Letters

Martin B Van Der Weyden Editor, The Medical Journal of Australia, Locked Bag 3030, Strawberry Hills, NSW 2012. editorialATampco.com.au In reply: Fate (or God) moves in both mysterious and wondrous ways. Maybe the manoeuvring and machinations of our health ministers in the consummation of the 2003–2008 Australian Health Care Agreements are worthy of: If you have a little ditty You would like to expose, Send it to the Journal We’ll publish your witty prose. All I can say is that the faux pas in the production process shows that, despite its high technology, it is still a human process. To err is human, so let’s not make a very public faux pas all consuming.

Martin B Van Der Weyden

To the Editor: Are we doctors, physicians, MDs, MBs or what? In the past 50 years or so, the address form “doctor” seems to have lost much of its meaning. Of course, academics holding non-medical doctorates in Australia have long nursed a grievance that graduates in medicine have no rightful claim to the title. Perhaps so, but, like it or not, it was thrust upon us at graduation as a courtesy title, and there is no doubt that in the 50s it was of value to patients in establishing the status of their medical advisers. The rightfulness of the use of the title “doctor” by medicos is supported by antiquity, although divinity, law and music might claim precedence over medicine in using the title. The ancient word “doctore” can be translated simply as “teacher”, and the title, or its equivalent, was so used in Roman and ancient Greek times. There is a reference to the term in its medical sense in a quote from Chaucer (c 1386) in the Oxford English Dictionary: “WiÞ vs Þere was a Doctur of Phesike”.1 At present in Australia we have dentists, veterinary surgeons and others who identify themselves as “doctors”. And then there are legions of PhDs in such diverse disciplines as demography, political science, nursing, economics, leisure industries, and so on. In Australia, where we have inherited much of our general medical culture from the United Kingdom, surgeons are often addressed as “Mr” (a legacy of the days of the barber-surgeons) within their hospitals, but “Dr” by their patients. In North America, where medicos acquire the letters “MD” on graduation, “physician” seems to be the generic term in professional circles, while for journalists, “a doctor” or “an MD” are interchangeable identifiers. We could anticipate that any trend away from “doctor” to “physician” in Australian medical literature to follow the US example would meet with strong opposition from internists protecting the integrity of their “physician” status conferred by the Royal College. Understandable opposition to the adoption of “MD” as a generic identifier could be expected from holders of Australian MDs gained by thesis. So is it time for a title change? Change would not be unprecedented. The University of Sydney changed the qualifying degrees from MB, ChB (1882) to MB, ChM (the by-laws being altered in 1884 so that the latter degree was conferred on those who elected to receive it). The first degree in surgery was changed again to BS in 1922 but remained optional until 1974.2 Several Australian universities have recently made radical changes to the content and duration of medical-school courses. Perhaps the indefinite term “an MB” could be adopted as a surrogate for the popular US term “an MD”. Perhaps a new, uniform Australian medical identifier will evolve. Or perhaps we will just muddle on, letting sleeping dogs lie and confusion continue. This seems to be the probable outcome, as good reason rarely prevails in the minds and hearts of men.

Dennis D Arnold MB BS, FRCS, FRACS · Thomas KF Taylor DPhil, FRCS, FRACS

To the Editor: Patiens in Latin refers to someone who is suffering. However, in the real world the word “patient” also, ironically, takes on elements of the more conventional meaning of the word in its adjectival form. A person becomes a patient when he becomes ill. From that moment onwards he begins to comprehend the indubitable reason for being tagged as a “patient”. He patiently bears the ride to the doctor’s office and waits with a dutiful patience, in a room appropriately dubbed the waiting room, until he is called into the consulting room. Like a zombie, he patiently waits in the consulting room, obeying the dictates of the nurse to either stand on a weighing scale or sit on a chair for blood pressure measurements, while he patiently answers a volley of insipid questions about his health. In between, he waits patiently, with a thermometer perched precariously in his mouth, as the nurse stares at her watch or waits for the thermometer to beep. Then he patiently submits to the discomfort of donating blood or the indignity of providing urine or sputum samples. Ultimately he gets the golden opportunity to understand the real meaning of patience as he patiently waits for the doctor to arrive. The doctor, knowing full well the patience of patients, takes his time to arrive at the clinic. Steadfastly ignoring calls from the clinic, he works diligently on grant proposals/lectures/administrative matters until finally, unable to quench persistent calls, he dashes out to see his patient patients. Now that the interminable wait is finally over, the patient patiently submits to an expert examination. He patiently describes his symptoms (again) and patiently listens to what the doctor has to say. The need to draw on a seemingly immense reserve of patience does not cease once the patient leaves the doctor’s surgery. After patiently waiting at the pharmacy for his prescription, he patiently takes the medicines according to the doctor’s orders. He then patiently waits for the medicines to take effect. Therefore, calling a sick person a “patient” is particularly apt. It becomes slightly complicated when the terms “inpatient” and “outpatient” are used. Does a lack of patience eventually turn a patient patient into an inpatient? When all’s said and done, it is always better to be a patient patient than an impatient patient who tries the patience of potentially impatient doctors who rely greatly on the potential patience of patients.

Biji T Kurien

To the Editor: The 25th Australian Conference of Health Economists was held in Canberra on 2–3 October 2003. This conference used to be held in shabby university seminar rooms, with dry biscuits and instant coffee. This year it was held in a modern facility — the SAS Visions Theatre at the National Museum — with all the usual conference embellishments, including brewed coffee and fresh pastries, plus an evening dinner at the lakeside restaurant within the museum. The conference was sponsored by Medicines Australia; Pfizer Pty Ltd; Bristol-Myers Squibb Australia Pty Ltd; AstraZeneca Pty Ltd; Sanofi-Synthelabo Australia Pty Ltd; Schering-Plough Pty Ltd; Bayer Australia Limited; and Merck Sharp & Dohme (Aust) Pty Ltd.1 Why are those traditional sponsors of medical gatherings, the pharmaceutical companies, subsidising the health economists’ conference? The immediate explanation is simple. Applications to the Pharmaceutical Benefits Advisory Committee for listing of a drug on the Pharmaceutical Benefits Scheme must now include a formal cost-effectiveness study. This requirement has generated a boom in this narrow technical aspect of health economics. Thirteen of the 32 papers presented to the conference reflected this area of interest.1 But are we seeing something more fundamental here? Are the canny pharmaceutical companies directing their largesse away from the once autonomous doctors to the dry bean counters who now make the real decisions? Or have the economists proved one of their own famous maxims wrong by demonstrating that there is such a thing as a free lunch?

