 No causative agent was actually identified. My investigation in the early 1980s of Toxocara pteropodis, a parasite of flying foxes, excluded it as a likely aetiological agent in the Palm Island outbreak, and compelled a critical reanalysis of other possibilities, which led me to conclude that subacute copper toxicity was the most plausible explanation. My rationale was published as a hypothesis.3 Sadly, discretion (to protect local technicians) compelled me to withhold critical information that explained how the community had been inadvertently exposed to excessive levels of copper in its water supply. Now that water management is becoming a major societal concern and algal blooms seem to be increasing in frequency, the issue needs to be resolved — and sufficient time may have elapsed for details to be revealed without impugning individuals. In 1985, having concluded that copper poisoning was the most likely explanation, I contacted the environmental health personnel who had overseen the mixing of algicide into the Palm Island water supply in 1979. They were aware that the actual volume of water to be treated had probably been grossly overestimated, because Solomon Dam’s water level was very low at the time. This meant that an excessive dose of copper sulfate was added to the dam, but it was assumed that this would be “erring on the safe side”. Further, the copper sulfate was not distributed uniformly through the water in the dam: a local resident with a dinghy had been contracted and instructed to spread the bags of copper salt around the dam, but had instead dumped it all at one place — immediately over the outlet pipe which carried the island’s drinking water. This would readily explain how the community encountered a sustained pulse of high copper levels in its tap water. While chronic copper poisoning can lead to infantile hepatic cirrhosis,4 acute gastrointestinal symptoms (as manifested during the Palm Island episode) are also well documented.5,6 In the absence of laboratory confirmation of copper toxicity, the cause of the “Palm Island mystery disease” must remain speculative. However, in any future similar outbreaks, copper poisoning should be excluded before attributing the cause to algal toxicity.

Paul Prociv

Christine B Phillips,* Suzanne Manning† * Senior Lecturer, Academic Unit of General Practice and Community Health, Australian National University Medical School, PO Box 254, Jamison Centre, Jamison, ACT 2614; † Intern, Department of Psychology, Australian National University, Acton, ACT. christine.phillipsATcalvary-act.com.au To the Editor: Since 1999, most asylum seekers in Australia who have been detained and subsequently found to be genuine refugees have been issued temporary protection visas (TPVs). Missing from much of the debate about management of asylum seekers has been the impact of the provisions of TPVs on children. A comparison of the entitlements of refugees on permanent and temporary protection visas is given in Box 1. To estimate the proportion of TPVs issued to children under 18 years of age, we analysed data provided by the Department of Immigration and Multicultural and Indigenous Affairs (DIMIA). The denominator population was drawn from data on numbers of temporary and permanent protection visas issued between June 1999 and June 2002.1,2 Numerator data were drawn from information provided by DIMIA on request.3 As shown in Box 2, we found that between October 1999 and June 2002, 23% of all TPVs were issued to children under the age of 18. Some of these children are now over 18 years of age. However, as children born to TPV holders in Australia are also given TPV status, more children will be recruited into this visa category. Australia is a signatory to the UN Convention on the Rights of the Child, which enshrines key rights for children, such as the right to health and safety.4 However, we believe that several of these basic rights are undermined by the lack of provisions afforded to TPV holders: they are prohibited from sponsoring family members, and they have limited access to settlement services for refugees (Box 1). Withholding of family reunion provisions increases the risks for children, as it makes it more likely that parents will take their children with them when they undertake hazardous travel to seek asylum. This is in contrast to the traditional model of families sending an index person, who then sponsors other family members. The lack of a comprehensive settlement package for TPV holders, and the temporary and indeterminate nature of the visas, is likely to compound the psychological distress experienced by both adult and child refugees. Children who have experienced ongoing adversity are vulnerable to developing psychological disorders.5 The children of TPV holders must also live in families where the parents bear an ongoing burden of fear and destabilisation. The effects of TPVs are borne by large numbers of children. There is a need for concerted advocacy by health professionals to ensure that the health consequences of TPVs for children are recognised and addressed. Addendum 13/07/04. While a recent federal government initiative will allow current Temporary Protection Visa holders to apply for permanent Australian residency, we urge ongoing review of refugee visas. 1 Comparison of entitlements of refugees on permanent and temporary protection visas Services funded by the Australian Government Refugees with permanent visas Refugees with temporary protection visas Settlement services Translating and interpreting service Eligible Not eligible Accommodation support Eligible Not eligible Assistance from Migrant Resource Centre Eligible Not eligible Early health and intervention service Eligible Eligible Torture and trauma counselling Eligible Eligible English language tuition Free tuition for adults and children Adults not eligible. Children eligible from July 2002 Family reunion May apply to sponsor family members Not eligible Employment Access to all assistance programs Not eligible except for most basic services Income support Eligible for full range of social security benefits Restricted entitlements Medicare Eligible Eligible Education Primary and secondary education Eligible Eligible Tertiary education Eligible for HECS Must pay upfront fees Travel Right of return if holder travels overseas No right of return if holder leaves country HECS = Higher Education Contribution Scheme. 2 Proportion of temporary protection visa (TPV) holders who were children when visa was granted (1999–2002) Years* No. of TPVs granted No. (%) < 18 years when TPV granted 1999–2000 871 108 (12.4%) 2000–01 4456 907 (20.3%) 2001–02 3196 952 (29.8%) Total 8523 1967 (23.1%) * Financial years.

