Letters

To the Editor: Humans may serve as intermediate hosts in hydatid disease, a parasitic infection caused by the tapeworm Echinococcus granulosus. They are infected through contact with infected dogs or by ingestion of tapeworm eggs in contaminated food, water, or soil.1 The larvae form cysts in body organs. Although the liver is the most common site, lung cysts are seen in up to 30% of cases of hydatid disease. Lung cysts are generally asymptomatic, but symptoms occur if the cysts rupture.2 Here, we describe an adolescent girl with a lung cyst that ruptured across the thoracic cage into the subcutaneous fascia, presenting as a breast swelling. A 14-year-old girl had had left-sided pleuritic chest pain, a high-grade fever, and marked swelling of the left breast for 10 days, which did not respond to antibiotics (oral amoxycillin and parenteral amikacin). Clinical examination revealed a slender, febrile and tachy-pnoeic patient with a tender swelling of the left mammary region. The swelling had a tense cystic feel, and transmitted impulses were felt when she coughed. A diffuse pleural rub was heard anteriorly, with reduced air entry. Investigations revealed a neutrophilic leukocytosis of 12.7 × 109/L. Chest x-ray showed diffuse opacification of the left hemithorax, and a computed tomography scan revealed a cystic, low-attenuation lesion in the left hemithorax extending into the submammary region (Figure A). On anterolateral thoracotomy, an infected ruptured cyst was seen in the left upper lobe of the lung, with degenerated membranes and pus extending across the chest wall into the submammary space. The cyst was removed, capitonnage of the residual cavity was performed, and pus and laminated membranes were removed from the submammary space. Small communications seen between the pus cavity and the bronchi were closed. After the operation, parenteral anti-biotics (vancomycin and amikacin) were administered for 10 days and albendazole for 4 weeks. Casoni’s skin test was positive and antihydatid antibodies were detected in serum. Surgically obtained pus revealed non-viable scolices of E. granulosus (many degenerated), and the histopathology of the surgical specimen was consistent with hydatid membrane (Figure B). Pulmonary hydatid cysts can rupture; however, rupture into the pleural cavity is rare.1-3 Although spontaneous rupture of a cyst into the pleural cavity, or rupture after trauma, has been reported,4,5 a rupture across the pleural cavity into the submammary fascial tissues has, to our knowledge, not been reported previously. A. Computed tomography scan showing a cystic lesion in the left hemithorax, extending into the submammary region (arrow). B. Degenerated hydatid cyst membrane (original magnification × 200).

Parvaiz A Koul · Abdul Wahid · Ghulam N Lone · Tariq A Bhat

To the Editor: St John’s wort (SJW) (Hypericum perforatum) is a natural medicine commonly used for treating depression. We recently encountered a case of an overdose of SJW leading to serious manifestations in the patient. A 16-year-old girl presented to the emergency department with seizures and confusion. She was intubated and admitted to the intensive care unit. The only relevant history was of febrile convulsions at the age of 4 years. There had been no head trauma. Results of a computed tomography brain scan and cerebrospinal fluid examination were unremarkable. Electrolyte levels were normal, and standard drug toxicological screens were negative. An electroencephalogram (EEG) confirmed diffuse spike wave activity consistent with generalised epileptic activity. On further questioning, it was found that she had taken large quantities of SJW — up to fifteen 300 μg tablets a day in the 2 weeks leading up to admission and an additional 50 tablets just before presentation — for a recent “depressive episode”. Depression had not been formally diagnosed, and the tablets had been obtained “over the counter” from a local pharmacy. A provisional diagnosis of seizures due to an overdose of SJW was made. High performance liquid chromatography was not performed to quantify hypericum extract in serum and urine, as these tests are not available in our hospital. A repeat EEG at discharge on Day 6 was normal, and there were no further seizures in the following 6 months. Psychiatric assessment during the patient’s hospital stay revealed a likely suicide attempt following recent social stresses. There is some evidence for the efficacy of SJW in treating depression.1 In the United States and Australia it is available without prescription, but in Germany, where it is prescribed more frequently than fluoxetine for depression, it is available by prescription only. The reported incidence of adverse drug reactions to SJW is 0–5.7%.2 Although these are usually minor and transient, more serious adverse reactions (such as serotonin syndrome) have been reported.3 SJW was implicated as a likely, but unproven, cause of seizure-related events in a recent review,4 but our case appears to be the most severe reported so far. Adverse reactions are thought to be more common if SJW is taken in conjunction with selective serotonin reuptake inhibitors, but have also been described when SJW is taken alone.5