William Coote

William J Glasson,* Robert A Bain† * Federal President, † Secretary General, Australian Medical Association, PO Box E115, Kingston, ACT 2604. To the Editor: The workforce article by Brooks et al1 identifies key factors causing the medical workforce shortage and notes, correctly in our view, that: “The full impact of these factors is yet to be felt, but might occur very rapidly”. However, the authors fail to address why this has occurred and what should be done. The answer as to why is quite simple. In the 1990s, the Labor and Coalition federal governments introduced a series of measures to ration the supply of doctors and the provision of services in order to restrain the health budget. Measures such as restrictions on medical student places, reduced training places, restricted provider numbers, failure to properly index the Medicare Benefits Schedule or introduce the Relative Value Study, and the move away from fee-for-service with the rapid expansion of red tape, were all designed to restrict services that cost the government money. The current doctor shortage, falling participation rates (the trend to doctors retiring early or working part-time) and demoralisation of significant sections of general practice are a tribute to the success of these policies. As the recent Australian Medical Workforce Advisory Committee careers study shows, the much-discussed feminisation of the GP workforce is as much a consequence of a declining number of young male doctors considering general practice to be a rewarding career as it is the result of a need by both male and female doctors for an occupation that allows a flexible work and family lifestyle.2 Nevertheless, the outcome — the falling participation rate among current and future general practitioners — is at the heart of the problem. The solution will require a total shift in policy direction from sticks to carrots. It will need to cover Medicare, training, working conditions, and the removal of red tape and all forms of restrictions not required to ensure good clinical practice. Attempts to use regulations or commercial levers to enforce bulk-billing in an already depleted workforce will only serve to exacerbate the current situation.

William J Glasson · Robert A Bain

Francisco J Ruiz-Ruiz,* Fernando J Ruiz-Laiglesia,† Juan I Perez-Calvo,‡ Carmen B Torrubia-Perez§ * Home Doctor; †,‡ Associate Professor of Medicine; § Staff Doctor, Servicio de Medicina Interna “B”, Hospital Clínico Universitario “Lozano Blesa”, Avenida San Juan Bosco 15, Zaragoza 50009, Spain. fjruiz1ATterra.es To the Editor: Sarcoid arthritis is often underdiagnosed because it may mimic reactive or rheumatoid arthritis. We report a case which was initially misdiagnosed. A 38-year-old white woman was admitted to hospital because of pain and swelling of her hands and feet. Two years earlier, she had been admitted because of joint pain and erythematous, painful round lesions on her shins. A chest x-ray at that time was normal. She was diagnosed with reactive polyarthritis based on positive serological tests for Rickettsia conorii and Coxiella burnettii. Doxycycline and indomethacin were given and her condition improved. Three days before the current admission her fingers, wrists and ankles had become painful and swollen. There was tenderness and swelling of the metacarpophalangeal, wrist and ankle joints. She was afebrile. Chest x-rays showed an enlarged left hilum. Computed tomography (CT) of the chest (Box) showed lymphadenopathy in the mediastinum and both hila. Her erythrocyte sedimentation rate was 104 mm/h (normal, 3–12 mm/h). Laboratory test results were normal, except for an elevated serum level of angiotensin-converting-enzyme (ACE). A mediastinoscopy was performed, and specimens obtained for biopsy revealed sarcoidosis. Prednisone (30 mg/day) was prescribed and she was discharged 7 days later with no symptoms. “Sarcoid arthritis” is a sarcoid process whose main or unique manifestation is joint disease. Some of its characteristics are seasonal clustering (typically in spring), higher incidence among non-smoking patients, and the presence of the human leukocyte antigen DQ2 (DQB1*0201) and DR3 (DRB1*0301) haplotypes. It occurs slightly more frequently in women. The median age of affected patients is 40 years. The process affects mainly ankle and knee joints symmetrically. Acute sarcoid arthritis is a self-limiting joint disease with a benign prognosis, but some patients can develop chronic sarcoidosis of the lungs, specially those who suffer recurrent episodes of arthritis.1,2 In our patient, the first episode, with associated erythema nodosum, was misdiagnosed as a reactive arthritis as there were false positive serological test results for Rickettsia and Coxiella secondary to an immune polyclonal response. In the second episode, the patient had mediastinal and hilar lymphadenopathy and an elevated ACE level. Although sarcoid arthritis is very often associated with lymphadenopathy and erythema nodosum (Löfgren syndrome), we should keep in mind other forms of joint involvement in sarcoidosis.3 Doctors should consider sarcoid arthritis in the differential diagnosis of seronegative arthritis. Chest x-ray and ACE assay are useful in identifying sarcoidosis. Computed tomography scan showing mediastinal and hilar lymphadenopathy

Francisco J Ruiz-Ruiz · Fernando J Ruiz-Laiglesia · Juan I Perez-Calvo · Carmen B Torrubia-Perez

Zhiqiang Wang,* Wendy E Hoy† * Senior Research Fellow, † Professor, Centre for Chronic Disease, School of Medicine, University of Queensland, Herston, QLD. zwangATccs.uq.edu.au To the Editor: In a recent article, Thompson and colleagues provided useful information on the prevalence of cardiovascular risk factors in urban Aboriginal people.1 Using the Sheffield table of absolute risk,2 the authors estimated that “15% men and 6% women had an absolute risk > 15% of a cardiovascular event within 10 years”. The Sheffield risk table was developed for assessing the risk of coronary deaths rather than the risk of cardiovascular events.2 Moreover, the validity of applying the Sheffield table and other risk assessment tools based on the Framingham risk functions to Aboriginal people is yet to be assessed. The lower risk estimate in women reported by Thompson and colleagues may simply reflect the higher cholesterol concentration cut-offs for women in the Sheffield table. The true risk difference between sexes in Aboriginal people may not be as dramatic as Thompson and colleagues suggest. Firstly, data in Box 1 of their article show that there was little difference between men and women as regards past history of cardiovascular disease. Secondly, Aboriginal women experience a higher prevalence than men of some cardiovascular risk factors such as diabetes,1,3 abnormal HDL cholesterol level and overweight.3 Thirdly, our own research suggests that there may be a substantial difference between estimated and observed risks. Using data from a cross-sectional study of 681 Australian Aboriginal people in a remote community,3 we performed a similar analysis to that of Thompson et al. Based on the Framingham functions,4 we estimated that 10-year risks of coronary heart disease for women were much lower than those for men in all age groups (a finding similar to that of Thompson and colleagues). However, in a related study of the same Aboriginal community (as yet unpublished), when we analysed cohort data from 838 participants with 13 years of follow-up, the observed coronary disease rates for women were as high as those for men (Box). The discrepancy we found between estimated and observed risks is a warning that researchers and clinicians need to be cautious when applying existing risk assessment tools to Aboriginal people. Incidence rates per 1000 person-years of coronary heart disease (95% CI), by age and sex (based on a cohort study of 838 Aboriginal people in a remote community) Age (years) Women Men 20–34 4.1 (1.8–9.1) 3.2 (1.4–7.0) 35–44 15.6 (9.4–25.9) 8.6 (4.5–16.5) 45–54 19.3 (10.9–33.9) 26.5 (15.0–46.7) ≥ 55 50.2 (32.4–77.9) 31.9 (16.6–61.2)

