Letters

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

Therese M Foran Medical Director, FPA Health, 328–336 Liverpool Road, Ashfield, NSW 2131. terrifashATfpahealth.org.au In reply: Mea culpa! Essure is, of course, a hysteroscopic rather than a laparoscopic method of female sterilisation and is described so in the text of the article. I apologise for not picking up this error while checking the proofs. Kerin is also correct in pointing out that Essure is made not from pure titanium but from a titanium alloy. The possible adverse effects, though rare, are listed among a number of others in the manufacturer’s information brochure.1 I am always extremely wary of ascribing a 100% effectiveness rate to any contraceptive method. Since Essure has been used so far on only small numbers of women, the figure I quoted was the upper limit of the failure rate in world literature for female sterilisation procedures.2 Although initial experience indicates that the eventual success rate should be very close to 100%, Kerin’s quoted 95% CI suggests that, at present, we can only promise potential Essure users a better than 99.5% effectiveness rate (ie, a failure rate quite close to the figure I used). I consider Essure to be an excellent new method of permanent contraception, and apologise if my article gave any other impression. I am certain that Australian women and their doctors will increasingly consider it an option in the future.

Therese M Foran

David H Eizenberg Obstetrician and Gynaecologist, Macquarie Chambers, 183 Macquarie Street, Sydney, NSW 2000 To the Editor: In their recent article on treatment of menstrual disorders, Hickey and Farquhar described three case scenarios to highlight alternative treatments for menstrual disorders.1 In Patient 1, a 39-year-old woman with dysfunctional uterine bleeding, the authors preferentially treated the patient with the levonorgestrel-releasing intrauterine system (20 μg per 24 h). Unfortunately, this device is available through the Pharmaceutical Benefits Scheme only for contraception, not treatment of menorrhagia. It would be difficult to explain to the government its use in this woman, who, according to the history, had had laparoscopic sterilisation. As a new intrauterine system has to be inserted every 5 years, and has a failure rate of 20% after 1 year, a 39-year-old woman would need at least another two inserted to control dysfunctional bleeding. The optimum method of management would have been simple vaginal hysterectomy. This was not mentioned in the article, which contrasted the intrauterine system only with abdominal hysterectomy. The authors also claimed that “cost–benefit analysis showed that [the intrauterine system] Mirena was three times cheaper than hysterectomy”. This analysis should include the cost of three Mirenas ($260 each), insertion, doctors’ visits for Pap smears for 30 years, tampons and pads. Is this cheaper? After all, hysterectomy means no periods, pain, pregnancies, Pap smears or pads. What is wrong with vaginal hysterectomy? The fact that the woman had had three caesarean sections and laparoscopic sterilisation was not a contraindication.2 Patient 2, a 45-year-old woman with menorrhagia and small fibroids, could also have been managed with vaginal hysterectomy.3 There is no evidence that hysteroscopic resection of fibroids in a multiple-fibroid uterus, as recommended by the authors, will improve menorrhagia. They also state that an alternative technique, embolisation, has been “widely used”. This technique is experimental and, as they state, “has been associated with serious side effects, such as infection, bowel obstruction and loss of ovarian function”, as well as death.4 In our quest for management innovations for women with dysfunctional bleeding, we should decide whether the new technique is better than the gold standard, hysterectomy. As hysterectomy can be vaginal, laparoscopic with vaginal assistance, totally laparoscopic, or abdominal, one cannot just use the word “hysterectomy”, one must specify. Studies reveal that the vaginal approach is superior.2,5

David H Eizenberg

Martha Hickey,* Cynthia M Farquhar† * Associate Professor of Obstetrics and Gynaecology, University of Western Australia, King Edward Memorial Hospital, 374 Bagot Road, Subiaco, WA 6008; † Associate Professor in Reproductive Medicine, National Women's Hospital, University of Auckland, Auckland, New Zealand. mhickeyATobsgyn.uwa.edu.au In reply: Eizenberg is correct in stating that the levonorgestrel-releasing intrauterine system Mirena is currently licensed as a contraceptive in Australia and not explicitly for treatment of menstrual disorders. He is also correct in stating that vaginal hysterectomy would be a management option for Cases 1 and 2 in our article.1 However, the purpose of our article was to explore newer options in management of menstrual disorders. This does not mean that “traditional” therapies such as hysterectomy are to be overlooked or superseded, and we did not attempt to compare the new therapies with hysterectomy. Dysfunctional uterine bleeding, although disruptive, is a benign condition, and treatment is symptomatic. We believe that women should be aware of all available therapeutic options, including hysterectomy, so that they can reach an informed decision.

