Letters

Suzanne P McEvoy,* Mark R Stevenson† * Research Fellow, Injury Research Centre, School of Population Health, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009; † Director, Injury Prevention and Trauma Care Division, Institute for International Health, University of Sydney, Sydney, NSW. scordovaATsph.uwa.edu.au To the Editor: Taylor et al found that: “Mobile phone use is common among Melbourne metropolitan drivers despite restrictive legislation” and suggest that this constitutes “a preventable exposure to injury risk”.1 This raises two questions: Does mobile phone use while driving affect road safety? If so, do hands-free devices reduce the risk? In their introduction, Taylor et al cited six publications to provide evidence that the use of a handheld mobile phone while driving increases the risk of a road crash. The studies by Lamble et al2 and McKnight and McKnight3 involved a hands-free device and examined driver impairment, not crash risk. The three papers by Violanti4-6 had significant limitations, including no phone billing information to demonstrate that drivers were using their phones at the time of the crash,4-6 reliance on police accident reports that may have involved more thorough investigations into fatal crashes than non-fatal ones,5 and small sample size with only 14 mobile phone users in one study.6 These limitations reduce the validity of the research. The best of the epidemiological studies was a case-crossover study of 699 drivers in collisions involving property damage only.7 However, the oft-quoted four-fold increase in risk comes from the analysis of mobile phone use in a 10-minute hazard interval before the collision. This does not provide conclusive evidence that these drivers were on the phone at the time of their crash and indicates a statistical association only. Although shorter hazard intervals were also examined, one needs to be wary of the potential for misclassifying post-crash calls as pre-crash calls because the time of collision may be imprecise, mobile phone use is common following a crash and a call to the emergency services may not be the first call made after the event. If we conclude that the data are valid despite these limitations, then the fact that hands-free models did not reduce the risk must be noted. Returning to our questions, although there is good evidence demonstrating driver impairment in laboratory-based studies, the epidemiological research has limitations that need to be dealt with to determine the real-world effect of mobile phone use while driving. We are currently undertaking two large epidemiological studies in Perth, involving about 2000 drivers over an 18-month period. The limitations have been addressed in the design of our studies. Furthermore, the evidence to date suggests that hands-free devices do not confer a safety advantage and this issue should not be ignored in driver education.

Suzanne P McEvoy · Mark R Stevenson

Ric Bouvier Community Safety Consultant, 200 Cotham Road, Kew, VIC 3101. ricbouvier7AToptusnet.com.au To the Editor: In “In this issue” of the Journal of 4 August 2003,1 you write regarding “Dialling drivers” that “the jury is still out on the health effects of mobile phones”. Well, the jury is back with a guilty verdict. In June 2003, Injury Prevention2 quoted an evaluation by the Harvard Center for Risk Analysis that “the use of cell phones by drivers may result in about 2600 deaths, 330 000 moderate to critical injuries, 240 000 minor injuries and 1.5 million instances of property damage in America per year”.3 Taylor et al suggest, “Further interventions aimed at decreasing mobile phone use among drivers should be considered.”4 Occupational safety professionals consider that a worker not complying with the safe practices for using a tool should be offered remedial education. If education fails, they stop the worker using that tool. Wise parents also consider taking away a child’s toy until the child can learn to use it safely. And so with mobile phones used while driving. Driver safety education is not very effective. Police have powers to impound items related to other offences, and so should have powers to impound mobile phones used when driving. The driver could then claim it, say, four weeks later, from the police station on payment of a fee-for-service to the police that covers, at least, the relative value of the expenses of the police. The driver would also incur demerit points. Repeated offences would mean they forfeit the phone or their licence.