Zhiqiang Wang · Wendy E Hoy

Peter L Thompson,* Pamela J Bradshaw,† Margherita Veroni,‡ Edward T Wilkes§ * Cardiologist, † Clinical Research Coordinator, ‡ Epidemiologist, Western Australian Heart Research Institute, Sir Charles Gairdner Hospital, Nedlands, WA 6009; § Senior Research Fellow, Centre for Developmental Health, Telethon Institute for Child Health Research, Subiaco, WA. peter.thompsonAThealth.wa.gov.au In reply: We appreciate the commentary by Wang and Hoy on the problems of the use of risk scores for assessing cardiovascular risk in Aboriginal people. In general, we agree that caution is essential in using tables that predict absolute risk of cardiovascular events. However, despite their limitations, absolute risk estimates are being encouraged by Australian, European, New Zealand and US authorities as a practical aid to targeting coronary disease preventive measures.1 An estimated risk of > 15% of a fatal cardiovascular event within 10 years, based on the Sheffield or Framingham scores, is now recommended as an indication for active treatment. Our prime purpose in providing an estimate of absolute risk in the Perth urban Aboriginal population was to demonstrate that a program of cardiovascular risk assessment with strong Aboriginal community support is capable of detecting high-risk people who will benefit from intensive risk-lowering strategies. Wang and Hoy’s caution about applying absolute risk estimates based on the Framingham population to unrelated populations is of particular importance in the case of Australian Indigenous people, in whom diabetes and the related metabolic syndrome may be the predominant risk factors. We have recently completed an analysis of the determinants of carotid atherosclerosis in the same population described in our earlier study.2 Our results confirm that, while the Framingham estimates (based on sex, age, LDL cholesterol and blood pressure) are indeed predictors of carotid atherosclerosis, their predictive value is significantly enhanced by the addition of markers of diabetes status and obesity. The 13-year follow-up study of the Aboriginal cohort referred to by Wang and Hoy will provide unique data to help identify reliable risk predictors specific to Aboriginal people, and we look forward to its publication.

Peter L Thompson · Pamela J Bradshaw · Margherita Veroni · Edward T Wilkes

John R M Caplehorn Senior Lecturer, Clinical Epidemiology, School of Public Health, University of Sydney, Sydney, NSW 2006. johncAThealth.usyd.edu.au To the Editor: The trial of buprenorphine-assisted heroin detoxification in primary care and a specialist clinic by Gibson et al1 was intended to compare the effectiveness and cost-effectiveness of buprenorphine-assisted withdrawal in a specialist clinic with treatment by general practitioners. However, of the average $191 for primary care staff costs, $69 was incurred at the clinic. As at least a third of interactions between patients and staff actually took place in the clinic, the primary care arm of the trial was really a combination of specialist clinic and primary care. Another design problem was the study’s lack of statistical power. A study would need 550 participants to have an 80% chance of identifying (at the 0.05 level of statistical significance) a difference of 50% in self-reported abstinence during the 8-day detoxification (ie, improving the percentage reporting abstinence from 22% to 33%). The trial by Gibson and colleagues had only 115 participants. As expected, the trial produced statistically non-significant results. Yet, the authors highlight the finding that 23% of primary care patients reported being abstinent during the 8-day detoxification, compared with 22% of the clinic patients, (95% CI risk difference, –14.1% to 16.5%; P = 0.9 [χ2]). Moreover, the clinic group performed better on an objective and more reliable measure of abstinence: 20% of clinic patients versus 14% of primary care patients gave morphine-free 8th day urine specimens, (95% CI risk difference, –7.7% to 19.8%; P = 0.4 [χ2]). As the confidence intervals for these risk differences include zero, the confidence interval for any estimate of incremental cost-effectiveness includes infinity. It is quite misleading for Gibson and colleagues to claim that “it costs $20 to achieve a 1% improvement in outcome in primary care”, as this ignores both the conflict and the variability in their clinical outcomes.1 Moreover, the statement ignores the variability in the estimated costs of treatment (eg, mean cost per clinic patient, $332; SD, $70). Surprisingly, Gibson and colleagues did not collect any information on continuing abstinence at the 13-week follow-up. Rather, they collected information on patients’ current treatment. While patients in whom detoxification therapy fails should be offered other treatment, post-withdrawal engagement in maintenance treatment is not a meaningful measure of the effectiveness of detoxification. If anything, it is a measure of failure. The trial needed sufficient statistical power to identify clinically meaningful differences in abstinence at the end of the 8-day detoxification and at 13 weeks. Staff working in the specialist clinic should not have been extensively involved in the delivery of primary care. Gibson and colleagues should have summarised their findings using appropriate estimates of clinical effect and cost-effectiveness with 95% confidence intervals.2

John R M Caplehorn

Amy E Gibson Senior Research Officer, The National Drug and Alcohol Research Centre, University of New South Wales, Sydney, NSW 2052. amy.gibsonATunsw.edu.au In reply: The primary focus of our study1 was retention in treatment, and not differences in abstinence. Caplehorn has previously argued compellingly that an orientation to abstinence can have an adverse impact on treatment outcomes in opioid dependence.2 We were using buprenorphine to redefine detoxification, not as a treatment producing lasting abstinence but as a way of promoting engagement in ongoing treatment. The power of our study was calculated on the basis of the proportion of subjects entering post-detoxification treatment, not on their self-reported abstinence levels. During the detoxification stage in the primary care setting, we used a shared-care dosing arrangement. This was primarily because of the need to give an initial research assessment to all participants before they were randomly allocated to treatment arms — something that would only occur in the context of a research study, and noted in the discussion. Further details of the health economic analysis are soon to be published.3 Ours was a study of the setting for buprenorphine treatment. Its critical finding was that patients were equally as likely to be engaged in maintenance treatment with practitioners in primary care as in specialist clinics.