Martha Hickey · Cynthia M Farquhar

Saul Wiener Allergist, Royal Melbourne Hospital, 46 Balaclava Road, East St Kilda, VIC 3183. To the Editor: In their study on the effectiveness of antivenom for redback spider bite, Isbister and Gray cast doubt on the current method of administering antivenom intramuscularly.1 Any study on the outcome of treating bites by venomous animals is limited by factors beyond the control of the investigator. These include the variability of the venom content in the animal’s venom apparatus, uncertainty regarding how much and where venom has been injected, and the delay before treatment. Between 1955 and 1957, I dissected the venom glands of 590 redback spiders for the production of antivenom.2 The yield of freeze dried venom per spider varied from 0.08 mg to 0.32 mg. Based on these findings, and to allow for dilution of antivenom by body fluids, “it was considered that 500 units of antivenene would constitute a suitable initial dose for the treatment of a bite by L. hasseltii”.3 This amount of antivenom will neutralise 5 mg of venom in vitro, and the antivenom is still issued in this strength by CSL Ltd. No fatalities have occurred from redback spider bite since antivenom became available in 1956,4 and reports from doctors have confirmed its efficacy and safety.5 If symptoms persist after the initial dose, or if diagnosis has been delayed, the initial dose of 500 units may have to be repeated. As Banham et al have wisely stated “treatment should be titrated against response”.6 Because of the risk of anaphylaxis, intramuscular injection, which has stood the test of time, is safer than the intravenous route.

Saul Wiener

Geoffrey K Isbister Clinical Envenoming Research Group, University of Newcastle, Newcastle Mater Misericordiae Hospital, Locked Bag 7, Hunter Region Mail Centre, NSW 2310 gsbiteATferntree.com In reply: We thank Wiener for his comments on our study. Although we challenge the use of intramuscular redback spider antivenom (RBS AV) in the article, we only suggested that the use of intramuscular antivenom needs review and that randomised controlled trials comparing intravenous and intramuscular RBS AV should be undertaken. Two such trials, in Western Australia and Newcastle, are currently in progress. There are no pharmacokinetic studies of RBS AV, but studies of other antivenoms suggest that the intramuscular route is less effective.1 In Tunisia, the intramuscular use of scorpion antivenom, which is also an F(ab')2 antivenom, similar to RBS AV, has been questioned for similar reasons.2,3 Studies in a rabbit model demonstrated that intramuscular antivenom induced only partial and delayed neutralisation of circulating toxins.3 More importantly, in a study of scorpion stings of children, the intramuscular administration of antivenom had far less effect on plasma venom concentrations and patient recovery times.2 We do not dispute that repeated doses of antivenom may be required, but the implication that only an initial dose was used in our study is incorrect. Half of the treated patients required repeat doses (6 ampoules in one patient). In a recent series of four patients with redback spider bites, intramuscular antivenom was ineffective, even though three patients received two or three ampoules. Subsequent intravenous antivenom was effective in all cases.4 There is no evidence that appropriately administered intravenous RBS AV (diluted in 200 mL of normal saline, over 20–30 minutes) is less safe than intramuscular antivenom. There is insufficient reason to prevent the use of intravenous antivenom if it is shown to be more effective than intramuscular antivenom. Although it is too early to change recommendations for the administration of RBS AV, it is essential that controlled trials be done.