Christine B Phillips · Suzanne Manning

Kim Hoe Chan,* Murugasu Segasothy† * Medical Registrar, † Associate Professor of Medicine, NT Clinical School of Medicine of Flinders University, Alice Springs Hospital, PO Box 2234, Alice Springs, NT 0871 m.segasothyATnt.gov.au To the Editor: A recent review suggests that acute rheumatic fever, osteoarthritis and systemic lupus erythematosus account for most rheumatic disease in Australian Aboriginals, and comments on the rarity of gout.1 Although the increased prevalence of hyperuricaemia in Aboriginals compared with non-Aboriginals has been described,2 clinical attacks of gout in Aboriginals have so far been extremely rare.1,3 This is in sharp contrast to various Polynesian and other indigenous populations, including Mäori in New Zealand, Filipinos in Hawaii and Alaska, Chamorros and Carolinians in the Marianas Islands, and Taiwanese aborigines. In these populations, increased prevalences of both hyperuricaemia and gout have been documented.4,5 In an extensive literature search, we found only one report of confirmed acute gouty arthritis in an Australian Aboriginal with normal renal function,3 although there have been several Aboriginals in the “Top End” with crystal-confirmed gout in association with chronic renal impairment.1 Between January 2001 and April 2004, we identified seven new cases of acute gouty arthritis in Aboriginals (Box), confirmed by joint aspiration revealing monosodium urate monohydrate crystals. Three of these patients had confirmed acute gouty arthritis without renal impairment. This series also includes the first reported cases of gouty arthritis in Aboriginal women. Our findings suggest that the prevalence of acute gouty arthritis in Australian Aboriginals is much higher than previously reported. Discussion with physicians at Alice Springs Hospital revealed that they too have encountered gouty arthritis in Aboriginals, but whether this was confirmed by joint aspiration is not known. It appears that gout has been misdiagnosed or under-reported, or both. Further epidemiological studies should be undertaken to confirm this hypothesis, and we must have a higher index of suspicion for gout when an Aboriginal patient presents with an arthropathy, as gout is a potentially disabling and yet easily treatable condition. Aboriginals with acute gouty arthritis, Alice Springs Hospital, January 2001 – April 2004 Age (years) Sex UA level (mmol/L) Site of joint aspiration Possible precipitating factors Joints involved 46 M 0.37 Right knee Alcohol Right knee 44 M 0.45 Right knee Acute renal failure, alcohol Right knee, left first metatarsophalangeal joint, left ankle 65 M 0.23 Right knee Renal transplant, cyclosporin Right knee, right foot 64 F 0.50 Right knee Chronic renal impairment Both ankles and first metatarsophalangeal joints, right knee 61 F N/A Right knee Acute-on-chronic renal failure, alcoholism Right knee 51 M 0.48 Left knee None identified Left knee 35 M 0.54 Right knee None identified Both ankles, right knee UA = uric acid. Reference range, 0.20–0.45 mmol/L. N/A = not available.

