Letters

To the Editor: Safety is a rather subjective concept, so to use the word without definition, as Clarke et al did,1 is somewhat misleading. One possible definition is that the complication rate for general practitioners is no greater than for anaesthetists in the same circumstances. In the study by Clarke et al,1 the GPs were allocated the lower-risk cases and the anaesthetists were allocated the more difficult ones. Direct comparison was made without any adjustment for this difference. The data suggest that the GPs had similar or higher rates of adverse events or interventions despite handling lower-risk cases. The most recent data on anaesthesia-related mortality reports 20 deaths at endoscopy from 1994–1996, with a note that this is likely to be an underestimate.2 Using the authors' denominator of 430 000 endoscopies per year, an estimated risk of anaesthesia-related death is therefore about 1 in 64 000. The risk of anaesthesia-related death for all surgery is quoted as 1 in 63 000, which implies that anaesthesia for endoscopy is of average risk. The sample size of 28 000 lacks sufficient power to make any comment on safety as regards the risk of death. Although I applaud the clinical standards of the authors' institution and fully agree that propofol has many clinical benefits over other agents, Clarke et al do not prove safety in the use of propofol by non-anaesthetists.

Patricia Mackay · Patrick J Hughes

To the Editor: We read with interest the article by Clarke et al1 and the accompanying editorial by Knoblanche,2 and are concerned that they may be interpreted as endorsing the use of the anaesthetic agent propofol in sedation techniques by personnel inadequately trained in anaesthetic techniques. Cases reported to the Victorian Consultative Council on Anaesthetic Mortality and Morbidity confirm the risk of serious morbidity and mortality associated with these procedures. Our report for the triennium 1997–1999 will include two deaths at endoscopy where a non-specialist administered the sedation or anaesthetic. In both of these cases, propofol was used. The circumstances described by Clarke et al are exceptional. They combine a scrupulous adherence to the professional guidelines3 and a significant involvement by the administration of the endoscopy centre in the selection, education and on-going training of the general practitioner sedationists. They include incident reporting of adverse events and non-standard treatments as part of a quality assurance program. Although not specified, there is also, presumably, access to high-quality back-up. This level of attention to detail is by no means universal. We would like to endorse several observations made in the articles: For a procedure to be considered sedation, it is imperative that the drugs used are not intended to, and do not, cause loss of consciousness or the loss of protective reflexes or spontaneous ventilation; by definition, this would be anaesthesia. Proper selection and careful medical assessment of patients is very important, and training must enable the identification of patients at higher risk. People administering sedation must have knowledge of the pharmacology of the agents being administered and modifications necessary because of concurrent therapeutic regimens or disease states. They must also ensure adequate intraprocedure monitoring is provided, that they have experience in interpretation of abnormal indices, and that they can manage any complications arising from the procedure, with particular emphasis on airway management and cardiovascular resuscitation. There may be benefits with the use of propofol, but the guidelines, designed for patient safety, clearly state: "Intravenous anaesthetic agents such as propofol must only be used by an anaesthetist."3 Technological advances in non-invasive and minimally invasive procedures have led to an explosion in demand for sedation of increasing complexity in areas removed from the traditional operating room environment. Consequently, demand for sedation by non-anaesthetists is likely to grow. It is important that the standard of care and patient safety be maintained in all these circumstances. The concern is not whether the practitioner administering the sedation is a general practitioner or a specialist, but whether he or she has the training and skills necessary to function as an anaesthetist. The terms "general practitioner sedationist" and "non-anaesthetist" might give an impression of diminished risk, which is not supported by the experience of this committee.

Jon P Clarke · Anthony C Clarke FRCP, FRACP · Lybus C Hillman MD, FRACP

In reply: We thank Clarke and Mackay and Hughes for their interest and comments. We accept that a sample larger than the 28 000 endoscopies we reported1 would be required to establish the true incidence of death or other catastrophic complications of our sedation service. As the mortality rate is expected to be so low, it would take many years to achieve an adequate sample size. It is even difficult to determine the mortality from endoscopy in Australia, as quantifying all the endoscopies performed is problematic, and the Royal Australian and New Zealand College of Anaesthetists believes that not all deaths occurring from endoscopy are reported to anaesthetic mortality committees.2 It is essential that any sedation service is carefully planned, and that all doctors providing sedation receive adequate training and follow the protocols and guidelines of the endoscopy centre. However, we challenge the opinion that only anaesthetists should use propofol. We have not been able to find any clinical safety studies that demonstrate that only anaesthetists are able to use propofol safely. We believe the results of our study show that, when propofol is used in the manner described in the article, the rate of ventilatory and other complications is low (but clearly not zero). There is no reason to believe that the propofol component of the sedation regimen increased the rate of ventilatory problems. Indeed, it might, through its short duration of action, minimise such problems. To arbitrarily exclude the use of propofol by appropriately trained GP sedationists would deny many patients the manifest benefits of this drug. Importantly, our GPs have been shown capable of successfully managing the problems of airway obstruction and apnoea that were encountered — whatever the cause. We agree with Mackay and Hughes that the GP sedationists need to have the anaesthesia skills necessary to maintain patient ventilation, as well as an excellent understanding of all the drugs they use. Anaesthetists play a major role in improving safety standards in the provision of sedation for endoscopy through codifying the standards required,3 assisting the training of staff, and delivering sedation services to high-risk patients. But many patients can be successfully sedated without a specialist anaesthetist being present. We argue there is no evidence that these patients should receive a suboptimal regimen. Most specialist anaesthetists have a more valuable role to fill than providing sedation for straightforward endoscopies.