Dharshi C Karalapillai · Rinaldo Bellomo

To the Editor: Sanderson et al provide an interesting viewpoint about how the community, including medical practitioners, have embraced complementary and alternative medicine (CAM).1 However, if we were reviewing this article for publication, we would ask the authors to: make a valid distinction between those complementary and alternative therapies promoted as curative versus those considered palliative; define how they decided which therapies belong to one or other side of the arbitrary CAM boundary; review and justify the boundaries for the “therapeutic footprint” in a more evidence-based and rigorous way; locate specific therapies inside the footprint; locate where chemotherapy lies within the footprint, in light of the recent review showing, for the vast majority of adult malignancies, its marginal survival benefits considering its high costs, both monetary and healthwise;2 emphasise that there are relatively few recorded adverse events for CAM compared with conventional cancer care (Therapeutic Goods Administration Medicine Summary reports 2003, 2004, 2005 — Dr K Mackay, Acting Director, Adverse Drug Reactions Unit, TGA, personal communication); and vigorously question the marketing of conventional medicines, such as trastuzumab (Herceptin, Roche), to vulnerable patients and an uncritical public when the evidence suggests huge expense and little, if any, survival benefit.3 Perhaps a distinction also needs to be made between CAM therapies, many of which provide proven symptomatic relief, and those lifestyle interventions, such as exercise,4 dietary change,5 and social support, which provide symptomatic relief and may also confer a survival benefit. It does not serve the profession well when many cancer patients and their carers have to go outside the medical system to access information, advice and therapies which they should have easy access to within the system. In fact, we might even question how helpful these arbitrary boundaries are when all that patients and doctors want is to use what works and what is safe.

Craig S Hassed · Vicki Kotsirilos · Marie Pirotta · Avni Sali

In reply: We would like to thank Hassed and colleagues for their comments on the “therapeutic footprint” and their questions about locating specific therapies within the model. While it was outside the scope of our article to critically analyse different treatments using the model (as benefits and risks will vary from patient to patient), we would like to direct Hassed et al to a more detailed consideration of the risks and benefits of chemotherapy.1 We do not see our model as a tool to categorise or economically appraise specific treatments, but rather as one to help conceptualise the key issues to be considered when proposing treatment — the evidence for benefits and risks, contextualised according to treatment goals. The model provides a basis for comparison, taking us beyond arbitrary and unhelpful arguments about the distinctions between complementary and alternative therapies and their boundaries. We hope that the model will encourage evaluation of evidence for all therapies and support critical evaluation not only of drugs, but also lifestyle interventions that may benefit patients. The primary or essential purpose of the model is to encourage the posing of questions like those articulated by Hassed and colleagues to any therapist — whether they identify as medical, complementary or alternative.

Christine R Sanderson · Bogda Koczwara · David C Currow

To the Editor: In From the Editor’s Desk in the 20 November 2006 issue of the Journal, Van Der Weyden acknowledged the 100th anniversary of the first performance of George Bernard Shaw’s play The doctor’s dilemma, and the fact that both society and medical practice have since changed dramatically in the ensuing century. He then asked: “. . . what is the modern doctor’s dilemma?”1 Contemporary Australian medical practice faces challenges posed by changes in community and government expectations, free market policies, workforce shortages and infrastructure changes, so this question should not be regarded as rhetorical. Answers to it will depend to some degree on the type of medical practice under consideration and where it is situated geographically, but to get the ball rolling, I suggest that in respect of general practice anywhere in Australia, a significant set of dilemmas surround notions of responsibility. Traditionally, general practitioners have held responsibilities primarily to individual patients. With increasing emphasis being placed, appropriately, on preventive and screening activities, to what extent should GPs’ responsibilities be extended to the community as a whole, and how should any such extension be resourced? Given that the interests of individuals and communities will not always be in accord, how might the resulting conflicts of interests best be managed? And, to increase the complexity of such considerations, to what extent ought responsibility to patients extend to responsibility for patients? Another dilemma for doctors in respect of responsibility relates to identifying the boundaries between altruism and martyrdom. To what extent should health care professionals be expected to put the interests of their patients or of the community before those of themselves and their families? To extend the notion of responsibility further, and with the GP’s role as patient advocate particularly in mind, to what degree should health care professionals be active against social injustices which impinge on their patients’ health? I know that in responding to the Editor’s question I have posed another set of questions, none of which are easily answered — if they could be, they would not be dilemmas. However, acknowledging and clarifying these questions is the first step towards answering them, and also towards preventing much community misunderstanding.