Amy E Gibson

Paul M Bailey Emergency Physician, Joondalup Health Campus, Shenton Avenue, Joondalup, WA 6027. pbaileyATiinet.net.au To the Editor: In the article by Davey1 no evidence other than deviation from a protocol published months before the study is produced to document the implied inappropriateness of single troponin assays. Emergency physicians are experienced in assessing undifferentiated chest pain. Acute coronary syndromes are but one cause of presentation to emergency departments (EDs) of patients with chest pain, and indeed are but one cause of elevated serum troponin levels. Many reasons may justify the “appropriate” ordering of single troponin assays. Some patients present to EDs many hours after their episode of chest pain. A single troponin test may be a very useful and sensitive test for a patient whose chest pain occurred yesterday. How many patients in the study group had their single troponin test done more than 12 hours after their episode of pain? How many patients discharged themselves against medical advice as they were unwilling to wait 6–8 hours for a second blood test to triage their risk for an acute coronary syndrome? How many patients died or were transferred to another hospital? How many patients had their single troponin test ordered in the investigation of a primarily non-cardiac illness, such as sepsis or pulmonary embolism? I have no doubt that many troponin assays ordered in the study population were inappropriate. But, by failing to conduct an explicit medical record review of those patients whose tests were deemed inappropriate, the author has failed to answer his stated aim of determining if the troponin assay is used appropriately when chest pain is encountered. We are left with no knowledge of whether this problem is small or large. Finally, does it matter? Are two consecutive negative troponin assays required to triage patients with chest pain? Recently, the Journal published a clinical outcome study that examined the implementation of a chest pain assessment protocol at a metropolitan university teaching hospital in Bankstown, Sydney.2 Patients presenting to the ED with “possibly cardiac” non-traumatic chest pain who were deemed to be low risk did not receive a second, late troponin assay, and yet this approach appeared to be safe. Those of us who have an interest in the rational use of diagnostic testing for patients with acute coronary syndromes eagerly await the publication of further evidence on this important matter.

Paul M Bailey

Richard X Davey Chemical Pathologist, Melbourne Health Shared Pathology Service, Western Hospital, Footscray, VIC 3011. Richard. DaveyATwh.org.au In reply: In acute myocardial infarction (AMI) diagnosis, the sensitivity and specificity of troponin rise with time after symptom onset. The sensitivity of troponin-I testing was shown to increase from 35% at 0–4 hours to 97% at 12–24 hours after an infarct.1 Similarly, a meta-analysis found that “multiple testing of individual biomarkers over time substantially improves sensitivity, while retaining high specificity” for AMI diagnosis.2 This position is taken by the National Academy of Clinical Biochemistry3 and European and American cardiologists.4 Furthermore, the diagnostic clock starts from a patient’s emergency department presentation if there is any unreliability suspected in the patient’s assessment of pain onset. Pain onset may have been stuttering, indeterminate, simply forgotten, some combination of these, or even absent. Bailey describes several situations such as these, thought to justify, or to explain, singlicate troponin testing, and suggests that, as I did not audit records, I was not able to quantify the true extent of inappropriate ordering. I acknowledged this shortcoming, but believe it does not detract from the endpoint found. The Bankstown low-risk patients5 are only a confounder here. In our protocol they probably would not have been thought to have cardiac pain, and all the remaining Bankstown patients had serial biomarker testing. In my audit,6 93% of singlicate troponin test orders did not diagnose an AMI, and if AMI were still considered, then the tests contravened the protocols.3,4 This is why they were called “inappropriate” — no arbitrary whim. I assumed, moreover, that no clinician ordered a troponin test unless seeking a cause for chest pain. Our protocol begins with chest pain, recognises uncertainty, and leads through to treating an AMI or reconsidering the diagnosis. Obliquely invoking Ockham’s principle is also dangerous here. Illnesses such as sepsis may “provoke” an AMI, but this must then be investigated independently, and according to its own rules of engagement, which do not alter solely because of the primary (co-)morbidity. In short, we did know what is appropriate troponin use, and surveyed it. Like Bailey, we look forward to seeing further evidence.

Richard X Davey

Lloyd K Morgan Retired General Practitioner, PO Box 150, Lorne, VIC 3232. To the Editor: New imaging and pathology investigations continually improve diagnostic accuracy. But tests must be used because they supplement clinical deduction, not because they are available, and the constellation of clinical features should not be ignored. The case report by Chatterjee and colleagues is valuable for describing delayed diagnosis of meningitis, based on imaging which suggested subarachnoid haemorrhage and aspiration pneumonia.1 The 4-day history, examination (raised respiratory and heart rates, high fever) and results of initial investigations (neutrophilia, raised C-reactive protein level, lung consolidation) suggested a primary respiratory infection. The absence of a typical history of onset of subarachnoid haemorrhage is excused by the 5.5- hour hiatus before the patient was found semicomatose. Subarachnoid haemorrhage was diagnosed because of density in the subarachnoid space on computed tomography (CT). The authors noted a 1980 report of this appearance in a patient with bacterial meningitis.2 They also noted only one previous report of purulent meningitis mimicking subarachnoid haemorrhage on CT scan (in 1994),3 but there is reluctance to publish “negative” outcomes. Aspiration as the cause of upper-lobe consolidation was unlikely. Bacterial pneumonia and chemical pneumonitis affect the lower lobe.4 Clinical findings were not consistent with subarachnoid haemorrhage, and meningitis was the differential diagnosis, so only the overweighted CT results prevented lumbar puncture on Day 0, which would have resulted in earlier, broader antibiotic therapy and possibly resumption of warfarin. By Day 1, it was too late to prevent permanent blindness (it was possibly too late on Day 0, but pupils were reactive at that time). Even on Day 1, repeat cranial CT showed infarction but less evidence of bleeding; “a disparity between the amount of [alleged] subarachnoid blood and the patient’s clinical condition” was followed by magnetic resonance imaging then angiography and venography, instead of lumbar puncture as suggested by hindsight in the last sentence of the report. Shadows do not always equate with pathology. Compare an article on the clinical diagnosis of meningococcaemia.5 Holistic care of Chatterjee et al’s patient included anticoagulation therapy. “It probably could have recommenced earlier” than after “a large pulmonary embolus” on Day 13 — perhaps, given the presence of long-term indications (lupus inhibitor, anticardiolipin antibody and previous thrombosis) and cerebral vessel inflammation causing infarction, on Day 1. The main lesson, which we were all taught as students but needs career-long reinforcement, is in the penultimate sentence of the case report: “Investigations should not be interpreted in isolation from the clinical picture”.