Jon P Clarke

To the Editor: The study by Douglas et al1 reports that the purposeful hastening of death in terminal illness is both widely practised and an acceptable method of palliative care for over a third of Australian surgeons. Yet the study is based on a questionnaire strongly favouring theoretical scenarios rather than actual practice. The framing of the questions maximises reporting bias towards "hastening death" by the use of absolute terms (eg, "Have you ever . . .?"; "[Are] there any circumstances . . .?"1). The study also fails to determine the stage in a terminal illness at which hastening of death had been, or might possibly be, acceptable to the surgeons, nor the reason for its implementation. If the patient's symptoms are already adequately controlled and the dying process is not prolonged, we do not see why it is necessary to administer doses in excess of those required to control symptoms. Whose symptoms are we treating?

Mathew Piercy · Gerald B Fogarty · Aubrey W Jansz · David M Gawler · Luis Vitetta · David Kenner · Avni Sali

To the Editor: We wish to comment on the article by Douglas et al about surgeons hastening death.1 Recently, Ray2 noted that, historically, surgeons have had to witness their patients' pain probably longer than any other medical specialty. Hence, it is not surprising to read Douglas and colleagues' report1 that more than a third of surgeons surveyed performed life-terminating events without explicit and persistent requests. The desire for death, as perceived by doctors and patients, has been correlated with ratings of pain, depression and poor family support.3,4 Surgeons, while intending "no harm", could be seen to be palliating themselves (relieving their own distress) as well as their patients' when performing life-terminating events. Helplessness, hopelessness and negative attitudes toward life-sustaining treatments are common and understandable in palliative care, and experienced by both doctors and patients.3,4 Surgeons are relatively new to palliative care and could have a significant contribution to make to the psychosocial support of cancer patients with terminal illness. Decisions by surgeons about hastening death may be modified by greater interaction with their patients' families and with other healthcare providers working with terminally ill patients. A clinical-outcomes study of 102 consecutive deaths of terminally ill patients admitted to hospice care during 1997–1999 highlights the importance of family support in the outcomes immediately before death.5 The study period coincided with a time of heightened awareness of euthanasia in Australia. Fifty-six per cent of the patients had received continuous family support and 44% sporadic support; these patients appeared to have less distress and better preterminal outcomes, despite 10% experiencing significant family conflict and distress. However, no spontaneous or other requests for euthanasia were recorded in patient files or notes by staff. This could reflect, in part, family support received in an environment conducive to positive interactions between patients, their families and health professionals. Involving such palliative care teams in surgeons' care for terminally ill patients may have a significant effect on both pre-terminal outcomes and hence requests for euthanasia.

Mathew Piercy MB BS · Gerald B Fogarty BSc, MB BS(Hons) · Aubrey W Jansz MB BS, FRACS · David M Gawler MB BS, FRACS, FRCS · Luis Vitetta · Avni Sali Professor and · David Kenner

To the Editor: We were interested to read the recent supplement on preventing osteoporosis.1 We could find only one reference to cigarette smoking, on page S13, where it is noted that "the role of lifestyle changes (including specific exercise regimens, changes in diet and quitting smoking) has not been evaluated adequately". The orthopaedic literature is replete with information and evidence on the adverse effects of cigarette smoking on bone density, healing of fractures, incorporation of bone grafts, etc. A meta-analysis2 has suggested that smokers have greater bone loss over time than non-smokers. Granted, there may as yet be no direct evidence that quitting smoking reduces "the fracture burden". However, to discuss osteoporosis and management of fractures without discussing the major adverse effects of cigarette smoking is akin to discussing the prevention of melanoma and the outcomes of treatment without discussing unprotected exposure to sunlight (for example). Could the "writing group" tell us what steps are being taken to inform Australians of the adverse effects of cigarette smoking on their bones, quite apart from the other public health issues surrounding this extraordinarily harmful habit?