Geoffrey K Isbister

John Boyages Executive Director, New South Wales Breast Cancer Institute, PO Box 143, Westmead, NSW 2145. johnbATbci.org.au To the Editor: I read with interest the position paper on breast self-examination by Crossing and Manaszewicz.1 I would like to point out an error of fact. The New South Wales Breast Cancer Institute (NSW BCI) has been promoting breast self-examination for many years. As a practising clinician, every month I see several women who have found small breast cancers using instructions from an old New Idea shower card or similar information. The position of the NSW BCI, which is stated clearly on our website, is as follows: Women should consider an annual breast examination by their general practitioner, particularly when they attend for a Pap test or a blood pressure check. Mammography should be performed at least every 2 years, particularly for women over 50 years, and earlier for women with a family history of breast cancer. Women should practise regular breast self-examination (BSE). Information about BSE can be obtained from GPs and the BCI has produced a fact sheet (www.bci.org.au/public/guides/g8bse.htm). BSE costs nothing and, in our opinion, does more good than harm. However, BSE should be combined with regular mammography and an examination by a GP. For a woman with a family history of breast cancer, or who has been diagnosed with breast cancer, BSE can be helpful in finding disease. Mammography is only about 95% reliable. BSE complements mammography. Certain types of breast cancer are often difficult to diagnose with mammography, for example “lobular” cancer, and BSE may help in finding such cancers. No evidence has been published that would justify a change in this position.

John Boyages

James E Fielding,* Heath Kelly† * Epidemiology Registrar, Communicable Disease Control Branch, Department of Human Services, PO Box 6, Rundle Mall, Adelaide, SA 5000; † Head, Epidemiology and Surveillance Division, Victorian Infectious Diseases Reference Laboratory, North Melbourne, VIC. james.fieldingATdhs.sa.gov.au To the Editor: In addition to a complicated ethical approval process, new privacy laws have presented challenges for multicentre research studies.1 In Victoria, an amendment to the Guardianship and Administration Act 1986 came into effect on 1 January 2003. We wish to highlight its unanticipated ramifications. We proposed to conduct a pilot study on the feasibility of ascertaining cases of Murray Valley encephalitis (MVE) in Victorian hospitals. Currently, there is no routine human surveillance for MVE, and we intended to perform diagnostic tests for several encephalitis aetiological agents on routinely collected samples. A study protocol was developed and submitted in November 2002 to five Human Research Ethics Committees (HRECs), one at the Department of Human Services and four at hospitals where the study was to be conducted. The case definition for encephalitis included the criterion that the patient had an “altered conscious state”, and could not therefore give informed consent. Informed consent was to be provided by the patient’s next-of-kin, but, in late December, an HREC representative alerted us to an imminent amendment to the Act which stipulated that only a guardian appointed by the Victorian Civil and Administrative Tribunal (VCAT) could provide consent to participate in “any procedure carried out for the purposes of medical research” on behalf of a disabled patient (in this instance, a patient with an altered conscious state). The Act does not further define medical research. Surveillance involves no intervention, and it is unclear to us (and some ethics committees) whether surveillance was considered a “procedure”. We indicated our uncertainty in a letter to VCAT in January 2003. If an application to VCAT were required for each patient we wished to enrol, then the study became unworkable. Under legislative requirements, VCAT is only obliged to “commence to hear” an application within 30 days of its receipt, which would prevent surveillance being conducted in a timely manner. Awareness of the legislative amendment differed between HRECs. In December 2002, two committees gave full approval for the study without reference to the amendment, while the remainder gave conditional approval, subject to complying with the amended Act. VCAT wrote to HRECs in February 2003 to clarify the amendment, and directly indicated to us that it did not apply to our proposed study. In May, despite the correspondence from VCAT, one HREC reaffirmed its position that applications must be made to VCAT for consent for studies such as this one. Despite attempts at clarification, a legislative amendment in Victoria has created ongoing confusion about obtaining consent on behalf of disabled patients. Researchers planning studies involving invasive procedures (eg, blood chemistry or seroprevalence studies) need to be aware of the amendment’s potential impact. Differences in interpretation of the amendment by the tribunal and various ethics committees highlight the need for further clarification of the Act, as well as for centralised and consistent assessment of HREC applications.