Ric Bouvier

Graham J Chalker,* Kenneth H Joyner,† Kelly S Parkinson† * Chief Executive Officer; † Technical Advisor, Health and Safety Committee, Australian Mobile Telecommunications Association, PO Box 4309, Manuka, ACT 2603. kellyATkppr.com.au To the Editor: The claim made in the recent article that mobile phone use while driving is more dangerous than drink driving is misleading.1 The 1997 study by Redelmeier is often misinterpreted and cited for the proposition that driving while using a mobile is the same as driving drunk. However, Redelmeier wrote to the New England Journal of Medicine to correct this inaccuracy, saying, “. . . alcohol circulates in the blood for hours, whereas a telephone call lasts only minutes. The cumulative risks associated with intoxication are greater than those associated with cellular telephones”.2 This is supported by a recent Australian study, which compared the blood alcohol levels of drivers involved in real car crashes, rather than driving simulators, and found the risk of an accident was increased by 25 times at a blood alcohol concentration of 0.08.3 Mobile phones have not been shown to present this level of risk in any research. In 2002 in the United States, alcohol was a factor in about 41% of all fatal traffic crashes and in 6% of all crashes.4 In comparison, data collected by about 20 state highway authorities show that mobile phones were a factor in an estimated one half of one percent of all accidents in the US last year. Furthermore, mobile phone subscribers provide the extra eyes and voice for police in reporting aggressive, reckless or drunk drivers, accidents and other road hazards. Almost a third of all genuine calls to 000 are made from mobile phones.5 A recent US survey found that at any given time only 3% of drivers are actively using their mobile phones,6 although it is legal to use a handheld phone in almost all states. Therefore, Taylor’s overall result that less than 2% of Melbourne drivers use a handheld mobile phone, while illegal in Australia and undesirable, is not unexpected. However, the unrelated and misleading comparison made with drink driving is not supported by the facts. No one is questioning that mobile phone use imposes physical, visual, and cognitive demands on the driver. Although technology can help to address physical and visual factors, education is required to address cognitive factors. The Australian Mobile Telecommunications Association has developed 10 safety tips for mobile phones and driving (see www.amta.org.au) and, by adhering to these simple common-sense practices, drivers can make full, productive and safe use of mobile phones.

Graham J Chalker · Kenneth H Joyner · Kelly S Parkinson

David McD Taylor Director of Emergency Medicine Research, Royal Melbourne Hospital, Grattan Street, Parkville, VIC 3050. David. TaylorATmh.org.au In reply: McEvoy and Stevenson raise some important issues. The first relates to the confusion between driver impairment and crash risk. Intuitively, this association seems valid, as any level of driver impairment could be expected to affect driving skill. However, they are correct to suggest that the two should not be used interchangeably without supporting evidence. Secondly, I agree that the quality of evidence directly linking mobile phone use with crash risk is poor.1-4 This largely relates to the difficulty in confirming mobile phone use at the exact time of the crash. Reported direct observation is uncommon, billing records are inexact, and self-report may be subject to prevarication bias. The use of hands-free devices was not examined in our study, mainly because of difficulties in detecting their use. There is anecdotal evidence of a trend towards the use of these devices while driving. However, while their use might avoid the need to physically hold the phone, they may not significantly diminish driver impairment resulting from distraction. Many questions remain, and I encourage McEvoy and Stevenson in their endeavour to more clearly evaluate the real-world risk of mobile phone use, both handheld and hands-free, by drivers. Chalker et al draw attention to the comparison of crash risk for mobile phone use while driving and drink driving. I acknowledge that interpretation of published studies is confusing. Redelmeier’s statement that alcohol circulates for hours and that a telephone call may last for only minutes relates to individuals. From the highway perspective, when one driver completes a call, another is likely to be starting one and effectively assuming the increased collision risk. This concept is consistent with our findings. Almost 2% of drivers were using mobile phones when they passed our observation points, and were therefore at risk at that time. The exact extent of this risk awaits clarification. Chalker et al provide US alcohol and mobile phone related crash statistics. Unfortunately, the latter were not referenced and their value is therefore questionable. Finally, Chalker et al are to be commended for publishing safety tips for mobile phone use while driving. However, their claim that common-sense practices can make mobile phone use safe is extraordinary and disregards emerging evidence. Indeed, this statement appears to contradict their first safety tip, which states “a hands free device can reduce the physical effort to make and receive calls; however, it alone doesn’t make using a mobile phone while driving safer”.5 At best, therefore, common-sense practices will not make mobile phone use while driving safe, only possibly safer.