Kim Hoe Chan · Murugasu Segasothy

Michael J Sinnott Emergency Physician, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, QLD 4102 michael_sinnottAThealth.qld.gov.au To the Editor: In physiology, the Frank–Starling curve demonstrates that cardiac muscle initially responds to an increased workload with an increased force of contraction.1 However, after the point of maximum efficiency is reached, further workload produces a decrease in both the force of contraction and the ejection fraction, leading to cardiac failure. It now appears that the same curve could describe the current situation in many Australian emergency departments. We used to operate at point A on the curve (Box). If there was a mini-disaster or a moderately large number of victims of a road accident, the department was able to increase output to cope with the situation. The “adrenalin stimulation” experienced by all members of the team meant that the department coped, and that staff were left with a sense of satisfaction. Now our department finds itself at point B on the curve. Extra workload can result in a decrease in performance and output. The patients obviously suffer, but so do the staff. The once-challenging and enjoyable parts of the job now generate frustration and exacerbate the background dysfunction. On a recent weekend, the emergency department experienced an influx of sick elderly patients as a result of a local heatwave, with temperatures reaching 42°C. The problem was identified as a mini-disaster only in retrospect. At the time it was thought to only exemplify another bad day. This is an example of the syndrome of “learned helplessness”2 that staff are experiencing. Politicians and health administrators need to understand that our public hospital emergency departments are struggling with their daily workloads and are no longer equipped to deal with medium- to large-scale emergencies. Access block as a medical model At point A, an increase in workload leads to increased performance to cope (moving to point A1). At point B, an increase in workload leads to a decrease in performance (to point B1).

Michael J Sinnott

Stacey L Emmett,* Joseph E Ibrahim,† Amanda Charles,‡ David L Ranson§ * Research Officer, † Physician, ‡ Clinical Research Nurse, § Deputy Director, Clinical Liaison Service, Victorian Institute of Forensic Medicine and the State Coroner’s Office, 57–83 Kavanagh Street, Southbank, VIC 3006 staceyeATvifm.org To the Editor: The Royal College of Pathologists of Australasia Autopsy Working Party highlighted the decline in the numbers of hospital autopsies.1 Forensic and hospital autopsies are a valuable safety and quality tool for improving healthcare systems. Autopsies provide an accurate cause of death and are a valuable audit tool to evaluate medical diagnostic processes and therapeutic interventions. Declines in both types of autopsies are cause for concern. A forensic autopsy is an integral part of the coronial process. The Coroner’s role is to establish the identity of the deceased, where he or she died, the cause of death and, perhaps most importantly, how the person died.2 Without an autopsy, it can be difficult to determine the cause of death. At the Victorian Institute of Forensic Medicine (VIFM), about 80% of all deaths that are reported to the State Coroner (in Melbourne and Geelong) undergo a full forensic autopsy. Senior next-of-kin can object to an autopsy being performed. Section 29 of the Coroner’s Act 1985 (Vic) details the objection process.2 The decision to grant an objection is dependent on the opinion of the Coroner and his or her view on the circumstances of death. We reviewed the number and rate of forensic autopsies performed by the VIFM between 1992 and 2002, as well as the number and rate of objections under Section 29. The rate of forensic autopsies remained relatively stable over the decade, at 80% of deaths reported to the State Coroner. There were 94 successful Section 29 applications in 1992. This accounted for 3.25% of all deaths reported to the Coroner. Objections to autopsies have been steadily increasing since 1992. In 2002, there were 212 successful applications, accounting for 7.1% of all deaths reported to the Coroner and representing about a 4% rise over the decade. When a coronial autopsy has been requested, but not carried out because of a Section 29 objection, substantial additional work is required. This includes medical record reviews; external forensic examinations; reviews of statements from treating doctors, independent experts and family; and inquests. The other major ramification associated with objections to autopsies is the discrepancies between causes of death that are determined clinically and at autopsy (with 28% of presumed causes wrong in one study).3 Without an autopsy, important pathology may remain unrecognised, and this can substantially affect the accuracy of the stated cause of death. The inherent right of next-of-kin to object to coronial autopsies will remain. However, healthcare professionals and coroners need to be aware of the public health implications associated with objections to autopsies.