James E Fielding · Heath Kelly

Martin B Van Der Weyden Editor, Medical Journal of Australia, Locked Bag 3030, Strawberry Hills, NSW 2012. editorialATampco.com.au Comment: Fielding and Heath raise two issues. The first is the increasing barriers to the conduct of research as the law and Human Research Ethics Committees (HRECs) quite rightly ensure the safety of participants in human research. In the words of Cicero, salus populi suprema est lex (“the welfare of the people is the highest law”),1 but the law is not immutable. The confusion uncovered by Fielding and Heath over the implications of the amendment to the Guardianship and Administration Act 1986 may prompt legislators to re-examine the purpose of the Act in the context of research involving patients with “altered conscious state”. The second issue raised is more general. The plurality of HRECs’ interpretations of the amendment may be difficult to fathom by ordered scientific minds: data are data, so why the differences in HRECs’ opinions? These frustrating differences are the bane of researchers involved in multicentre research.2,3 The 1999 National statement on ethical conduct in research involving humans4 empowers HRECs to minimise duplication and allows for ethical and scientific assessments made by one HREC to be accepted by others.5 Nevertheless, HRECs value their independence and are unlikely to relinquish it to others easily.6 Various states are considering the feasibility of centralised ethical bodies,5 but bureaucracy moves cautiously and change is always slow.

Martin B Van Der Weyden

Steve Lontos,* Robert M Jones,† Peter W Angus,‡ Paul J Gow§ * Liver Transplant Registrar, † Director, Liver Transplant Unit, ‡ Director, Department of Gastroenterology, § Gastroenterologist, Austin and Repatriation Medical Centre, Studley Road, Heidelberg, VIC 3084 paul.gowATarmc.org.au To the Editor: We wish to report a case of acute liver failure associated with the use of a herbal preparation that contained several ingredients, including Cimicifuga racemosa (black cohosh). In January 2003, a 52-year-old woman was referred to our unit with acute liver failure. She had taken a herbal preparation for three months (for severe tinnitus), but ceased four weeks before admission. The preparation was made and provided by a pharmacist. The preparation was supplied in a 200 mL bottle and contained a mixture of the fluid extracts of Nepeta hederacea (ground ivy) 80 mL, Hydrastis canadensis (golden seal) 20 mL, Ginkgo biloba (ginkgo) 40 mL, Avena sativa (oats seed) 40 mL and Cimicifuga racemosa (black cohosh) 20 mL. According to the information supplied by the pharmacist, one gram of herb was contained in each 1 mL of extract, with the exception of golden seal, for which 0.5 g of herb was contained in each millilitre. The oats seed fluid extract was supplied by Southern Cross Herbal School (Gosford, NSW), and all other fluid extracts were supplied by the Herbal Extract Company of Australia (Sydney, NSW). The patient took a total of 600 mL over the 3-month period (7.5 mL bd orally as required). Before developing symptoms of liver failure, the patient had taken no other medications and had no risk factors for the acquisition of viral hepatitis. On arrival, she was deeply jaundiced but not encephalopathic. Liver span was reduced and there were no signs of chronic liver disease. The international normalised ratio was 3.0 (normal, 1.0–1.2), and she had serum concentrations of albumin, 26 g/L (normal, 35–50 g/L); bilirubin, 368 μmol/L (normal, < 18 μmol/L); alkaline phosphatase, 230 U/L (normal, 35–104 U/L); alanine aminotransferase, 1380 U/L (normal, < 55 U/L); and g glutamyl-transpeptidase, 134 U/L (normal, < 45 U/L). Extensive investigation excluded other recognised causes of acute liver failure. Her condition deteriorated over the following week, with the development of hepatic encephalopathy and hepatorenal failure. She underwent liver transplantation in early February 2003, and had an uneventful postoperative course. Examination of the explanted liver revealed massive hepatic necrosis. Following transplantation, the pharmacist supplied samples of the individual extracts to the Therapeutic Goods Administration (Canberra) for analysis. The analysis revealed no undeclared pharmaceutical drugs. Assay of the individual extracts of golden seal, ginkgo and black cohosh revealed the listed ingredients to be present. The presence of ground ivy and oats seed in the extracts has not yet been confirmed owing to the lack of a suitable reference standard. It is not possible to determine the individual ingredient, or mixture of ingredients, that resulted in acute liver failure in this patient. However, this is the third case of acute liver failure associated with black cohosh ingestion to be reported recently in Australia.1 In this instance, liver failure progressed despite cessation of the herbal therapy, and transplantation was required, suggesting that a process of irreversible liver injury had been initiated before treatment was ceased. It should be noted that ground ivy contains pulegone, a known hepatotoxin. However, the concentration of pulegone in ground ivy is accepted to be vastly less than in pennyroyal, where pulegone-induced hepatotoxicity has been reported.2 To our knowledge, there are no reports of golden seal, oats seed or ginkgo causing hepatotoxicity. The popularity of herbal therapies is due in part to their perceived lack of side effects. It is important for the medical and broader community to be aware of the potential toxicity of these preparations. In any patient presenting with unexplained hepatitis it is essential to determine if there has been exposure to herbal therapies, since early cessation of treatment may be life saving.