Lloyd K Morgan

Taposh Chatterjee,* John R Gowardman,† Tony D Goh‡ * Registrar, † Intensivist (corresponding author), ‡ Radiologist, The Canberra Hospital, PO Box 11, Woden, ACT 2605. John.gowardmanATact.gov.au In reply: We agree with Morgan that the symptoms, signs and laboratory investigations in our case report, although non-specific, supported a diagnosis of infection.1 The C-reactive protein level was not available for 24 hours. The unwitnessed drop in level of consciousness that occurred between 09:00 and 14:30 could have been secondary to meningitis or an acute cerebral event, and, while it is true that the lower lobes are predominantly involved in aspiration, they are not solely involved. Consolidation in other gravity-dependent segments, including the posterior segments of the upper lobes, can occur.2 The suggestion that “permanent blindness” could have been prevented is not supported. Fortuitously, an appropriate antibiotic to which the organism was fully sensitive was given from Day 0 (ceftriaxone). Adjunctive supportive care was quickly provided. In retrospect, anti-coagulation therapy could have recommenced earlier, but this remained a difficult decision in the context of the computed tomography findings. It remains unclear how this would have modulated the meningeal process, but it possibly contributed to the complication of pulmonary embolism. We agree that there is a reluctance to publish what may be perceived as “negative” outcomes, but, educationally, these may be the most rewarding. This case was an uncommon presentation of a common disease, and we considered it sufficiently important to notify other practitioners. Of most importance in this era when technology in medicine advances exponentially, any investigation must be considered only an adjunct to, and not a replacement for, thorough clinical evaluation.

Taposh Chatterjee · John R Gowardman · Tony D Goh

Amanda J Caswell Managing Editor, MIMS Australia, Locked Bag 3000, St Leonards, NSW 1590. amanda.caswellATmims.com.au To the Editor: Tan et al outline deficiencies in product information documents (PIs) as published in MIMS.1 It needs to be clarified that MIMS Australia is not responsible for the content of PIs — this is specified and approved by the Therapeutic Goods Administration in consultation with the sponsoring company. The conclusion by the authors that the “PIs for many prescription products listed . . . do not adequately detail paediatric doses” should not be specifically attributed to MIMS, as all published medicines information that relies on approved PIs will suffer from the same deficiencies.

Amanda J Caswell

Michael J O’Leary Intensive Care Physician, St George Hospital, Gray Street, Kogarah, NSW 2217. m.olearyATunsw.edu.au To the Editor: Hore and colleagues argue for “integrated critical care” as a solution to the problem of providing intensive-care cover for patients in rural and non-tertiary metropolitan hospitals.1 They claim that such an approach is required uniquely in these hospitals, whereas in tertiary centres “subspecialists would be involved in each phase of the management process”. That this occurs is undisputed; however, it is far from the optimal model of care.2 Over the past 3 decades, the management of critically ill patients has evolved to require its own specialty. Other than in the traditional critical-care disciplines of anaesthesia and emergency medicine, training in critical care is not a significant component of specialty training programs. Within tertiary hospitals, therefore, the requirement that critically ill patients be cared for by specialists trained in critical-care medicine (and not a “committee” of subspecialty experts) is no less important than in the rural setting. There is consequently little difference between the skills and experience required of tertiary and rural critical-care specialists, and the continuum of critical care is the same in both settings. The recent creation of the Joint Faculty of Intensive Care Medicine by the Royal Australasian College of Physicians (RACP) and the Australian and New Zealand College of Anaesthetists (ANZCA) has enabled many of the past artificial barriers to effective critical-care training and accreditation in Australasia to be broken down. It is now possible to enter intensive-care training from varied training programs, including those of the Australasian College for Emergency Medicine, the RACP and the ANZCA. Completion of training is recognised by successfully passing a broad-based critical-care examination. The argument that training could and should include rural practice is well made. However, any comprehensive critical-care training will inevitably require some high-volume experience only available within a tertiary institution. That there are differences in emphasis in the workload of our rural colleagues should be recognised. However, our job is essentially the same. There is no need for a separate specialty, but there is a need to ensure provision of high quality critical-care services to all patients into the future.

Michael J O’Leary

Neil T Matthews Dean, Joint Faculty of Intensive Care Medicine, Australian and New Zealand College of Anaesthetists and Royal Australasian College of Physicians, 630 St Kilda Road, Melbourne, VIC 3004. jficmATanzca.edu.au To the Editor: The article by Hore et al1 raises many important issues for acute-care medicine in rural settings, including the need for specialists to be multiskilled and collaborate across disciplines, the lack of professional support for rural training programs and rural specialists, and the difficulty of overseeing multidisciplinary credentialling. These issues are not unique to acute-care medicine or to the Joint Faculty of Intensive Care Medicine (JFICM). They are problems for other faculties and colleges, rural healthcare facilities and governments. Many rural specialist services in Australia and New Zealand have the benefit of considerable expertise provided by medical practitioners who are not necessarily Fellows of the relevant specialist colleges. They should be supported by collaborative efforts of the relevant colleges, which should develop initiatives to increase the numbers of specialist medical practitioners working in rural settings. The JFICM, representing some 464 Fellows and 391 trainees, has been developing frameworks to support rural intensive care. JFICM’s goals are to develop a more flexible training program to encourage rural training; to establish a rural officer on the JFICM Board; to support a rural focus group, working through rural structures with the Committee of Presidents of Medical Colleges; and to explore liaisons with other colleges. The argument for developing a specialty of integrated critical-care medicine implies that current programs are deficient and cannot provide a holistic, integrated approach to rural acute care. Hore and colleagues argue that “there is no formal program for training specialists for multidisciplinary rural critical-care practice”. I must correct them on this point. Their proposal in fact eloquently describes the elements of the JFICM training program, which has existed since 1977. An internationally recognised and comprehensive intensive-care/critical-care training program, its status has been confirmed with its successful accreditation by the Australian Medical Council. The authors also suggest that “critical care” is in some way different from “intensive care”. This is not contemporary reality. The terms “intensive care” and “critical care” are one and the same. Healthcare workers in rural and remote locations have collaboratively developed multidisciplinary working relationships that provide comprehensive acute and non-acute healthcare. The same approach should be used by authoritative bodies to resolve important issues for rural specialists and training programs. The issues do not require establishing a separate specialty. The above comments notwithstanding, the suggestion by Hore and colleagues that specialties involved in acute care lead a collaborative process to strengthen clinical links is to be applauded. The discussions need to be inclusive of medical specialists working in intensive care medicine.