David E Smith

To the Editor: I am one of the septuagenarians described by Arnold in his cri de coeur over the demise of professional courtesies.1 In my medical student days, my teachers extended the courtesy of free medical treatment to my parents. I have continued this tradition, in the certain knowledge that this will be the only situation in which medical students save their parents money. Such professional courtesies are still the norm in Western Australia. But, with the exception of medical colleagues, I have only once, in the 30 years of operation of Medibank/Medicare, had a bulk-billed patient realise that he has received a discount. I recently asked a picture framer/patient for a 40% discount and he laughed. When I explained that by bulk-billing I was effectively giving him a 40% discount, he was incredulous, but he did reciprocate. In the 1970s, Australian Medical Association spokesmen and medical educators often confused etiquette (a code of desirable behaviour between doctors) with ethics (a more important set of moral principles underlying a person’s general behaviour). This is no longer the case, and etiquette has disappeared from undergraduate and postgraduate medical curricula. I think it is time to reintroduce the topic into the education of both our future doctors and our patients.

Max Kamien

To the Editor: There would be few medical students who have not had drummed into them the tautological aphorism, “Common things occur commonly!” And few practising clinicians who have not come across or read about a serious adverse event arising from the actions of a colleague or nurse who thought, “It was only X, which is so common at this time of the year/around these parts/among these people. I didn’t think it was anything serious.” The patient might have been a child with meningitis sent home with a diagnosis of a winter upper respiratory tract infection or a very anxious young woman with an intracranial haemorrhage discharged with a diagnosis of tension headache. Guided by this aphorism, we doctors will almost always make the correct diagnosis, and nurses an accurate assessment of a patient’s complaints, and we will glow with professional satisfaction. But how does this boost to our professional confidence measure up against what should be our paramount concern — the safety of each patient in our care? When assessing junior colleagues, we must, above all else, be seeking reassurance that patients will be safe in their hands. We do not want to hear a junior doctor brushing aside a commonly occurring symptom or clinical sign as of little importance merely because it is common. But we do want to know that he or she has considered, “What is the most serious condition that this could be?”, followed by relevant enquiries into the patient’s history, appropriate clinical examination and warranted laboratory or other investigations. Knowing that the doctor has checked that there is no suggestion of a serious illness, we can be reasonably assured that the patient will be safe. An excellent candidate would make the correct diagnosis sooner and perhaps with less pain, discomfort and inconvenience for the patient, and at less cost to the health care system, than a less able colleague. But the patient will be safe with either doctor, as a dangerous, perhaps life-threatening, illness has been excluded. All that remains is for the correct diagnosis to be made and appropriate treatment administered — a burden for the patient perhaps, but not a disaster. I suggest that readers of the Journal, in their role as teachers, advise their students to abandon that inane and dangerous “commonness” tautology, and replace it with: “Exclude the worst possibility and then assist Nature in its healing processes”.