Steve Lontos · Robert M Jones · Peter W Angus · Paul J Gow

Michael D Coory Medical Epidemiologist, Queensland Health, GPO Box 48, Brisbane, QLD 4001. michael_cooryAThealth.qld.gov.au To the Editor: The randomised controlled trial associated with the Women’s Health Initiative (WHI) found that long-term hormone replacement therapy (HRT) with combined oestrogen–progestin causes net harm.1 Both the article by Baber and colleagues on HRT2 and a previous editorial by Patel and colleagues3 imply that the method used to calculate the confidence intervals in the WHI report is questionable. Baber et al suggest that “a trial such as this, with multiple endpoints, should use adjusted rather than nominal confidence intervals to test individual endpoints for significance”.2 It is important that this issue is clarified. In the WHI report in JAMA, Table 2 shows both nominal and adjusted confidence intervals for the primary and secondary outcomes.1 Nominal confidence intervals are appropriate for the preselected primary outcomes of the trial — breast cancer, coronary heart disease and the composite global-index score.4 Confidence intervals adjusted for multiple comparisons are possibly appropriate for the multiple secondary endpoints in the study, but are not advocated by all statisticians.5 In any case, the decision of Baber and colleagues to concentrate on adjusted confidence intervals for the preselected primary outcomes is not valid.4 The purpose of confidence intervals is to assess the effects of random variation or chance. It is not sensible to suggest that the extra harm that occurred in the combined HRT arm of the WHI study could be due to chance. Moreover, 42% of women in the HRT group stopped taking the drug, and 11% of women in the placebo group started taking it.1 Therefore, the reported findings of the intention-to-treat analysis underestimated the true harm to individual women taking long-term HRT. Also, if duration of treatment is important (as appears the case with breast cancer risk), and because compliance decreased over time, 5-year results underestimated longer-term treatment harm.4 The aim of the WHI trial was to assess whether long-term HRT is a useful preventive intervention for postmenopausal women. It did not assess the short-term use of HRT to relieve severe hot flushes. As Sackett points out, curative and preventive medicine are absolutely and fundamentally different in their obligations and implied promises to the individuals whose lives they hope to modify.6 As a long-term preventive intervention, HRT causes more harm than good. Although the absolute risks were small, millions of women were prescribed this treatment worldwide, causing harm to thousands. Billions of dollars were spent on an ineffective preventive intervention.6 The thousands of Australian women who stopped taking HRT on learning the results of the WHI trial made a sensible decision.

Michael D Coory

Rodney J Baber,* Justine L O’Hara,† Frances M Boyle‡ * Clinical Senior Lecturer, Department of Obstetrics and Gynaecology, University of Sydney, NSW, 2006; † Medical Student, ‡ Oncologist, Royal North Shore Hospital, Sydney, NSW. rbaberATmail.usyd.edu.au In reply: We acknowledge that not all statisticians agree on the place of adjusted confidence intervals. However, we and others1,2 believe they represent a conservative choice for secondary endpoints in a study with multiple endpoints, such as the WHI trial. Results of recent randomised controlled trials of hormone replacement therapy (HRT) and cardiovascular disease certainly support the notion that HRT confers no protection. However, any real harm of HRT must be questionable in light of the rapid review by Beral and colleagues, which, also using nominal confidence intervals, showed no change in relative risk for HRT users.3 We are surprised that, having emphasised the importance of nominal confidence intervals for primary endpoints, Coory did not mention that the breast cancer risk in the WHI report was not statistically significant using either nominal or adjusted CIs, or that the global index used was a non-validated instrument designed for and used only in the WHI study.4 Intention-to-treat analysis is used to avoid overestimates of both harm and benefit. While drop-in and drop-out rates (equal in both arms) may have led to underestimates of harm from HRT, they may also have led to underestimates of benefit, with no net change to risk–benefit assessment. The aim of the WHI trial was to assess the benefit or otherwise of long-term HRT on disease processes in otherwise healthy women. There seems little doubt that in the group of older, overweight, somewhat hypertensive, women enrolled in this trial the use of HRT was not beneficial. The aim of our article was to assess the case for and against HRT use.5 In reaching our conclusions, we drew on a broad range of published data, including, but not confined to, the WHI data. Our conclusions make it clear that we believe the use of HRT is primarily for short-term relief of symptoms during the menopause transition. However, we sought to defend the right of a small number of women to choose to continue HRT for long-term improvement of quality of life and symptom relief after appropriate, balanced, individualised counselling about the risks and benefits of such a decision. We do not agree with Coory’s final comment. The thousands of Australian women who stopped taking HRT on learning the results of the WHI trial did so in fear and ignorance in an environment where their physicians were unable to offer balanced counsel — hardly a formula for good medicine.