Roy PL Carey · Walter E Plehwe · Peter R Ebeling

In reply: On behalf of the writing group, I wish to thank Carey and Plehwe for their perceptive comment on the effects of cigarette smoking on bone health. The focus of our supplement was the prevention of fragility fractures, and unfortunately there is no evidence that smoking cessation reduces fracture rate. However, the authors are correct to emphasise the negative impact of cigarette smoking on fracture healing, bone graft incorporation and bone density, the last factor being a strong predictor of fragility fracture. The meta-analysis that Carey and Plehwe refer to1 showed that hip bone mineral density (BMD) in current smokers was one-third of a standard deviation below that of people who had never smoked. This meta-analysis and another recent study2 showed that these effects are greatest in men and are dose-dependent. Prospective studies also show that smokers have higher rates of bone loss than non-smokers. Extrapolations from these BMD data suggest smoking increases the lifetime risk of vertebral fracture by 13% in women and 32% in men, while hip fractures are increased by 31% and 40%, respectively. In response to the question of what steps are being taken to publicise the effects of smoking on bone health, we would like emphasise that further prospective studies are urgently required to assess the effect of smoking cessation on fracture risk, BMD and bone turnover; and the message that smoking has a negative impact on BMD should be incorporated into public education campaigns run by government and non-government organisations for both osteoporosis prevention and smoking cessation. This area of bone health is eminently suited to successful intervention.

Roy PL Carey FRACS · Walter E Plehwe MB BS FRACP PhD · Peter R Ebeling MD FRACP

To the Editor: I applaud the ideology of the Journal in its pursuit of evidence-based excellence, drawn to our attention by Rosselli in a recent letter.1 Based on data that the MJA is at the top of the list of English-language journals publishing "evidence-based medicine" references, Rosselli asks "could it be that MJA readers are three times more interested in EBM-related topics than BMJ readers?". My response is that the editors (and perhaps also reviewers) of articles for the MJA may well be more interested in EBM than their BMJ counterparts, but this does not necessarily apply to readers. Without actual evidence of what interests MJA readers, it is not possible to draw any conclusions. Perhaps the readers should be asked?

C Ross Philpot

To the Editor: It was a most interesting idea to call for a list of favourites books.1 I have some of my own to add. The death of Ivan Ilyich, by Tolstoy — all the different responses to a dying man handled in the way only Tolstoy can. Interestingly, the most comforting presence was that of his illiterate man-servant, Gerassim. The doctor, his patient, and the illness, by Michael Balint — this was introduced to me by a very thoughtful medical student when I was a surgical registrar in England 40 years ago. A new edition edited by Balint's son has appeared in the past year or two. Contrary imaginations, by Liam Hudson — the advice in this book on selecting medical students and introducing first-year students to clinical medicine is now being carried out by many teaching schools 35 years after it was written! A long season in hell, by Gail Graham — the story of a mother's fight to rehabilitate her head-injured son. This book has all the characters that a doctor should be aware of — good doctors, bad doctors, unimaginative bureaucrats and politicians, helpful people and an inspiring physiotherapist who lost her husband, apparently through suicide, during the period she was fighting for her son. The book would be an ideal seminar topic for medical students and ethics discussion groups. Lastly, Intellectual impostures, by Sokal and Bricmont — a book with little medical content, but which should be read by every intelligent person. Sokal submitted pretentious gobbledygook to a postmodern journal, which was published. He then exposed the hoax, creating an enormous stir. This book is an expansion of that exposure.

Aubrey W Jansz

To the Editor: Recent astronomic awards for medical mishaps, and the follow-on medical indemnity crisis, bring back memories of an earlier editorial I wrote for the Journal dealing with some aspects of this problem. Its message is worth repeating. In 1990, a letter by Armstrong was published in the Journal,1 which enclosed a newspaper advertisement for a firm of solicitors, Messrs Stern, Stern & Tanner, inviting custom from anyone who may have been a victim of "obstetric negligence", "even if your child was born as long ago as 1965 or even earlier. Initial consultation free". The Journal's then editor invited me to write an accompanying editorial. The editorial, published simultaneously with Armstrong's letter and accompanying advertisement, was headed "No hawkers, canvassers or solicitors".2 It began with a quotation from United States Chief Justice Burger: "Never, never, never under any circumstances hire an advertising lawyer!".3 It noted that some solicitors claimed to possess special expertise in asbestos-related diseases, others claimed to know all about defoliants. I suggested, in those innocent days, that "obstetric negligence" was a new subspecialty which should henceforth be known as Stern–Tanner disease. (If Drs Guillain and Barré were to be forever enshrined in medicine's Hall of Fame, why not Messrs Stern and Tanner?) My editorial suggested a remedial response, stating that "the law permits parties to any contract to abrogate, limit or qualify their legal rights, duties, liabilities and remedies which might otherwise arise. Thus, while the courts — both here and in the United Kingdom — tend to lean against total exclusion from liability, they are, surprisingly, more benevolent towards clauses which limit liability, however contemptuous the specified amount." I adhere to that view. I can see no reason why doctors — save in an emergency — cannot demand that patients enter into a written "contract of treatment" which limits the treating doctor's liability to a specified amount. And while such contracts will not be valid against children born impaired as a result of "obstetric negligence", I can see no reason why the courts should deny the validity of such contracts as a matter of public policy. Why should "contracts of treatment", entered into between consenting adults, be any different from those entered into with lawyers or dry cleaners? It may seem a trifle offensive, but then the practice of medicine is treated in law as a business, much the same as touting lawyers or dry cleaners. If doctors were once put on a pedestal, this pedestal has been effectively knocked down by astronomic awards of damages freely awarded by the courts — whether by judge or jury — largely as a result of the freely expanded constituent elements of the tort of negligence. I researched the law relating to "limitation of liability" clauses, which was published in the Australian Law Journal4 and quoted in the MJA editorial: "Why the courts should be more benevolent to clauses of limitation than to clauses of exemption is not easy to comprehend. . . . The principle, it seems to the present writer, is much the same: Exclusion clauses save a party from having to pay anything, whilst a limitation saves him from having to pay as much as he would otherwise have to pay. [ . . . ] Alas, the last word on this seems to have been spoken for some time to come." As far as I am aware, the law has not changed since the publication of my earlier research.