Peter C Arnold

To the Editor: The National Health and Medical Research Council’s National statement on ethical conduct in research involving humans1 recognises that prisoners can participate in research, but categorises them as “persons in dependent or unequal relationships”. They have limited capacity to provide informed consent. Responding to the high levels of transmission of bloodborne viruses in Australian prisons,2 the Australian Red Cross Blood Service excludes prisoners from donating blood and ex-prisoners are excluded for 12 months after they have been released from prison.3 The New South Wales Human Tissue Act 1983 is silent on whether prisoners can donate organs. We report here the case of a prisoner organ donor, highlighting the administrative, legal and operational hurdles that needed to be overcome. A 53-year-old male prisoner was a suitable living kidney donor for his first cousin. He provided consent willingly and without coercion. At initial assessment, the prisoner’s classification required that he be escorted to hospital and that constant surveillance by prison officers be maintained — at a cost of $1000 per day, for at least 7 days. These costs would have been borne by the family. Furthermore, as Australian prisoners are ineligible for Medicare under the Australian Constitution, the donor, as an uninsured patient, and his family would have been required to pay for all pre-, peri- and postoperative care. The donation was deferred for 14 months while these two administrative hurdles were overcome to permit the donation to proceed: 1. The Commissioner for the Department of Corrective Services gave approval for the prisoner to be reclassified to the lowest security classification, thus removing the need for surveillance while in hospital; and 2. A rarely used provision within the NSW Crimes (Administration of Sentences) Act 1999 was applied. Section 26(1) of the Act allows the Commissioner to issue a permit allowing an inmate to be absent from a correctional centre: (a) on such conditions and for such period as may be specified in the permit, and (b) for such purpose as the Commissioner considers appropriate. This allowed the prisoner to be temporarily reinstated to receive Medicare entitlements. The nephrectomy and transplantation were successfully performed. The donor returned to prison on the seventh postoperative day. The donor organ is functioning 4 months after the operation. Prisoners have a right to participate in organ donor programs; however, their precarious position to provide informed consent needs to be protected.

Elizabeth Magee · Michael H Levy

To the Editor: An important factor in the well documented shortfall of organs and eyes for transplantation is the apparent reluctance of people to agree to donate.1 One nearly universal strategy in attempting to raise donation rates has been to encourage individuals to register their wishes about donation. Although evidence that this strategy increases donation rates is lacking, there is some evidence that more individuals make and communicate a decision with appropriate education.2 Most families consent to donation when the deceased had indicated this was their wish, and virtually none override a stated wish not to donate.3 When wishes are unknown, half of families consent and half refuse.3 Encouraging declaration of intention aims to increase the rate of consent for families who would otherwise not know the deceased individual’s wishes. For this to be successful, most individuals newly recording their wishes must indicate a desire to donate. This assumption has underpinned Australian education campaigns, including “Talk about it”, “Share your life, share your decision”, and most recently the national “Sign on to save a life” campaign.4 A simple review of New South Wales Roads and Traffic Authority organ donation data over the period of these campaigns suggests this assumption may not hold. From 1997 to 2004, a significant proportion of drivers licence holders newly indicated a preference about donation; the proportion indicating some decision rose from 59.4% to 78.6%. Over the same period, the proportion indicating yes to donation of all organs rose from 35.6% to 41.9% (a 17.7% increase); however, the proportion indicating no to any donation rose from 19.9% to 31.4% (a 57.8% increase).5 These results raise the possibility that encouraging individuals to make a decision about donation may increase the number of families who refuse donation. Individuals who had previously not made a decision about donation, when encouraged to do so, displayed an unwillingness to become organ donors at twice the rate of those who indicated willingness. Although it is imperative to recognise and respect the decision of individuals to refuse organ donation, this unwillingness may reflect either formalisation of a considered desire not to donate, or a decision made without personal discussion of fears and concerns about donation. Generalised education campaigns are limited in that they encourage action without addressing fears and concerns. Further policy should recognise a possible danger in simply exhorting the public to make a decision, and research should investigate why individuals are refusing to become organ and eye donors.