Neil T Matthews

John Stokes Director of Intensive Care, Mater Private Hospital, Fulham Road, Pimlico, QLD 4812. john.stokesATmatertsv.org.au To the Editor: Hore et al1 raise some very pertinent issues relating to the delivery of integrated critical care in the rural setting and raise the possibility of a new specialty to help solve the problem. The issue of providing many services in rural, remote and regional Australia will not be solved by more subspecialisation, which is actually having the effect of centralising services in major metropolitan centres distant from important and productive portions of our population. Rather than propagate another group of subspecialists, our medical colleges, and in particular the Australian Medical Council (AMC), need to look at new ways to empower specialists and generalists who work in regional areas to continue to provide services without their expertise being undermined in the eyes of the public. We need to encourage state governments to spread services more widely rather than to centralise and remove rural services. The push for so-called “centres of excellence” that draw all patients to a few centres is for the convenience of the few and is financially attractive to governments. Artificial standards for care (produced by the medical colleges), with restrictions on practice related to the number of patients treated or the number of patients ventilated, are unrelated to the quality of care delivered to individual patients. These restrictions may soon lead to many specialties not being sustainable outside capital cities or major urban centres because of insufficient caseload to meet the guidelines. In regional areas, specialists (such as anaesthetists) who have the experience to provide additional services (eg, intensive care), but not the formal recognition, are being discouraged from doing so by the college guidelines and the current legal climate. My observation of the actions of most medical colleges is that, by their good intention to maintain standards, they are supporting the concentration of services but are discouraging the wide delivery of services. Surely, when we do studies that demonstrate that care is better delivered in special or centralised units, the aim should be to find out why, and to seek ways to deliver that expertise in less specialised and more decentralised units, rather than to immediately call for more centralisation of services. This, I believe, is the real challenge for our AMC and our Committee of Presidents of Medical Colleges.

John Stokes

Craig T Hore,* William Lancashire,† John B Roberts,‡ Robert Fassett§ * Director of Critical Care, † Director of Critical Training, ‡ Director of Emergency Medicine, Port Macquarie Base Hospital, PO Box 2466, Port Macquarie, NSW 2444; § Director of Renal Unit, Department of Medicine, Launceston General Hospital, Launceston, TAS. horeATmaynegroup.com In reply: We thank the correspondents for their interest, insights and discussion. In general, there appears to be much common ground between our views and theirs, although a few points of clarification need to be made. We do not argue that a “committee of subspecialty experts” undertakes critical care in tertiary centres, as O’Leary suggests. The subspecialists we refer to are those within the discipline of critical care, particularly intensivists, emergency physicians and anaesthetists. In tertiary settings, these specialists operate predominantly within their base critical-care “subspecialty”. In rural settings, they are also involved in the other phases of critical care on a regular basis. Hence, while the principles of critical care are similar in rural and metropolitan settings, their effective delivery differs. We do not question that the Joint Faculty of Intensive Care Medicine (JFICM) provides a comprehensive intensive-care training program. However, there are very few JFICM-accredited intensive-care units in Australia outside metropolitan centres, and few JFICM-endorsed specialists working in the public sector in rural and remote intensive-care units.1 Unfortunately, this suggests that the current JFICM program is not addressing the needs of rural and remote centres. Indeed, in their recent review, the Australian Medical Council encouraged the JFICM to give more opportunity and encouragement for trainees to gain rural experience.2 The steps being undertaken by the JFICM that Matthews outlines are encouraging. We believe the statement by Matthews that “intensive care and critical care are one and the same” is insular and at odds with the reality of critical care, especially outside tertiary metropolitan centres. It is pleasing to note that O’Leary includes emergency medicine as a “traditional critical-care discipline”. There are strong clinical and curriculum similarities between emergency medicine and intensive-care medicine that cannot be overlooked. In this respect, rural centres may be leading the way in further breaking down barriers. The formation of the JFICM has been a positive step, but it remains a liaison of only two bodies. A greater presence from emergency medicine, rural anaesthesia, rural medicine and surgery would be beneficial and a significant step towards a truly multidisciplinary specialty. We reaffirm that, to ensure high standards of critical care for rural patients, solutions need to match the existing realities of rural practice. We agree that these must be collaborative and inclusive. The integrated critical-care model has been successful in a number of rural hospitals and offers potential for wider implementation.

Craig T Hore · William Lancashire · John B Roberts · Robert Fassett

Ian G Jacobs,* James Tibballs,† Peter T Morley,† Jennifer Dennett,‡ Jeff Wassertheil,§ Vic Callanan,¶ John Hall** (ARC executive committee on behalf of the Australian Resuscitation Council) * Chairman, Australian Resuscitation Council, C/- Royal Australasian College of Surgeons, Spring Street, Melbourne, VIC 3000; † Physician, Intensive Care Unit, Royal Children’s Hospital, Melbourne, VIC; ‡ Nurse Unit Manager, Central Gippsland Health Service, Sale, VIC; § Director of Emergency Medicine, Peninsula Health, Frankston, VIC; ¶ Head, Anaesthesia, Townsville Hospital, Townsville, QLD; ** Superintendent, Divisional Office, Ambulance Service of NSW, Hurstville, NSW. ijacobsATcyllene.uwa.edu.au To the Editor: With the increasing availability of biphasic defibrillators for use in both the manual and shock-advisory modes, considerable confusion has developed as to the appropriate energy levels to be used with these devices. This confusion has arisen partly because of differing recommendations from manufacturers, partly as a result of limited clinical evidence and partly because of the clinical availability of both monophasic and biphasic defibrillators. The differences between these waveforms are the way energy is delivered. Biphasic energy is delivered in two directions, whereas monophasic energies are delivered in one direction. Recommendations of the International Liaison Committee on Resuscitation state that biphasic energies less than or equal to 200 J are as efficacious as escalating higher-energy monophasic shocks.1 Lower-energy biphasic shocks cause less myocardial injury and postresuscitation myocardial dysfunction, and so potentially improve the likelihood of survival.2 Faced with the lack of data with respect to biphasic energy levels, the Australian Resuscitation Council makes the following recommendations: 1. When using manual biphasic defibrillators, energy levels of 150 J should be used for defibrillating ventricular fibrillation and pulseless ventricular tachycardia in adults. The basis of this recommendation is as follows: one randomised controlled trial in people in out-of-hospital ventricular fibrillation compared monophasic and biphasic shocks delivered by automated external defibrillators (AEDs).3,4 This study showed that 150 J biphasic shocks achieved higher rates of defibrillation and return of spontaneous circulation than higher-energy (200 J/200 J/360 J) escalating monophasic shocks. No differences were observed in the proportion of patients discharged from hospital. As clinical superiority of one particular biphasic waveform over another has yet to be demonstrated, it is appropriate to recommend this single energy level to achieve a consistent approach. 2. Biphasic energy levels of 1–2 J/kg should be used for defibrillating ventricular fibrillation and pulseless ventricular tachycardia in children. The basis of this recommendation is as follows: extrapolation from adult data, supported by studies in “child” and “infant” animal models, suggests that the dose for biphasic shocks in children should be 1–2 J/kg (about half the monophasic dose). Higher doses (up to 4 J/kg) are not likely to be harmful and are more efficacious than equivalent monophasic shocks.5 Biphasic shocks may be delivered in a fixed dose of 50 J by an AED. The use of AEDs in children less than 1 year of age is not recommended, as in this situation these devices are unable to differentiate between shock-able and non-shockable rhythms (eg, ventricular fibrillation v pulseless electrical activity). Energy levels for AEDs when used in automatic mode have been pre-set by the manufacturer, and do not require an energy level to be set by the user.