Paul Gerber

To the Editor: The ME/Chronic Fatigue Syndrome Association of Australia Limited. has expressed its concern over the content of the Royal Australasian College of Physicians' clinical practice guidelines on chronic fatigue syndrome, published as a recent supplement to the Journal.1 Recognising a shared objective to overcome the challenges of chronic fatigue syndrome (CFS), neither the Association nor the College believes that conflict will provide a useful path to future answers. Accordingly, as the Chairman of the ME/Chronic Fatigue Syndrome Association of Australia and the President (at the time the guidelines were published) of the Royal Australasian College of Physicians, we would like to document the common ground we have identified. We acknowledge, as do the guidelines, that CFS is a serious, disabling illness. There is no evidence that the illness is primarily psychological in origin. There is significant evidence of a range of biological abnormalities occurring in people with CFS. It remains unclear whether these are primary or secondary. Treatment should be personalised according to the symptoms and circumstances of the individual patient. Treatment plans should be worked out by the patient together with a healthcare professional and designed to be within the capabilities of the patient. Scientific evidence on aetiology, pathophysiology and treatment is, at this stage, grossly deficient. More research is required to understand the biological mechanisms involved and to clarify the role that genetic, environmental and infectious agents might have in the aetiology and pathophysiology of this complex and debilitating illness. The medical community, other health professionals and patients and their families should work together to encourage increased funding and research into the epidemiology, aetiology and pathophysiology of CFS so that we may find more effective treatments for this condition (or these conditions). All clinical guidelines should be viewed as documents that will, in time, require refinement, rewriting and replacement. Doctors must be cognisant of the limitations of all such guidelines and be aware that the investigation and management of a patient's condition must be determined with the assistance of the best and latest information as it emerges and, in all instances, be tailored to the needs of the individual patient.

Richard G Larkins · Simon R Molesworth

To the Editor: I read with interest the article by Goldsworthy and McFarlane on Howard Florey, Alexander Fleming and penicillin.1 With regard to the cause of Florey's "famous pinched smile", which allegedly hid tooth erosion caused by his drinking dilute hydrochloric acid prescribed for achlorhydria, a more prosaic yet interesting explanation is found in the memoirs of Raymond Valentine Hennessy. Hennessy was Senior Ear, Nose And Throat Surgeon at St Vincent's Hospital, Melbourne, between 1928 and 1951.2 Howard Florey in the late 1930s In August 1936, Florey, who was then Professor of Pathology at Oxford, visited his dying mother in Melbourne. He and his family stayed with his sister, Dr Hilda Gardner. Florey had a supply of sulfanilamide, probably the first in Melbourne, to treat his daughter, who was convalescing from a recent mastoid operation. During his stay, Florey attended a local dentist for treatment of a painful lateral incisor tooth. Some days later (on a Saturday evening), his face had become swollen and he began having rigors. His sister, a medical graduate who was then working as a clinical pathologist and microbiologist at the Melbourne Hospital, appreciated the danger — an abscess of a lateral incisor tooth can produce a cavernous sinus thrombosis — and quickly contacted Raymond Hennessy, who lived nearby. Hennessy had graduated as a dentist before pursuing a career as an ear, nose and throat surgeon and had written about the dangers of a lateral incisor dental abscess.3 After examining Florey, Hennessy told him that the offending tooth required extraction that night. Initially, Florey refused to heed his advice, preferring to see his own dentist the following Monday. Fortunately for Florey, he was persuaded by his sister to have the extraction. Hennessy then telephoned a dentist colleague, and they all met at the latter's surgery in Collins Street, where Hennessy gave Florey a gas–oxygen anaesthetic, and the nervous dentist proceeded to extract the incisor. However, he extracted the normal central incisor, not the offending lateral! On realising his mistake, the dentist "went to water", but Hennessy immediately rose to the occasion and extracted the correct tooth. When Florey woke from the anaesthetic, as Hennessy well remembered, he was not amused. Later, he had a dental plate made but did not like wearing it. Whether he took the sulfanilamide is not known. This episode is not mentioned in Gwyn Macfarlane's biography of Florey.4 However, the photograph of Florey in the frontispiece of this book shows the gap in his upper incisors (pictured). I believe this is the explanation for Florey's "famous pinched smile".