Stacey L Emmett · Joseph E Ibrahim · Amanda Charles · David L Ranson

Gaston R B Arnolda Honorary Associate, Department of Public Health, University of Sydney, QEII Institute for Mothers and Babies, Building DO2, Sydney, NSW 2006. garnoldaATperinatal.usyd.edu.au To the Editor: O’Grady and Noland, concerned about the consequences of privacy legislation,1 draw attention to “. . . the findings of an Australian survey in which 61% of adults believe that even their de-identified health information should not be used for research purposes without their consent”. Unfortunately, they do not point out that the survey,2 commissioned by the Office of the Federal Privacy Commissioner, had a 20% response rate, making it effectively useless in determining what Australian adults really think about the use of their de-identified health information. Alarmed at the possibility that “evidence” of this quality could be used to aid decision-making that had important implications for rigorous research, I turned to Google (<www.google.com>) for assistance. A Google search using the words “61% de-identified health information roy morgan” generated 21 hits, 15 of them unique, and only five related to the subject. One of the five was the letter by O’Grady and Noland, one was the report of the survey, and three specifically cited this survey result: Privacy Victoria,3 Privacy NSW,4 and the Office of the Federal Privacy Commissioner5 all used the result in formal submissions to reviews of privacy-related issues — without revealing the survey’s appalling response rate. We have privacy commissioners who are powerful advocates of the principles of respect for privacy and autonomy. Perhaps the time has come for Australia to have “public interest commissioners” who can powerfully advocate for the public interest in high-quality health research.

Gaston R B Arnolda

Gary C Morgan Executive Chairman, Roy Morgan Research Pty Ltd, PO Box 2282U, Melbourne, VIC 3001. Gary. MorganATroymorgan.com In reply: In a world in which people are increasingly busy and mobile, increasingly concerned about invasions of privacy and increasingly approached to participate in surveys, survey response rates that could be readily achieved 25 years ago are now very much more difficult to attain. High response rates (ie, 60% and over) are still very desirable and can still be achieved. We have conducted surveys on sensitive issues, such as drug-taking, and achieved response rates that would probably satisfy even Arnolda. But this requires very intensive field activity that is not always justified by the nature of the project. The survey in question was not a health survey. It set out to provide general background information, exploring comparative levels of concern about, and the relationships between, a very wide range of privacy issues on a scale adequate to allow relatively small groups within the population to be examined. It was not intended to yield precise and critical measurements. Measures of “concern” or “reluctance” are highly context-dependent, “soft” measures, subject to interpretation, both by the respondents and by end-users. External validity is therefore not the issue: a response rate of 80% would not have made the figures demonstrably more “accurate”. Given the imprecise nature of the measures obtained, overengineering the sample relative to other components of the survey design would have been a waste of (public) money, better devoted to further research. The survey was part of a wider-ranging project and was planned in close consultation with the Office of the Privacy Commissioner in the light of their needs and priorities. It is appropriate that this issue arose out of a debate on privacy. As privacy constraints bite harder, whether imposed by statute or codes of practice, or arising through increasing resistance from subjects, medical researchers are going to have to come to terms with problems of non-response in the same way that social-survey researchers have. How are researchers going to react when only 20% of potential subjects consent to have their information used? Will they use words like “appalling” and “effectively useless” to dismiss any studies based on such a subset? Or will they perhaps learn to use them, with due caution, for the valuable information they nevertheless contain? One does not have to look very far in the history of medicine or public health to find major advances in knowledge using less than perfect statistics.