David McD Taylor

Donna B Mak,* Graeme H Johnson,† Lewis J Marshall,‡ Jacqueline K Mein§ * Public Health Physician, Department of Health Western Australia, 189 Royal Street, East Perth, WA 6000; † Medical Officer, Derby Aboriginal Health Service, Derby, WA; ‡ Head, Sexual Health Service, Fremantle Hospital, Fremantle, WA; § Public Health Medical Officer, Kimberley Population Health Unit, Broome, WA. makhoATbigpond.com To the Editor: We were pleased to read Chen and Donovan’s editorial which highlighted sex-based inequalities in control of genital chlamydial infection and argued for more screening of men for this infection.1 In the Kimberley region of Western Australia, where rates of genital chlamydial infection are among the highest in Australia, control strategies encompass both sexes.2 Although chlamydial infection was not notifiable in WA until 1993, it has been part of the sexually transmitted infections (STI) control program of the Kimberley Public Health Unit (now the Kimberley Population Health Unit) since the 1980s. Since 1989, regional STI management guidelines have recommended that testing for chlamydial infection (and gonorrhoea, syphilis, hepatitis B and HIV infection) be offered to all patients presenting with STI symptoms or as a sexual contact of an STI patient, and as part of antenatal, prison and well-person’s screenings.3,4 In 1996, empirical treatment for chlamydial infection with single-dose azithromycin (funded by the Kimberley Public Health Unit) was added to the standard treatment regimen, and antibody testing and culture were replaced by nucleic acid testing, which is more transport-robust and sensitive. This led to the introduction in 1997 of active health-service-initiated contact tracing for chlamydial infection (ie, sexual contacts reported by patients with chlamydial infection are actively sought by health staff and offered an STI consultation and empirical treatment). Between 11 June 2001 and 29 June 2002, WA Health Department staff (who contribute over 70% of the region’s STI notifications) notified 94 cases of chlamydial infection in female patients and 56 in male patients.5 Coinfection was common, with 61 patients (41%) also having gonorrhoea and four (3%) also having syphilis. Of the female patients, 30% were tested for chlamydia because they had self-presented with STI symptoms, 32% as part of antenatal or well-person’s screening, 36% because they had been reported as a sexual contact of a patient with STI, and 2% for unknown reasons. The corresponding proportions in male patients were 45%, 7%, 45% and 4%, respectively (Pearson χ2 = 12.6, df = 3; P = 0.006). Prevalence of chlamydial infection in the Kimberley antenatal population (69% of whom are screened for chlamydia) is 3% (95% CI, 2%–6%).6 Prevalence in 93 Kimberley men screened consecutively on admission to prison during 18 weeks in 1998–1999 was also 3% (95% CI, 1%–9%). During this same period, prevalence among 59 Kimberley men and 68 women presenting consecutively as STI contacts was 19% (95% CI, 11%–31%) and 22% (95% CI, 14%–33%), respectively (Mak DB, unpublished data). These data demonstrate that contact tracing contributes significantly to chlamydial case-finding, and support the addition of azithromycin to the Kimberley’s empirical STI treatment regimen. Empirical treatment and contact tracing for gonorrhoea over more than 15 years have been associated with decreases in the rate of gonorrhoea and the male : female ratio of cases in the Kimberley (Box). Seven to 8 years after introducing empirical treatment and contact tracing for chlamydial infection, rates have increased in both sexes, as has the proportion of male notifications (Box). Further progress in control of chlamydial infection requires continued provision of STI screening, treatment and contact-tracing services that are acceptable and accessible to both men and women. Notifications of chlamydial infection and gonorrhoea in the Kimberley region, 1993–2002

Donna B Mak · Graeme H Johnson · Lewis J Marshall · Jacqueline K Mein

Neil R Parker Public Health Physician, Darling Downs Public Health Unit, Public Health Services, Queensland Health, PO Box 1775, Toowoomba, QLD 4350. neil_parkerAThealth.qld.gov.au To the Editor: In May 2000 and December 2001, I vaccinated two women for Q fever (Q-Vax, CSL). Both had negative blood tests (IgG < 1:10 by immunofluoresence) and skin tests. Both had local reactions similar to those described by Mills et al.1 In both women, the skin test became positive after vaccination. The first woman had visited a farm on weekends, but had had no direct exposure to cattle, sheep or goats. Swelling at the vaccination site occurred within 72 hours, forming a lump 70 mm x 30 mm in size and causing significant discomfort. The skin test became positive at the same time. A surgeon excised the lesion 5 months after vaccination, and scarring resulted. The histological appearance was similar to that described by Mills et al,1 including a granulomatous panniculitis. The tissue was weakly positive for Coxiella burnetii by a polymerase chain reaction test (Professor B P Marmion, Institute of Medical and Veterinary Science, Adelaide). The skin test was still positive 7 months after vaccination. The second vaccine recipient lived on a cattle property and was involved with calving. She reported that her skin test became positive 5 weeks after vaccination (an observation confirmed by me a week later). The test was still positive at my final review 4 months after vaccination. Although the swelling at the vaccination site reached 50 mm × 20 mm, it caused little local pain or inconvenience. The lesion resolved spontaneously without scarring. The first of these cases had a much shorter onset period than that described by Mills et al.1 Their article did not document the fate of the skin tests, but based on the two cases I report here, and other cases notified to me by general practitioners, I suspect that prolonged positivity may be the rule rather than the exception.