Ivo D Vellar · Thomas B Hugh

To the Editor: The patronising article by Goldsworthy and McFarlane on the discovery of penicillin1 depicts the popular heroic view of Alexander Fleming as a myth, but also promulgates myths of its own. Their description of the Fleming saga is historically accurate. Fleming searched for an answer to the riddle of infection, and, to paraphrase Pasteur, chance in the form of a spore of a rare subtype of Penicillium favoured his prepared mind. Whether or not the spore came through an open window is irrelevant, but the windows in Fleming's laboratory — now preserved as a museum (pictured) — could be opened3 and probably were on occasion, as Fleming was a heavy smoker. Fleming perceived the significance of inhibition (or, more correctly, lysis) of staphylococcal colonies, named the active agent "penicillin" and studied its effect on animals. Goldsworthy and McFarlane are "astonished" that he failed to inject it into infected animals to investigate its therapeutic effect, but the reason is simple: Fleming discovered that penicillin was rapidly inactivated by serum, dashing his hopes for its use as a systemic agent.3 Although he met opposition from his chief, Almroth Wright (known to his students as "Almost Right"), who rejected the view that penicillin might be a useful therapeutic agent, it is absurd to say that Fleming was "a victim of the pessimistic mind-set against toxic chemical antimicrobials". His confidence in its lack of toxicity led him, in 1929, to use penicillin to treat pneumococcal conjunctivitis in one of his assistants, with dramatic success.2 Site of Fleming's laboratory The Clarence Wing, St Mary's Hospital, London, in 1910. Fleming's laboratory, where penicillin was discovered in 1928, was on the third floor of the tower on the right. The windows of the laboratory could be opened by an internal system of ropes and pulleys, but a more likely source of the Penicillium spore was a dumb-waiter shaft communicating with a mycology laboratory on the floor below.2 To say that "Fleming had little idea what to do with his mould apart from dabbing it on infected wounds" unfairly trivialises his actions after the discovery. In addition to clinical and animal studies, he had the mould identified, deposited a culture with the collection held by the Medical Research Council and published his observations. He set two researchers to work purifying the active principle of the mould broth, and established that penicillin was soluble in alcohol and that its stability was pH-dependent. He also developed an assay for penicillin and defined the range of organisms that were sensitive to it. He sent cultures of the penicillin-producing strain to many laboratories, including Oxford, where that very culture later provided the starting point for Chain and Florey's work. Fleming's subsequent work on penicillin was stalled by his lack of biochemical expertise; he was unable to overcome the difficulties of purification and stabilisation.2 Fleming is recorded as saying, "It's up to the chemists now, I'm no chemist".2 It is quite untrue that "he then effectively forgot about it for 13 years". Although Fleming ceased clinical work on penicillin in 1934, he continued with laboratory studies. A contemporary at St Mary's Hospital, Dr A G Cross, recalled that in the 1930s "penicillin was on his mind all the time and in the minds of those who worked with him".2 Fleming had his faults, but the genius of his prepared mind did indeed present humanity with a fairy tale come true. Perhaps Ernst Chain, who did not particularly like Fleming, should have the last word: "There is no doubt that this discovery, which changed the history of medicine, has justly earned [Fleming] a position of immortality."2

Ivo D Vellar · Thomas B Hugh · Peter D Goldsworthy MB BS · Alexander C McFarlane MD, Dip Psychother, FRANZCP

In reply: Our article aimed to show how history is often rewritten in narrative forms that are more appealing to the human need for heroes and for clear, memorable moral lessons.1 The challenge is to sort out whether the matters at stake are those of narrative style or substantial differences of fact. Hugh felt our approach was patronising to Fleming — but we were at pains to emphasise his "genius" for making important causal connections. He also had a genius for seeking adulation — which in no way disqualifies him from deserving to share the Nobel Prize for Medicine with Chain and Florey. Hugh also criticised our assertion that "Fleming had little idea what to do with his mould apart from dabbing it on infected wounds" — yet his counterexample, that in 1929 Fleming used "penicillin to treat pneumococcal conjunctivitis in one of his assistants", illustrates the point. Let us also not forget that a Belgian group had discovered the penicillin mould in 1920, and recognised its antimicrobial properties well before Fleming did. The challenge is to foresee and drive the application of knowledge rather than to leave facts in a dormant but pregnant state. Vellar's fascinating letter proposes that a dental abscess and two extractions, rather than Florey's drinking of hydrochloric acid, caused his "pinched smile". A mutually compatible hypothesis is that Florey was prone to this infection because of tooth damage caused by the acid. Vellar also provides further support for the quixotic spread of knowledge and the personal motivations and obsessions that influence researchers. Florey's transport of sulfanilamide to Melbourne was apparently not to popularise the new and revolutionary drug, but to treat his daughter. It also raises a fascinating, if ironic, possibility: was Florey's life saved by sulfanilamide, allowing him to continue on his yet-to-be-forged endeavour of the purification of penicillin?