Gary C Morgan

Sharon J Gardiner,* Evan J Begg,† Carl M J Kirkpatrick,‡ Robert B Buckham¶ * Drug Information Pharmacist, † Professor of Medicine, Christchurch School of Medicine and Health Sciences, Private Bag 4345, Christchurch, NZ; ‡ Lecturer, School of Pharmacy, University of Queensland, Brisbane; ¶ Drug Information Pharmacist, Christchurch Hospital, NZ sharon.gardinerATcdhb.govt.nz To the Editor: We wish to commend the Australasian Diabetes in Pregnancy Society (ADIPS) ad hoc working party for providing an update on the safety of metformin in pregnancy.1 However, we would like to comment on the information they provided on the safety of this drug in breastfeeding. Metformin can be regarded as a well studied drug with respect to its distribution into human breastmilk;2,3 most drugs are not as well served in this regard. As Simmons et al indicated,1 the infant “dose” in breastmilk is small at less than 0.4% of the maternal dose, corrected for body weight. This is substantially lower than the arbitrary cut-off of 10% used to guide drug use during lactation and thus implies safety.4 Further evidence for the safety of this drug in breastfeeding arises from failure to detect metformin in blood sampled from four of six infants exposed via breastmilk (limit of detection, 5–10 μg/L) and lack of adverse effects noted in nine exposed infants.2,3 Simmons et al stated that infant exposure to metformin could be reduced by breastfeeding immediately before maternal dose ingestion and then avoiding feeding for at least 2–3 hours after the dose. For drugs with a short elimination half-life, this recommendation — avoiding feeding at peak drug concentrations in the milk — may reduce infant exposure. However, this is not the case for metformin. Two studies investigating metformin in breastfeeding have shown that the metformin peak plasma concentration occurs about 2–4 hours after the dose, while milk concentrations are “flat” across the entire dosing interval. This is distinctly different from most drugs, in which the drug concentrations in milk mimic the rise and fall of plasma concentrations, consistent with passive diffusion.2,3 The flat profile observed with metformin raises the possibility that the distribution of metformin into or out of breastmilk may involve an active process such as organic cation transporter(s), in addition to passive diffusion Given this unusual concentration profile in breastmilk, infant exposure (albeit small) will not be reduced by the practice of avoiding breastfeeding for a few hours after maternal dose ingestion, as suggested by Simmons et al. In other words, mothers may feed their infants at any time during the dosing interval and this will not affect infant exposure to metformin. We believe that there is sufficient evidence for metformin to be considered a safe therapeutic option in the treatment of diabetes or polycystic ovary syndrome in breastfeeding mothers, with the usual caveat of weighing up the risk–benefit ratio in each case.

Sharon J Gardiner · Evan J Begg · Carl M J Kirkpatrick · Robert B Buckham

David Simmons,* Barry N J Walters,† Janet A Rowan,‡ H David McIntyre§ * Professor of Medicine, Waikato Clinical School, Waikato Hospital, Hamilton, NZ; † Clinical Associate Professor, Department of Women’s and Children’s Health, King Edward Memorial Hospital, Subiaco, WA; ‡ Physician, Department of Obstetrics, National Women's Hospital, Auckland, NZ; § Director of Endocrinology, Mater Hospital, Brisbane, QLD. simmonsdATwaikatodhb.govt.nz In reply: We thank Gardiner et al for their commendation and support for our update on the safety of metformin in pregnancy.1 We agree with their analysis regarding the timing of the use of metformin during lactation. Nevertheless, we would like to highlight that the safety of metformin can not be assumed from the studies they quote, as these included very few subjects. Such studies, helpful as they may be, provide no imprimatur for the long-term safety for the growing infant and subsequent adult. While no babies had side effects reported during these studies, this may not be the case for other babies. Should a woman decide against the use of insulin to control hyperglycaemia postnatally, then the risk of potential known and unanticipated side effects of metformin should be discussed while obtaining informed consent for metformin use. However, during this discussion, it would also be prudent to weigh-up metformin use against breastfeeding with continued hyperglycaemia, an activity associated with greater obesity and impaired glucose tolerance in the offspring.2

David Simmons · Barry N J Walters · Janet A Rowan · H David McIntyre

Clive D Hadfield Gastroenterologist, 30 Megan Street, Cairns, QLD 4870. chadfieldATaustarnet.com.au To the Editor: In their recent study, Scott and colleagues demonstrated benefit from a program to standardise clinical management of cardiac conditions in Queensland hospitals.1 They found differences in the effect on “low-intensity intervention” hospitals compared with “high-intensity intervention” hospitals. The former were, by and large, district-type hospitals and the latter tertiary hospitals. The study found that about 50% more patients in the larger hospitals had assessments of left ventricular function. Three times as many patients in the larger hospitals accessed rehabilitation. Nearly three times as many patients in the smaller hospitals were readmitted with a diagnosis of acute coronary syndrome within 30 days, perhaps a surrogate for angiography rates, which were not reported differentially. It may be that the most urgent intervention required is “high-intensity” funding of district hospitals, so that they can achieve rates of echocardiography, rehabilitation and coronary angiography approaching those of tertiary hospitals. This intervention would need no further justification than that the population served by the district hospitals has paid its share for these treatments. Let us hope that the remaining comparative outcome data are published.