Neil R Parker

Sandy J Berenger,* John K Ferguson† * Area Infection Control Consultant (and Clinical Nurse Consultant, Hunter Area Pathology Service, University of Newcastle), † Director, Department of Microbiology and Infectious Diseases, John Hunter Hospital, Locked Bag 1, Newcastle, NSW 2310. sberengerAThunter.health.nsw.gov.au To the Editor: Collignon and colleagues decry the reuse of “single-use” medical devices.1 Unfortunately, the focus on reuse of items labelled as single-use detracts attention from some of the more serious issues with cleaning of reusable instruments. All hospitals have cleaning failures that occur because some instruments are virtually impossible to clean. Examples include hollow instruments such as bone reamers, biopsy needles and tissue forceps. The actual sterilisation process (as described under Australian Standard [AS] 41872) is not at issue here. Rather, it is the poor design of instruments, and the lack of any standardised assessment process to determine whether an item is capable of being cleaned against that standard. One study found that most “sterilised” artery forceps had residual tissue, visible by light microscopy, representing an unknown, but real, infection risk.3 Most Australian hospitals do not examine surgical instruments under the microscope for grooves or cracks, and instrument sets remain in circulation for many years. In contrast, the most common “single use” critical items that are reused in many Australian hospitals are electrophysiological stimulation (EPS) and aberrant cardiac pathway ablation catheters; there have been no reports of significant mechanical or patient safety issues from reuse of a wide range of cardiac catheters, including EPS and ablation catheters.4 The sterilisation process itself has been validated for these items.5 At John Hunter Hospital, the process of reuse is controlled by a quality system that is far more stringent than the existing AS 4187 Standard. Devices are used for a set number of times before discard, and each catheter use is tracked to the specific patient and procedure. After cleaning, each catheter is examined under x 10 magnification to detect defects. The catheters are tested electrically at the point of use and patient consent is obtained before the procedure. The John Hunter Hospital program has operated for 6 years with an estimated cumulative cost saving of $6 million (compared with no reuse). Patient outcomes are monitored, and no adverse events have been detected. Clinicians express a high degree of satisfaction with the program. The same standard of equipment design, assessment and cleaning should be applied to all instruments that contact sterile tissue. Whether or not a company chooses to label its product “single-use” should not determine whether the item should or should not be reused. More often than not, such labelling serves to benefit financial return rather than patient safety. Hughes entreats us to cease reuse practices until there is incontrovertible proof of the safety of reuse.6 This statement should also apply to routine surgical items. In this era of zero risk tolerance, perhaps the consent process should make patients aware that reusable instruments processed under AS 4187 cannot be guaranteed to be free from human tissue contamination.

Sandy J Berenger · John K Ferguson

Clifford F Hughes Head, Department of Cardiothoracic Surgery, Royal Prince Alfred Medical Centre, Suite 304, 100 Carillon Avenue, Newtown, NSW 2042 (and former Chairman, Therapeutic Device Evaluation Committee). clifford.hughesATemail.cs.nsw.gov.au In reply: Berenger and Ferguson correctly raise the issue of sterilisation procedures for devices used in surgery. They have also described specific measures taken at their hospital for a specific device and, more importantly, have developed a system to ensure the highest quality of sterilisation process in a medical device. Of course, the use of any surgical device should be subject to the strictest sterilisation procedures. Most reuseable surgical instruments do have documented sterilisation protocols which include verification of the process used. All surgical instruments, whether designed for reuse or not, whether used for the first time or the tenth time, should be subject to the scrutiny, surveillance and meticulous records demonstrated by the John Hunter Hospital system. This hospital is to be congratulated on its attention to detail. Were similar stringent protocols in place across all disciplines and in all hospitals, the debate would cease to rage. More importantly, many devices could be safely and efficiently reused. Others may be considered too difficult to resterilise. Nevertheless, asepsis would, once again, be positioned where it belongs, as one of the key principles of surgery.