Ian G Jacobs · James Tibballs · Peter T Morley · Jennifer Dennett · Jeff Wassertheil · Vic Callanan · John Hall

Judy A Seal,* Eric M Johnson,† Zelda Doyle,‡ Kelly Shaw§ * State Nutrition Officer, † State Food Officer, § Public Health Registrar, Public and Environmental Health, Department of Health and Human Services, GPO Box 125, Hobart, TAS 7001; ‡ Field Officer, Broad Street Consultants, Tasmanian Iodine Monitoring Program, Lauderdale, TAS. judy.sealATdhhs.tas.gov.au To the Editor: Tasmania has been recognised for many years as an area of endemic iodine deficiency.1 According to the World Health Organization, populations are considered iodine sufficient if population median urinary iodine (UI) levels exceed 100 μg/L, with less than 10% of the UI levels below 50 μg/L.2 Two random surveys (1998–99 and 2000–01) of Tasmanian school children aged 4–14 years suggest mild iodine deficiency. Median UI levels were 75 μg/L and 77 μg/L, with 13% and 21%, respectively, of the UI levels below 50 μg/L.3 In response to these findings, an iodine supplementation program was introduced in October 2001. Tasmanian bakeries were encouraged to switch to using iodised salt in place of regular salt. The program is voluntary, with participating bakeries asked to sign a memorandum of understanding. Industry advice suggests that bakeries that have signed the memorandum produce about 80% of the bread available for consumption in Tasmania. The Tasmanian Iodine Monitoring Program commenced in July 2002. Its objectives are to determine the effect of iodine supplementation of bread on the general population and on high-risk groups, and to identify any negative health effects associated with the program. Preliminary results from the monitoring are encouraging. Children were selected using a random cluster sampling approach. The sampling frame included all Grade 4 classes in all government, Catholic and independent schools in Tasmania. To date, 148 urine samples have been collected, with results from 124 available (test completion rate, 84%). The median UI level from the preliminary results is 97 μg/L (95% CI, 90–109 μg/L), with 10.5% below 50 μg/L. Ongoing monitoring will provide a more rigorous evaluation of the effects of the iodine supplementation program. Early indications suggest the supplementation program may be achieving its goal of improving the iodine status of the Tasmanian population. The monitoring program will continue for the next 4 years, with regular surveys to detect any changes in the population’s iodine status. It will be challenging to retain the ongoing participation of the bread industry if, in the future, there is increased reliance on premixed and ready-to-bake products from outside Tasmania. Maintaining bread supplementation in Tasmania would then require cooperation from interstate suppliers to ensure iodine supplemention of these premixes and ready-to-bake products. Given that recent research has shown mild iodine deficiency in other parts of Australia and New Zealand, perhaps it is time for a bi-national solution to the problem.4,5

Judy A Seal · Eric M Johnson · Zelda Doyle · Kelly Shaw

Donna B Mak,* Eleanor M Platt,† Christopher H Heath‡ * Public Health Medical Officer (currently, Adjunct Research Fellow, School of Population Health, University of Western Australia, Nedlands, WA 6009); † Senior Public Health Nurse, Kimberley Public Health Unit, Derby, WA; ‡ Infectious Diseases Physician and Clinical Microbiologist, Royal Perth Hospital, Perth, WA, and Clinical Senior Lecturer in Medicine, University of Western Australia. makhoATbigpond.com To the Editor: The World Health Organization has established the Global Alliance for the Elimination of Leprosy, which aims to eliminate leprosy from every country by 2005.1 Elimination is defined as reducing the disease prevalence to below one case per 10 000 population. Australia has met this goal. Nevertheless, leprosy transmission still occurs in parts of Australia. Between 1986 and 2002, 28 new cases of leprosy were notified to the Kimberley Public Health Unit (KPHU). All patients except one were Indigenous. At diagnosis their ages ranged from 8 to 63 years. In several recent cases, diagnosis was delayed despite multiple presentations to primary healthcare staff and medical specialists. Eleven patients (39%), including the most recently diagnosed case, had multibacillary disease (WHO classifies leprosy as paucibacillary [< 6 skin lesions with no bacilli on skin smears] or multibacillary [≥ 6 skin lesions and/or positive skin smears]2). People with multibacillary leprosy can transmit the disease. This epidemiological pattern is also seen in Australia’s Northern Territory, where a third of the 236 new cases of leprosy between 1970 and 1997 were multibacillary.3 In leprosy-endemic countries, the proportion of cases that are multibacillary ranges from 32% in Guinea to 84% in Egypt.4 The long incubation period of leprosy (usually 2–5 years, but possibly decades) makes it likely that new cases will occur in Australia over the next few decades. Management of patients in the Kimberley region is challenging, not only because of remoteness, patient mobility and the prolonged treatment and follow-up required, but because adverse reactions to leprosy treatment are common, and may occur weeks to months after starting therapy with antileprotic agents. With all presentations of leprosy, the KPHU informs patients and relevant health professionals about these reactions, including how to recognise them and where to seek specialist advice. The region’s frequent turnover of healthcare professionals and its increasing reliance on short-term and overseas-trained doctors makes this a time-consuming undertaking. With increasing movement of people into and out of leprosy-endemic areas like the Kimberley, or leprosy-endemic countries, Indigenous Australians who have not yet been exposed to leprosy may now be at greater risk of encountering and acquiring the disease. In addition, Indigenous Australians from leprosy-endemic areas may develop symptoms of leprosy when they are no longer in leprosy-endemic areas, and may attend health professionals unfamiliar with leprosy, resulting in delayed diagnosis.5 In the 21st century, the medical community still needs to be alert to the possibility of leprosy in patients with chronic dermatological or neurological conditions, and needs to enquire about exposure to leprosy (eg, living in a leprosy-endemic area, history of leprosy in relatives — both by blood and by marriage). Otherwise, we will fail to diagnose and appropriately manage this disease, risking further outbreaks of leprosy in Indigenous Australian populations.