Clive D Hadfield

Ian A Scott,* Irene C Darwin,† Kathy H Harvey,‡ Andy B Duke,§ Nicholas D Buckmaster,¶ John Atherton,** Hazel E Harden,†† Michael Ward,‡‡ for the CHI Cardiac Collaborative * Director of Internal Medicine, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, QLD 4102; † Program Manager, ‡ Project Manager, § Senior Analyst, Collaborative for Healthcare Improvement, Queensland Health; ¶ Director of Medicine, Caboolture Hospital; ** Director of Cardiology, Royal Brisbane Hospital; †† Program Manager, Integrating Strategy and Performance, Queensland Health; ‡‡ Program Director, Queensland Health Skills Development Centre, Royal Brisbane Hospital. ian_scottAThealth.qld.gov.au In reply: We agree with Hadfield that optimising cardiac care may require extra resources targeted at increasing access of patients in regional Queensland to specific interventions, such as coronary angiography, cardiac rehabilitation and echocardiography, in addition to the quality-improvement strategies used within our collaborative. We contend that both approaches are necessary, and that the magnitude of improvement achieved by either will depend on the intensity with which they are applied. Indeed, the “high-intensity” quality-improvement hospitals in our study were defined on the basis of more funding being made available to undertake quality-improvement activities at those sites. We concede that some of the differences in quality indicators between “high-intensity” and “low-intensity” quality-improvement hospitals may be attributable to inequities in capital expenditure on service delivery that we did not measure. However, some of the differences may have also arisen from variation in systems for identifying and referring those patients who have most to gain from receiving the care targeted by our collaborative.

Ian A Scott · Irene C Darwin · Kathy H Harvey · Andy B Duke · Nicholas D Buckmaster · John Atherton · Hazel E Harden · Michael Ward

Barry E Christophers Retired General Practitioner, 1/12 Tollington Avenue, East Malvern, VIC 3145 To the Editor: I write concerning the recent article about my letters to the MJA in the 1950s and 1960s drawing attention to Indigenous health issues.1 Mention is made in the article of the campaign waged by the Federal Council for the Advancement of Aborigines and Torres Strait Islanders concerning the exclusion of Queensland Aboriginal patients with tuberculosis from the generous allowance paid to other TB patients. This campaign was successful. The Tuberculosis Act was amended so that Aboriginal people were not excluded from receiving this allowance. The Australian Medical Association supported this campaign. Without its support it would have failed.

Barry E Christophers

Subhash C Arya,* Nirmala Agarwal† * Clinical Microbiologist; † Chief of Gynaecology and Obstetrics, Sant Parmanand Hospital, 18 Alipore Road, Delhi-110054, India. subhashjiAThotmail.com To the Editor: The recent editorial by Burgess and McIntyre on the recommended vaccination schedules in Australia1 points to the fiscal constraints on offering the new, costlier vaccines. Overcoming these constraints would not be insurmountable if vaccinations were to be linked with annual festivals and celebrations in the life of individuals and the community. Birthday celebrations are important for infants and preschool children. Rather than giving conventional birthday gifts, varicella vaccine, costing $40, would be most appropriate. For those in the sixth or higher decades of life, gifts of influenza vaccine, 23-valent pneumococcal polysaccharide vaccine or the adult formulation of the diphtheria–tetanus vaccine would be memorable on Mother’s Day or Father’s Day and silver, golden or platinum wedding anniversaries. Similarly, slight adjustments to the allocation of funds for celebrating festivals such as Christmas and New Year, Dewali or Eid could make costly vaccines available to all. Vaccine producers, like department stores, could gear up for a Christmas vaccine sale. The public should be motivated to consider vaccines the most appropriate gifts. This is bound to address any poor coverage of costlier vaccines, such as varicella or the pneumococcal polysaccharide vaccine.