Mitchell Lawlor · Frank A Billson

To the Editor: Opdam and Silvester concluded that the small pool of organ donors limits the potential for organ donation in Victoria.1 According to the definition of death in the Human Tissue Act 1983 (NSW): a person has died when there has occurred: (a) irreversible cessation of all function of the person’s brain, or (b) irreversible cessation of circulation of blood in the person’s body. Current cadaveric organ donation takes place predominantly after brain death, although it is also possible after cardiac death. This was previously described as “non-heart-beating organ donation”, but the name was changed to “donation after cardiac death” (DCD) to emphasise that organ donation occurs only after death. DCD can be classified by the Maastricht criteria (Box).2 Category III is relevant in select patients undergoing planned withdrawal of therapy in intensive care units (ICUs). Planned withdrawal of therapy is said to occur in about 60% of all ICU deaths.3 Permission for organ donation is required before the planned withdrawal of life support, so the donor organ retrieval teams can be available and ready to retrieve organs soon after a 5-minute “cooling off” period after circulation ceases. These 5 minutes also allow families to spend time with the deceased after death. A period of less than 60 minutes between withdrawal of therapy and cessation of circulation is recommended to minimise warm ischaemia time in the retrieved organs. Withdrawal of life support may occur in the ICU or in the operating room complex, and local hospital guidelines should address the issue of where this occurs. Between 1989 and 2004, 30 Australian organ donations involved non-heart-beating organ donors (data from the Australia New Zealand Organ Donor Registry). In 2005, eight New South Wales organ donations, accounting for 14% of all cadaveric renal transplantation, proceeded after cardiac death criteria were applied. In our unpublished retrospective audit, 7% of patients who had planned withdrawal of therapy in the ICU met the criteria for eligible organ donors after cardiac death. The organ donor pool for organ donation after brain death was 1.7% in Opdam and Silvester’s study.1 The long-term function of transplanted kidneys is not significantly different for organs retrieved after cardiac death compared with organs retrieved after brain death.4 Liver and lung transplantation are also possible from organs retrieved from non-heart-beating organ donors. Draft guidelines for DCD in NSW are soon to be released by NSW Health. Similar guidelines in other states and education of staff involved in organ donation would no doubt increase the organ donation pool and the potential for organ donation. Maastricht donation after cardiac death protocol categories2 I Dead on arrival (uncontrolled) II Failed resuscitation (uncontrolled) III Withdrawal of support (controlled) IV Arrest following brain death (uncontrolled)

Deepak Bhonagiri · Patricia Wills

To the Editor: In 2004, there were 580 cases of suicide in Queensland, and not 453, as reported by the Australian Bureau of Statistics (ABS) on 14 March 2006.1 These data alone reverse the declining trend for suicide mortality nationally in the most recent years. The Queensland Suicide Register, maintained by the Australian Institute for Suicide Research and Prevention (AISRAP), receives data directly from the Office of the State Coroner, and crosschecks them with other Queensland coroners, the John Tonge Centre (the Queensland Health Scientific Services mortuary), and the National Coroners Information System (NCIS). The ABS receives data from the state registries of births, deaths and marriages, and crosschecks them with the state coroners’ offices. The agreement between the two agencies has been decreasing in recent years, with AISRAP detecting 550 suicide cases in 2003 and 588 in 2002, compared with 466 and 537, respectively, detected by the ABS (Box). The ABS has acknowledged difficulties in getting reliable data for 2004 in a number of endnotes to its yearly report.1 Most of the problems were related to a very large backlog of cases still under investigation by coroners, a phenomenon that is reported as increasing in recent years. A confirmation of problems in official data comes from the NCIS, whose most recent report has evidenced, from 2000 on, declining percentages of completeness in mortality data in Queensland and elsewhere in Australia, with the most incomplete figures in 2004.2 It is important to note that cases that are under investigation and those that end with an open verdict would not enter official suicide mortality data, as these are never reconciled. Following the example of many European countries, it would be desirable to start a periodical publication (eg, every 3–5 years) to provide a more comprehensive picture of suicide mortality, including finalised investigations, reclassified (ex-accidental or ex-undetermined) causes of deaths, and deaths that occurred (especially in hospitals) with a delay from a self-injurious event. This would provide a more credible depiction of suicide mortality in the country, and permit better research.3 Meanwhile, efforts should be made to homogenise certification procedures (International classification of diseases, 10th revision terminology has yet to be extensively adopted) and streamline the bureaucratic procedures (we still suffer from a number of “lost in the system” data). In the registries of births, deaths and marriages, by law, the word “suicide” (or analogous term) does not appear. Frequently, the ABS, which collects data from the registries each month, has to reclassify the data obtained, and integrate the information received with further enquiries. Apart from being time-consuming, this routine does not provide foolproof results, and has potential for improvement. Some underreporting in suicide statistics is virtually ubiquitous,3,4 and has to be tolerated (eg, misclassification as accident, road accident, or disease-related, particularly in the elderly; cover-up because of stigma, sociocultural norms, or insurance reasons; or remoteness of location). However, federal and state governments in Australia are committed to suicide prevention plans that require credible baselines for evaluating their effects. All relevant parties need to work jointly on improving data quality. This is of crucial importance for scientists and policymakers, and for those personally affected by a suicide death. Number of suicides in Queensland according to the Australian Bureau of Statistics and the Queensland Suicide Register (QSR) QSR data were provided by the Office of the State Coroner, the National Coroners Information System and the John Tonge Centre. “Possible” suicides are not included. Data for 2005 are an estimate.