Rodney J Baber · Justine L O’Hara · Frances M Boyle

Donna B Mak,* Alastair MacKendrick,† Max K Bulsara,‡ Sharon Weeks,§ Lewis Leidwinger,¶ Harvey Coates,** Francis J Lannigan,** Deborah Lehmann†† * Public Health Physician, ¶ Audiologist, Kimberley Public Health Unit, Derby, WA; † Ear, Nose and Throat Surgeon, Southern Corridor ENT Services, South Fremantle, WA; ‡ Biostatistician, Biostatistical Consulting Service, School of Population Health, University of Western Australia, Crawley, WA; § Audiologist, Disability Services Commission, West Perth, WA; ** Ear, Nose and Throat Surgeon, Department of Otorhinolaryngology – Head and Neck Surgery, Princess Margaret Hospital for Children, Subiaco, WA; †† Senior Research Fellow, Centre for Child Health Research, University of Western Australia, Telethon Institute for Child Health Research, Subiaco, WA. Correspondence: Dr Donna B Mak, 189 Royal Street, East Perth, WA 6000. makhoATbigpond.com To the Editor: Chronic suppurative otitis media is very common among Australian Aboriginal children, resulting in hearing loss and educational and social disadvantage.1 Reconstructive middle-ear surgery has been part of the accepted treatment for decades. However, there are no publications about long-term outcomes in Aboriginal populations.2 We report here the results of a study of long-term postoperative outcomes in Aboriginal children following reconstructive middle-ear surgery. We studied all Aboriginal children aged ≤ 15 years who underwent middle-ear surgery for a tympanic membrane perforation (excluding cholesteatoma) in the Kimberley region of Western Australia between 1 October 1986 and 31 December 1995. Data had been collected prospectively during a previous study, and long-term follow-up was undertaken as part of a recent study of middle-ear surgery outcomes.2,3 Ethical approval was obtained from the WA Aboriginal Health Information and Ethics Committee. The study population consisted of 93 children (57 girls, 36 boys), aged 5–15 years (mean, 10 years; median, 10 years) at the time of operation. Preoperative air–bone gap (ABG) measurements ranged from 8.75 to 58.75 dB (mean, 36.7 dB; median, 36.25 dB). The operations were performed by nine surgeons at three hospitals and included tympanoplasty using temporalis fascia (73%), dura (13%), and other graft materials (8%), and mastoidectomy (6%). Sixty-four children (69%) underwent early postoperative review (median follow-up interval, 11 months) and 73 children (78%) underwent late postoperative review (median follow-up interval, 103 months). More of the patients had a late review because, at the time, additional resources were available to actively locate the patients for follow-up. At late postoperative review, 56/93 (60%) patients had a successful outcome (intact tympanic membrane and normal hearing) and 17/93 (18%) did not (20/93 [22%] did not undergo late postoperative review). Of the 32 patients who had a successful outcome at the early postoperative review (median follow-up interval, 5 months), 26 (81%) underwent late postoperative review; 24/26 (92%) still had an intact tympanic membrane and ABG ≤ 25 dB at late postoperative review (median follow-up interval, 109 months) (Box). These findings indicate that successful tympanic membrane closure with hearing improvement after middle-ear surgery in Aboriginal children is probably longlasting. The major limitation of our study is the absence of clinical information in the time period (mean, 8 years) between the early and late postoperative reviews. An unknown (but likely to be small) number of patients may have had further operations and/or conservative management, which may have influenced their ear health status at late postoperative review. Collection of these data would have been extremely difficult given the nomadic lifestyle of many patients and the logistical realities of remote-area healthcare. Our findings support the current recommendation of the Office of Aboriginal and Torres Strait Islander Health that Aboriginal children should be offered tympanoplasty if conservative management of chronic suppurative otitis media is unsuccessful.4 Postoperative review status of 93 Aboriginal children who underwent middle-ear surgery for a tympanic membrane (TM) perforation* in the Kimberley region of Western Australia between 1 October 1986 and 31 December 1995† * Excluding cholesteatoma. † If a patient had more than one operation, the first ear operated on during this time period was included in the analysis. If a patient had operations on both ears on the same date, the ear with the largest preoperative hearing loss was included. If hearing loss was the same on both sides, the right ear was chosen.