Subhash C Arya · Nirmala Agarwal

Ronan J Murray,* Kishore Sieunarine,† Peter B Ward,‡ John W Pearman§ * Senior Microbiology Registrar, § Clinical Microbiologist, † Vascular Surgeon, Royal Perth Hospital, Perth, WA; ‡ Senior Scientist, Department of Microbiology, Austin Repatriation Medical Centre, Heidelberg, VIC. ronan.murrayAThealth.wa.gov.au To the Editor: Previous articles in the Journal have described the emergence of Staphylococcus aureus with reduced susceptibility to vancomycin (also known as heteroresistant vancomycin-intermediate Staphylococcus aureus, or hVISA) in populations where methicillin-resistant S. aureus (MRSA) is endemic in healthcare settings.1,2 We describe a case of infection caused by hVISA from a region where healthcare-associated MRSA infection is relatively uncommon.3 A 79-year-old woman with an extensive medical history, including type 2 diabetes mellitus and multiple bypass procedures for lower-limb ischaemia, presented with critical ischaemia of the right lower leg. After above-knee amputation, she developed a discharge from the stump wound from which multiresistant MRSA was cultured. Despite receiving several courses of intravenous vancomycin (a total of 25 days of therapy over 5 months), the infection did not resolve. Extensive debridement surgery, with removal of multiple grossly infected vascular grafts, was performed, and MRSA was cultured from the graft material. Subsequently, the patient developed a discharging sinus from which MRSA with reduced susceptibility to glycopeptide antibiotics was cultured (vancomycin minimal inhibitory concentration [MIC], 8 mg/L; teicoplanin MIC, 24 mg/L). This isolate was shown to be hVISA by population analysis profiling (PAP). When the original MRSA isolate was subsequently tested by PAP, heterogenous subpopulations of bacteria with reduced susceptibility to vancomycin were present which had not been detected by routine susceptibility testing (ie, the isolate was already hVISA). Review of the patient’s medical records from other Perth healthcare institutions revealed no evidence of vancomycin administration before the initial isolation of MRSA, or contact with known MRSA-colonised patients or healthcare workers. Multilocus sequence typing and staphylococcal cassette chromosome mec allotyping identified the MRSA strain as ST239-MRSA-III, a multiresistant “international” MRSA clone frequently isolated in Australia, mainly on the east coast.4 Despite further surgery and institution of alternative antimicrobial therapy (initially rifampicin and fusidic acid and subsequently linezolid), the patient died of ongoing ischaemia and uncontrolled infection. Prolonged or repeated use of vancomycin in patients with implanted prostheses that are infected with MRSA should be discouraged, not only because it is commonly futile, but also because it may promote the emergence of subpopulations of S. aureus with reduced susceptibility to vancomycin, as occurred in this case. The fact that these resistant subpopulations were detected in an isolate before the commencement of vancomycin therapy (and then only with specialised testing) reinforces our recommendation.

Ronan J Murray · Kishore Sieunarine · Peter B Ward · John W Pearman

James D Kidd Retired General Practitioner, The Medical Centre, 125 River Road, Emu Plains, NSW 2750. To the Editor: Although I am retired, I wish to make some comment on the controversy about the use of ciprofloxacin in the treatment of chronic suppurative otitis media.1 I still feel uneasy when there is mention of the topical use of an antibiotic that may be used either orally or parenterally. Many years ago, when I had a large practice, including paediatric patients, chronic suppurative otitis media was common, although most cases responded to the classical ear drops. However, some persisted and, not infrequently, a new patient would present with this problem. As mentioned, most were the result of a pseudomonas infection. Pseudomonas was then a common problem in chronic leg ulcer of the elderly, and I had found that treatment with Burrow’s solution (aluminium sulfate [2.25 g], acetic acid [33%], tartaric acid [0.45 g], calcium carbonate [1 g], purified water [7.5 mL]) was very successful and continued to be successful right up to my retirement, even in new cases which had been treated unsuccessfully with ciprofloxacin. Before the advent of ciprofloxacin, I used Burrow’s solution ear drops in many adult cases of chronic suppurative otitis media with great success. As the number of children with this problem grew, I attempted to get advice on the use and any toxicity of Burrow’s solution ear drops in children. I could not find anyone at the Children’s Hospital with any experience, but the consensus was that it was unlikely to be toxic. Although at first I had difficulty in getting the chemist to make up ear drops for adults, by this time there was little problem getting them made for children, and the results were dramatic. There were recurrences, but these responded as well as they did the first time they were treated. Advice on correct aural hygiene after swimming and bathing was important. Burrow’s solution kills pseudomonas. Am I too old fashioned?

James D Kidd