Ivo D Vellar

To the Editor: Perhaps for reasons of space, Tobin et al, in their article on community versus individual benefit,1 have omitted an important public health justification for confidentiality. If patients are fearful that the doctor's obligation to notify the authorities could lead to a loss of privileges (in the case cited, a driver's licence), they may fail to attend for diagnosis and treatment. This understandable anxiety warrants a mention in this debate.

Peter C Arnold · Bernadette M Tobin · Steven R Leeder · Ernest R Somerville

In reply: Arnold makes a good point. We agree with him, and would resist today's increasing tendency, on public health grounds, to make it mandatory for doctors to report a variety of conditions suffered by their patients. In general the community is well served if doctors have the discretion to decide, in any particular case, whether the public interest in maintaining a patient's confidentiality is outweighed by the public interest in breaching that confidentiality in order to protect innocent third parties.

Peter C Arnold · Bernadette M Tobin MA PhD · Steven R Leeder PhD FRACP FFPHM · Ernest R Somerville MB BS FRACP FRCP

To the Editor: End-of-life issues: Case 11 illustrates an increasingly common scenario confronting physicians caring for older patients. The case example of a nursing home resident with stroke, dementia and the onset of pneumonia highlights the importance of encouraging patients to prepare for future medical decision-making. This can be done through the use of enduring guardianship, medical powers-of-attorney or advance care directives ("living wills"). Documenting these matters allows people to appoint others to make healthcare decisions on their behalf, and to indicate what treatment they would want in various clinical circumstances, should they no longer be competent to do so. If "Mrs W" had appointed an enduring guardian to deal with issues of healthcare and medical consent, or had indicated in an advance care directive what her wishes would be if she were to become seriously ill, the decision-making process may well have been clearer. The other issue this scenario raises is the need to check whether Mrs W's daughter could have made medical decisions for her mother. In New South Wales, if the daughter had been in a caring role for her mother before nursing-home placement, she could be considered the "person responsible" (similar to the old concept of "next of kin"). Under the Guardianship Act 1987 (NSW), the "person responsible" is able to act as a substitute decision-maker for healthcare and medical treatment. While it would clearly still be good, sensible medical practice to involve other family members in discussion about Mrs W's future, it would ultimately be the daughter, as the "person responsible", who would be able to make those decisions.

Susan E Kurrle

In reply: We agree with Kurrle about the importance of encouraging patients to prepare for future medical decision-making. The strategies she suggests are practical and useful. However, we believe that the difficulties confronting physicians in caring for older patients require us to go further and to rethink what represents excellent care at the end of life. Today, death from acute illness has largely been superseded by death from chronic illness, and the latter generally follows one of three main trajectories: cancer, organ system failure or dementia/frailty.1 Our systems of care for people who are near the end of life need to reflect the ways in which elderly people actually decline and die. If we wish to promise elderly people what a decent society should be able to promise them (accurate diagnoses, excellent control of symptoms, the absence of any gaps in care and of any "surprises" in their condition and its treatment, clarity about the role of their family in caring for them, a way of dying that accords with their hopes, and, most importantly, help to live the remaining part of their lives "to the full"), we need to rethink the care provided during hospitalisation of older people at the end of their lives.1

Susan E Kurrle · Bernadette M Tobin MA PhD · Ian D Cameron FACRM FAFRM PhD

To the Editor: Community-acquired methicillin resistance in Staphylococcus aureus was only reported in eastern Australia as recently as 1998.1 We report a case of community-acquired methicillin-resistant Staphylococcus aureus (CAMRSA) causing cellulitis and bacteraemia. A 30-year-old man presented to the emergency department with a short history of heel pain. There was no history of trauma, diabetes, drug misuse, contact with hospitals or previous antibiotic treatments before the current illness. Examination showed that he had a temperature of 37.7°C and sinus tachycardia of 120 beats per minute. There was extensive cellulitis surrounding a superficial collection of pus over the left heel; this was incised and drained. Initial investigations showed only neutrophilia. Blood cultures, but no swabs, were taken. Therapy with daily intravenous injections of 1 g ceftriaxone, given at home by an ambulatory care service, was initiated. The following day, blood cultures showed the presence of gram-positive cocci identified as a Staphylococcus sp., and the treatment was changed to 2 g of cephazolin 12-hourly, intravenously. On the second day Staphylococcus aureus resistant to oxacillin was isolated. There was susceptibility to erythromycin, clindamycin, tetracycline, ciprofloxacin, vancomycin, rifampicin and fusidic acid. Treatment with vancomycin (1 g 12-hourly, by means of a peripherally inserted central catheter) resulted in clinical improvement within 48 hours and was continued for a total of two weeks, followed by oral rifampicin and fusidic acid. A bone scan and echocardiogram showed no significant abnormality. Resolution was complete at six weeks and the patient returned to work. Methicillin-resistant Staphylococcus aureus (MRSA) is now a common cause of skin and soft tissue infections.2-4 MRSA was not acquired outside hospital until the 1980s, when intravenous drug users from Detroit were reported with MRSA bacteraemia. Such community-acquired strains have now been reported worldwide, including in Australia.5 These strains are usually non-multiresistant MRSA,3 which are highly pyogenic, readily communicable and predominantly cause skin and soft tissue infections. However, CAMRSA endocarditis and a bacteraemic osteomyelitis have been described. We believe this to be the first case of CAMRSA bacteraemia to be reported in Australia. Community-acquired MRSA strains have become a common cause of community-acquired staphylococcal infection in Australia.2,3 It is now recommended that swabs be routinely taken to cover the possibility of drug-resistant organisms such as MRSA.1-3 The appropriate initial management of suspected or high-risk cases is unclear, but might include treatment with vancomycin or gentamicin before the availability of antibiotic sensitivity test results.