Clifford F Hughes

Bryan G Walpole Emergency Physician, Australian Antarctic Division, Channel Highway, Kingston, TAS 7050. bwalpoleATtassie.net.au To the Editor: Your otherwise excellent issue on chronic illness (1 September 2003) was timely and appreciated. However, the article by Zajac on the future of public hospitals1 left me pondering how frequently he patrolled the wards and the emergency department. Most public hospitals have undergone the very revolution he adumbrates. Patients now arrive with automated medication records and problem lists from their general practitioner; GP liaison doctors from the Divisions attend discharge planning committees; discharge summaries are delivered by fax on discharge; multidisciplinary clinics abound for complex and chronic illness, but invited GPs claim that time commitments and insufficient payment often preclude attendance; there are target waiting times for clinic appointments; often there is a quality assurance unit, with a complaints or grievance procedure; day surgery and day of admission surgery is now the norm (and strict guidelines help control the morbidity Zajac bemoans), with vastly improved throughput; endoscopy and emergency cardiac catheterisation or angioplasty on demand are commonplace; we now acknowledge, document and rectify system errors with alacrity, without the rancour and recrimination of years ago; and evidence has replaced the wise maxims of the physician. Admittedly, all is not rosy and funding remains a perennial problem, but within available resources the public hospital is a completely different place from 15 years ago. A major issue, and Zajac agrees, is the place of general medicine in the public hospital, being rapidly subsumed by sub(super)-specialists together with emergency physicians, as they are available round the clock, skilled and equipped to perform the assessment and early management of most medical patients, while the physicians are in rooms or at home. We welcome the presence of general physicians in the emergency department, and encourage twice-daily rounds on admitting day with shared care, but so far the rhetoric of general medicine has rarely been matched by attendance. The real challenge for public hospitals at present is to effectively manage and discharge frail elderly patients, and those with cognitive impairment, thus keeping beds free to reduce access block; otherwise general medicine may suffer the fate Zajac reserves for public hospitals and become “a thing of the past”.

Bryan G Walpole

Jeffrey D Zajac Head, Department of Medicine, Austin Hospital, Level 7, Lance Townsend Building, Studley Road, Heidelberg, VIC 3084. j.zajacATunimelb.edu.au In reply: Walpole and I agree that public hospitals have changed significantly. Where we seem to disagree is that he suggests that we have got to where we are going and all the problems have been solved. Walpole clearly works in a different world from me. Even a short visit to the wards and emergency department reveals that, despite good will, planning and many of the changes Walpole lists, things are far from perfect. System errors, major and minor, occur far more commonly than they should, elderly patients spend more time as inpatients than they should, and stresses in the system continue to impair quality and efficiency. I think we need to keep working on these issues, and not pretend that they are fixed. I note with dismay the description of general physicians occasionally visiting Walpole’s emergency department, while other specialists work diligently, 24 hours a day, to heal the sick. These comments demonstrate one of the main problems with doctors in public hospitals, namely, the territorial imperative in full flight. We should be finding ways to work together.

Jeffrey D Zajac

Ron J Lord Editor, Healthcover, 28 Hereford Street, Glebe, NSW 2037. hcoverATihug.com.au To the Editor: The Editor’s article on health reform and the Australian Health Care Summit,1 in which he expressed sentiments with which I agree, included a Box setting out the “egalitarian and socially cohesive principles underpinning Australia’s healthcare” reaffirmed by the Summit. However, the Box contained a Christmas tree and an invitation to readers to enter a poem in the MJA’s Christmas Competition 2003. Among the lines were: “’Tis Christmas, the season to be kind”. While obviously the result of a glitch in the production process, you managed — much to the envy of other editors and publishers seriously wounded by such glitches (to the extent that entire print runs have had to be pulped and then reprinted) — to fall on your feet. I could not think of a better (or more comprehensive) set of principles to underpin our healthcare system than those embodied in the message and spirit of Christmas. Perhaps God moves in mysterious ways.

Ron J Lord

Robert A Jones Specialist Gynaecologist, Adelaide Private Menopause Clinic, Memorial Medical Centre, 8/1 Kermode Street, North Adelaide, SA 5006. robjonesAT senet.com.au To the Editor: 9/15 was disaster day at the MJA.1 Not only was the Editor guilty of printing perseveration, but his “Box” seems to have been transmogrified from . . . “(the) socially cohesive principles underpinning Australia’s healthcare” to an invitation to “expose” the readers of the Christmas journal to some “witty prose”. Perhaps the “healthcare dialogue” has indeed been reduced to rhyming couplets, possibly accompanied by the health ministers fiddling while the rest of us burn?

Robert A Jones

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