Donna B Mak · Alastair MacKendrick · Max K Bulsara · Sharon Weeks · Lewis Leidwinger · Harvey Coates · Francis J Lannigan · Deborah Lehmann

Rosie G Scott,* John T Edwards,† Richard M Mendelson,‡ Geoffrey M Forbes§ * Research Fellow, ‡ Radiologist, Department of Diagnostic and Interventional Radiology; † Gastroenterologist, § Gastroenterologist (corresponding author), Department of Gastroenterology and Hepatology; Royal Perth Hospital, PO Box X2213 GPO, Perth, WA 6000 geoff.forbesAThealth.wa.gov.au To the Editor: The burden of colorectal cancer can be minimised, firstly, by early and appropriate investigation of symptoms; secondly, by screening those at higher-than-average risk without symptoms; and thirdly, by community-based screening of asymptomatic people aged over 50 years who are at average risk. Major screening programs using faecal-occult-blood testing (FOBT)1-3 or flexible sigmoidoscopy4 have not necessarily made this differentiation. These tests lack the sensitivity of colonoscopy, which is generally indicated for those with symptoms or a strong family history of colorectal cancer. In our recent community-based screening program in which we used virtual colonoscopy, we excluded those at higher than average risk for colon cancer (that is, they were symptomatic or had at least one first-degree relative with colon cancer), as our standard of care for these patients is colonoscopy. They were given verbal and written advice to see their general practitioner, with the expectation that most should have colonoscopy. They were followed up an average of 12 months (range, 6–15 months) later, by letter and telephone, to determine the outcome of this advice. Of 2000 participants aged 50–69 years who were offered screening, 90 (4.5%) described having symptoms or a first-degree relative with bowel cancer, but had not undergone investigation. Follow-up information obtained from 71 of these people indicated that 21 had a relevant family history and 50 described recent bowel symptoms. Only 35 (49%) had discussed further investigations with their GPs — 19 (27%) had undergone colonoscopy, and five of these (26%) had advanced colorectal neoplasia (CRN). One had tubular adenoma (> 1 cm), one showed villous architecture, one had intramucosal carcinoma, and two had cancer. Four other participants had had negative results on other investigations. These were FOBT alone in three (two symptomatic, one with family history) and barium enema in one who had bleeding. Common reasons for not consulting their GPs were because of good health (15 participants), resolution of symptoms (12), and perceived lack of need for tests (10). These data have important implications for CRN screening programs, including recently commenced Australian pilot programs (www.cancerscreening.gov.au). Firstly, there is likely to be an improved yield of advanced CRN when a previously uninvestigated high-risk group is identified within a screening program. Secondly, people identified as having higher-than-average risk for CRN need special attention to ensure there is adherence to advice on appropriate follow-up. Thirdly, procedures are required to ensure colonoscopy is appropriately undertaken when participants do consult their GPs. Accordingly, rather than adopting an exclusion policy within a screening program based on FOBT or flexible sigmoidoscopy, we believe it is appropriate that people at greater risk for CRN are identified and offered colonoscopy within that program.

Rosie G Scott · John T Edwards · Richard M Mendelson · Geoffrey M Forbes