Nicholas Collins · lain B Gosbell · Stephen F Wilson

To the Editor: The recent article by the Obstetric Medicine Group of Australasia alluded to the increasing relevance and importance of thrombophilia screening following adverse pregnancy outcomes, namely recurrent miscarriage, stillbirth, retarded intrauterine growth and pre-eclampsia.1 Formerly, these outcomes were generally attributed to "placental insufficiency", where a cause was not readily identified. Screening for disorders in the uteroplacental circulation after such adverse pregnancy outcomes was formerly confined to investigations for an autoimmune basis, such as antinuclear antibodies, anticentromere antibodies, anti-DNA antibodies and the lupus inhibitor. However, in recent years, it has become more apparent that inherited or acquired thrombophilias may play a significant role in certain adverse pregnancy outcomes.2-5 Reports from Israel2,3 and elsewhere have suggested that thrombophilias can be found in up to 65% of women with recurrent pregnancy loss of unknown cause, as well as in cases of intrauterine growth retardation, stillbirth, placental abruption and pre-eclampsia. It is also known that certain thrombophilic factors are more likely to produce thrombogenic changes and hence are possible deficiencies in the uteroplacental circulation. Preliminary work has shown that treating women who have had recurrent pregnancy loss complicated by thrombophilia with antithrombotic agents (low molecular weight heparins) is beneficial, with improved pregnancy outcomes in a significant number of these cases.3 With the growing understanding of the role of thrombophilias in pregnancy, it seems that thrombophilia screening will assume a more prominent role in investigating patients after recurrent miscarriage, stillbirth, intrauterine growth retardation and pre-eclampsia.

David Morgans

To the Editor: I agree with the assessment by Del Mar and colleagues of available data according to evidence-based guidelines on hormone replacement therapy (HRT) after mastectomy.1 As they note, these data are not definitive. Standard practice has been to avoid oestrogen use in women with a history of breast cancer. Ours is an increasingly litigious society and courts make decisions according to different criteria than do scientists. In particular, precedent is very important to the law of tort, even if the scientific basis for the precedent is unproven. For some years now, I have seen 100 or more new patients per year with recently diagnosed early breast carcinoma. By the time I see them, every single one already knows that: anti-oestrogens are used in treatment of breast cancer; and women are at least 30% more likely to develop breast cancer after five years of HRT. Further, these women fear recurrence of breast cancer more than any other health problem. Hence, I am concerned that the sound evidence-based conclusions reached by Del Mar and colleagues could be successfully challenged in court by a woman who developed recurrence of breast cancer while receiving HRT. In addition to the costs and stress for the individual practitioner involved and other members of his medical indemnity organisation, such action would set back scientific enquiry into this important subject, possibly forever. There is a wealth of well conducted research into non-oestrogenic management for menopausal symptoms. Lifestyle measures (clothing and activity) and dietary modifications (avoiding spicy foods, alcohol) have a role in well-being. Oral progestogens, clonidine, venlafaxine, black cohosh, and probably tibilone, all produce better outcomes than placebo.2 Evening primrose oil, pyridoxine, dong quai, Chinese herbs, progestogen and yam creams, and phytoestrogens do not work better than placebo.3 The last may actually be harmful. Advisory statements for general practitioners about oestrogen replacement therapy for managing menopausal symptoms after breast cancer should be prefaced with this information, as should any discussion with patients. I do prescribe oestrogens for distressing menopausal symptoms after breast cancer treatment, but only after several consultations to allow time for women to appreciate the uncertainties involved.

Robert N Hitchins

To the Editor: I was pleased to see the issue of hormone replacement therapy (HRT) after breast cancer raised by Del Mar and colleagues in a recent issue of the Journal.1 However, I was a little disappointed to see that Australian research in this area had been "missed" by their search.2,3 There are a number of other studies that I am aware of which would suggest to me that perhaps their search technique was not particularly thorough.4-7 Nonetheless, I should add that I do agree with their conclusions. In fact, I am not aware of any clinical trials that have shown an adverse effect of HRT after a diagnosis of breast cancer. However, the studies examined by Del Mar and colleagues are all population studies and not randomised controlled trials. I also think it's important that the readers of the Journal understand that there are other strategies for controlling menopause symptoms after breast cancer, such as the use of progestins, antidepressants and stress-reduction techniques. Even though the evidence we have suggests that HRT after breast cancer is "safe", we do not have even one published randomised trial on this question, so caution should be the rule. HRT after breast cancer should always be viewed as a last resort.