Diego De Leo

To the Editor: We read with interest the “Diagnostic Dilemma” by Peter et al.1 The case raises interesting management issues. The first is initiation of antibiotics. Despite 1 week of fever, rigors, haematuria and loin pain, we are informed that the patient was in no distress at initial assessment. In this situation there is, despite the anxieties of resident staff, no urgent need to administer antibiotics; hospitals are controlled, monitored environments in which observation, review and investigation can be undertaken, within reason, if a diagnosis is not immediately made. The second issue is antibiotic selection. The provisional diagnosis was a urinary tract infection, and ceftriaxone and gentamicin were administered. The justification for the use of two agents with a similar spectrum of antimicrobial activity is not given.2 Likewise, no justification is given for the use of a potent nephrotoxin in the presence of moderately severe acute renal failure. Flucloxacillin was added “to broaden the gram-positive antibiotic cover”. It is not apparent why staphylococcal cover was sought at this stage. All cultures (blood, urine and pleural fluid) remained negative. At Day 14, ceftriaxone and gentamicin were changed to ticarcillin/clavulanic acid and ciprofloxacin “because of persistent fever and rising [white cell count]”; this decision in the absence of positive cultures is not explained. The patient’s renal function deteriorated further and he became profoundly acidotic. In fact, the patient’s renal function had performed heroically, given administration of gentamicin for 2 weeks in the presence of acute renal failure at admission. In the intensive care unit, flucloxacillin was replaced with vancomycin; the rationale is not explained. This case illustrates important points regarding antibiotic use. Despite significant renal impairment at admission, the patient was administered a 2-week course of a nephrotoxic antibiotic, which contributed to renal collapse. This situation would have been terminal if not for supportive intensive care. The treating team appears to have managed the patient as if sepsis were a given, and yet all cultures remained negative. This illustrates a basic but crucial teaching point — fevers, chills, rigors, raised inflammatory markers and neutrophilia do not necessarily equate with sepsis. If this experience reflects routine practice elsewhere (and it is our experience that it does), is it any wonder that we have reached an era in which we now encounter organisms so resistant that they are essentially untreatable?3

Mark A Boyd · Stephen Hedger

In reply: Boyd and Hedger have raised concerns regarding the initiation and choice of antibiotics in our recent case report.1 Several aspects of this correspondence need to be addressed. The primary focus of the article was to highlight an important and probably underrecognised cause of unexplained metabolic acidosis, and discussion regarding antibiotic choice was not within the scope of the article. Further, the patient’s management before admission to the intensive care unit was by a different treating team. Subsequent case-note review did not reveal reasons for initiation or choice of antibiotics other than described in our article, although it was evident that gentamicin doses were adjusted based on drug levels. We agree that a less nephrotoxic agent could have been chosen and that the profligate use of antibiotics in the absence of strong evidence of infection could have been avoided. The excessive use of antibiotics in the current medical milieu may stem from a physician’s lack of confidence, or even legal ramifications of “watching and waiting” in the setting of “fevers, chills, rigors, raised inflammatory markers and neutrophilia”, as encountered in our patient.