Donna B Mak · Eleanor M Platt · Christopher H Heath

Michael South Paediatrician, General Medicine, Royal Children’s Hospital, Flemington Road, Parkville, VIC 3052. mike.southATrch.org.au To the Editor: The recent study by Wilson,1 and its accompanying editorial by Walters and colleagues,2 highlight a number of issues about written asthma action plans (AAPs). The utility of AAPs is controversial. However, a number of points are more certain: AAPs will achieve nothing unless they are part of a comprehensive program of therapy, patient education and review. AAPs must be individualised, and must cover several aspects of self-management, including ongoing maintenance therapy and future acute episode treatment (including the current episode if this has triggered the patient’s attendance). AAPs cannot improve patient care if doctors don’t take the time and effort to write them, and if patients don’t have them available at the time of need, particularly during acute episodes. AAPs are a useful communication tool, and an aid in consistency of care, provided patients and all their doctors have up-to-date copies of the same plan. To help with the complex and time-consuming task of producing customised AAPs, we developed a computerised AAP generator which runs in a standard web browser. Individualised AAPs are produced with minimal typing and a few mouse clicks in less than 45 seconds. All plans have sections for future acute episodes. Sections for preventer medications and the current episode only appear when selected. All asthma medications currently available in Australia are selectable from drop-down menus, and these lists are updated regularly. There are several prompts to encourage best-practice care. Enough copies are produced for the family, school, kindergarten, child minder, grandparents, general practitioner, and hospital notes. The AAP generator was made available on the Royal Children’s Hospital intranet in July 1999. This intranet version logs, in detail, all use of the plan and the recommended therapies, without any patient identification. About 19 500 plans have been generated since. We have not formally evaluated this system, but we do know, from informal feedback and from our records showing that many of them have used it hundreds of times each, that our staff find it useful. AAPs are only a part of the “education package” required for patients with asthma. If it is quick and easy to generate good AAPs, it is to be hoped this will encourage doctors to produce them, while also giving them more time to concentrate on the explanation and discussion of care. The AAP generator is available for free download from our website (www.rch.org.au/clinicalguide/asthmaPlanRequest.php).

Michael South

Milton G Roxanas Psychiatrist, The Epping Clinic, PO Box 288, Eastwood, NSW 2122. mroxanasATbigpond.net.au To the Editor: I wish to report hyponatraemia in a patient commencing therapy with mirtazapine — this is the first such report from Australia. An 86-year-old widow with depression had had a previous episode of hyponatraemia while taking venlafaxine. Anticipating the possibility of further hyponatraemia, I prescribed mirtazapine 15 mg nightly — half the recommended starting dose. At this time, she was also taking amiodarone, gliclazide, l-thyroxine, irbesartan with hydrochlorothiazide, alendronate, omeprazole, atorvastatin and zolpidem. Her baseline serum sodium level was 135 mmol/L (normal range [NR], 135–149 mmol/L), but 4 days later it had fallen to 130 mmol/L, with serum osmolality of 294 mosmol/kg (NR, 280–295 mosmol/kg), urine osmolality of 398 mosmol/kg (NR, 50–1200 mosmol/kg), spot urine sodium concentration of 42 mmol/L, and plasma antidiuretic hormone (ADH) level of 0.7 pmol/L (NR, 0.1–7.0 pmol/L). Mirtazapine therapy was stopped after a further 2 days, and 10 days later her serum sodium level was 134 mmol/L, serum osmolality 296 mosmol/kg, urine osmolality 419 mosmol/kg and spot urine sodium concentration 27 mmol/L. Her plasma glucose level varied from 7.4 mmol/L to 9.2 mmol/L (NR, 3.4–5.4 mmol/L). Her condition was subsequently stabilised on mianserin (20 mg nightly) without electrolyte abnormalities. There are 12 reports worldwide of hyponatraemia due to mirtazapine (manufacturer’s data “on file”). This antidepressant inhibits α2 auto- and heteroreceptors, blocks 5-HT2 and 5-HT3 receptors, and acts via noradrenergic and 5-HT1A receptors. The mechanism of hyponatraemia is thought to be via α1 or serotonergic stimulation of ADH, but other possible causes include increased osmoreceptor sensitivity, reduced renal ability to conserve salt and water in the elderly, enhanced renal action of ADH1 and reduced metabolism of the antidepressant. There is no known interaction between mirtazapine and amiodarone or irbesartan or thiazides to account for hyponatraemia. This patient had risk factors — she was elderly, female, was taking diuretics and had had hyponatraemia with another antidepressant medication. As in previously reported cases the ADH level was not elevated, although the syndrome of inappropriate ADH secretion (SIADH) is not always accompanied by raised ADH levels.2 Hyponatraemia is seen more often these days because of greater awareness, the increasing proportion of elderly people in the population and the trend towards polypharmacy in the elderly. Many drugs have the potential to produce SIADH; one report has indicated that almost all antidepressants are implicated.3 Amitriptyline-induced hyponatraemia was first described in 1974, and a recent retrospective study of elderly patients found an incidence of 32% with selective serotonin reuptake inhibitors and an unusually high 71% with venlafaxine.4 In the face of an increasingly common phenomenon, I recommend that patients aged over 65 years should have baseline measurements of electrolyte levels before starting therapy with an antidepressant, and that these should be repeated 2–7 days later to detect possible hyponatraemia and initiate treatment.

Milton G Roxanas

John F Kerin Professor, Reproductive Medicine Unit, University of Adelaide, and Adelaide Fertility and Gyn-Endoscopy Centre, “Timara”, 154 Barton Terrace West, North Adelaide, SA 5006. kerinjfATsenet.com.au To the Editor: In a recent article by Foran,1 information provided on the new Essure (Conceptus, Inc) permanent birth control or sterilisation method was inaccurate in several respects. Firstly, Foran stated, incorrectly, that the Essure method is performed laparoscopically (it is actually a hysteroscopic method). This is a significant error, as one of the unique advantages of this method is the avoidance of incisional surgery, particularly laparoscopy and a general anaesthetic. This hysteroscopic procedure is well tolerated and can be performed with minimal or no sedation, followed by a rapid postprocedure recovery and early return to normal activity.2,3 Secondly, the failure rate in terms of postprocedure pregnancy is much less than the 0.6% quoted by Foran. To date, no pregnancies have been recorded in Phase II2 or Phase III3 multicentre, prospective, single-arm clinical trials conducted according to US Food and Drug Administration guidelines between 1998 and 2003. To date, no pregnancies have occurred in women relying on this intratubal microinsert during a combined 15 635 women-months of follow-up. The effectiveness rate for pregnancy prevention after 2 years of follow-up is 100% (95% CI, 99.5%–100%). Thirdly, it is not a titanium insert. The metal used in the outer dynamic coil is a nickel–titanium alloy commonly known by the trade name Nitinol. Fourthly, the adverse effects claimed (infection, bleeding) are misleading and incorrect. No infections within the uterus, tubes or pelvis have been recorded, and abnormal bleeding is not a feature of this form of sterilisation.2,3 Essure is the first hysteroscopic method of female sterilisation to gain regulatory approval for clinical use (in November 2002). This method of sterilisation offers women the choice of a less invasive, safe and reliable choice of sterilisation in the future.

John F Kerin