Robert N Hitchins MB BS, FRACP, FAChPM · Christopher M Pyke MB BS, FRACS, FACS

To the Editor: While I have little concern with the conclusion of the article by Del Mar and colleagues,1 I have some concerns about its use to portray a mode of healthcare delivery where any given health practitioner, armed only with what can be gleaned from the Internet, can issue advice. For example, in such a circumstance, should not the general practitioner also refer to the National Health and Medical Research Council clinical practice guidelines on the management of early breast cancer,2 which suggests that the "safety of oestrogen replacement therapy in women with breast cancer has not yet been established", and, further, that "HRT [hormone replacement therapy] and women with breast cancer" is an area where research is needed? Should the doctor also point out to the patient that she is eligible to enter a prospective randomised trial looking at the use of HRT following breast cancer treatment versus the best non-hormonal treatment of menopausal symptoms, currently being administered by the Australian and New Zealand Breast Cancer Trials Group (as part of International Breast Cancer Study Group trial 17-98)? How should practitioners protect themselves when they find the management they are recommending is outside that recommended in the evidence-based guidelines published by specialty groups? A few other minor points: the content of the article refers to women with breast cancer, whereas the title refers only to women who have had mastectomy, and the imaginary patient asked about loss of libido, which was not addressed at any subsequent point in the article.

Christopher B Del Mar MD FRACGP FAFPHM · Paul P Glasziou PhD FRACGP FAFPHM

In reply: Eden, Pyke and Hitchins are happy with the findings of the rapid literature search that we performed for the general practitioner who wanted to know about the safety of HRT in a woman treated for breast cancer. However, they have concerns with the process. Eden is worried that we missed two Australian publications on the issue. In fact, they misunderstand our intentions. Firstly, we did not raise the issue, nor deliver an "advisory statement". It was the general practitioner who asked the question. We were trying to provide a rapid (few days) and responsive service to provide credible information to help a doctor manage a patient. Secondly, we were not able to undertake a full systematic review (which would take a full-time researcher as long as six months and would cost accordingly).1 Instead, our best strategy was to use a cascade process of searching, looking first for the most rigorous study types that would answer the clinical question. If not available we go to the next most rigorous, and so on, stopping when we find the relevant evidence.2 For this question, the ideal study type would be a meta-analysis of randomised controlled trials (RCTs). However, no RCTs were available (as Eden, and the guidelines to which Pyke refers, note), and we had to content ourselves with observational studies. We should remember that no evidence for safety is not the same as evidence for danger. What is important is that we did not miss any trials. Legal issues worry many doctors, even when decisions are supported by best research evidence,3 but, rather than pose a medicolegal threat, we believe that this evidence-based approach is more likely to protect doctors. Why? Failures in communication are the most common preventable cause for doctors being sued by patients.4 Yet, taking the trouble to find empirical information such as this and then discussing it with the patient is surely the most effective way of communicating the pros and cons of different treatment strategies (including, we agree, alternatives such as those mentioned by Hitchins). In the end the patient has to decide on the basis of the risks and benefits, and the choice can often be extremely difficult. It is likely to be more dangerous to assume the patient has abdicated this responsibility to the doctor without checking first. Can doctors be sued for a "safe" decision that leaves a patient exposed to unnecessary symptoms? It may be dangerous to assume that doctors can play "safe" in any one direction. Why do experts take exception when non-experts delve in their areas for the best evidence to manage patients? After all, a cat may look at a king.5 Experts seem to welcome the attention, but seem to think they should be dispensing the information. However, until the information can be delivered more effectively, this sort of stopgap system will have to do.

Robert N Hitchins

To the Editor: Fitzgerald and Isaacs' recent article on genotype–phenotype correlations in healthcare professionals describes some truly original research in an area of exceptional relevance.1 However, some of their conclusions fail the analytical technique described by others as "the common sense test".2 Most obviously, the finding of complete deletion of all personality genes in orthopaedic surgeons sits uncomfortably with clinical experience, which suggests a plethora of witty and indeed charismatic members of that specialty. The authors have erred in making an admission of reading The Medical Journal of Australia on at least a semi-regular basis as an inclusion criterion for the study. As this would include only a minuscule proportion of the orthopaedic population, their sampling was surely unrepresentative. By the same criterion, it is likely that there are few theatre sisters who would admit to being semi-regular readers of the Journal. Those who do are probably married to members of the medical profession, which would explain the (bel) indifference phenotype.

Dominic A Fitzgerald · David Isaacs