John V Peter · Natasha Rogers · Sandra L Peake

To the Editor: Primary care skin cancer clinics continue to receive negative publicity. We have previously reported on the workload profile of one network of clinics.1 We report here the profile of clinical activity of the four MoleScan skin cancer clinics situated on the Sunshine Coast, Queensland. Between them, these clinics have been open for a total of 22 years, ranging from 2 years to nearly 9 years of operation. MoleScan is a service company with clinics across Australia. Doctors are employed as subcontractors and are provided with digital dermascopes. The clinics do not have dedicated day surgery facilities, and surgical procedures are conducted in the consulting rooms (http://www.molescan.com.au). Using Medicare Benefits Schedule item number billing data (as previously reported1), we calculated the number of consultations, biopsies, excised lesions (benign, non-melanoma skin cancers [NMSCs] and melanoma), surgical repairs, non-surgical treatment of skin cancers, and non-surgical treatment of other skin lesions. We also estimated the number needed to treat (NNT), defined as the number of benign lesions removed per melanoma. There were 98 276 consultations at the four clinics during the 22 years of operation (Box). In all, 14 982 skin cancers were treated: 395 melanomas and 7468 NMSCs by surgical excision, and 7119 NMSCs by non-surgical methods. The estimated NNT was 22.5. Of the 16 962 lesions excised, 11% (1812) were repaired by a skin flap, 68% (1226) of which were simple flaps. Our previous report, on a different network of clinics,1 showed a different pattern of surgical repairs: 33% (2651) of the 8055 lesions excised were repaired by a skin flap, 45% (1187) of which were simple flaps. Clearly, the clinical practices of these two clinic networks vary. Another area of apparent difference between the two clinic groups is the NNT — 22.5 reported here, compared with 28.6 from the other network.1 The lower NNT in these MoleScan clinics may result from the use of digital dermoscopy, but this requires further study. These early findings from our analyses of MoleScan data highlight the dangers of generalising about the activities of primary care skin cancer clinics from one dataset. Workload profiles of different clinical services may vary markedly, and the widely expressed concern about large numbers of inappropriate surgical repairs may not be warranted. Activities billed at four MoleScan skin cancer clinics on the Sunshine Coast, Queensland, over a total of 22 years of operation * Eyelid, nose, ear, lip, neck, hand, digit or genitals.

Deborah A Askew · David Wilkinson · Gordon L Patrick

To the Editor: We read with interest the article by Couper et al on the psychosocial impact of prostate cancer (PCA) on patients and their female partners.1 We agree that involvement of partners in the research pro-cess is pivotal to understanding the relational dimension of how PCA is both understood and approached by men and their partners.2 However, this could be extended to consider the unique experiences of gay men diagnosed with PCA and their partners. Heteronormative viewpoints are commonplace in PCA research. This bias is unfortunate, as there is a 28% possibility that one of the men in a gay relationship will develop PCA over the course of his lifetime.3 While it is probable that gay men and their partners have some of the same concerns regarding PCA as heterosexual couples, there are also unique concerns that are specific to gay men and their partners. Such considerations may include (but are not limited to): the prostate gland as a site of sexual pleasure and the associated implications of being able to engage in penetrative anal sex after prostate surgery;4 homophobia and/or disregard for sexuality within the health care system5 when being diagnosed with and treated for PCA; and the impact of polygamous (open) relationships and the ambiguous position of gay partners having to care for their mates.4 At this stage, the above concerns are purely speculative, as there is a paucity of literature on gay men and PCA.4,6 We believe future research on the psychosocial impacts of PCA should consider the experiences and special concerns of gay men with PCA, as well as those of their partners.

James A Smith · Shaun M Filiault · Murray J Drummond · Robert J Knapman

In reply: We thank Smith et al for their acknowledgement of the importance of the relational dimension to understanding how prostate cancer (PCA) is understood and approached by men and their partners. The psychosocial implications of prostate cancer for same-sex couples are important and need specific investigation. However, there are methodological difficulties in attempting to quantify the impact of PCA on same-sex couples and in comparing their experience with other couples. In our review of the literature,1 we discovered that where previous researchers had included same-sex partners in their studies, insufficient numbers were recruited for meaningful quantitative statistical comparisons. For example, Perez and colleagues,2 Neese and colleagues3 and Davison and colleagues4 each recruited only one same-sex couple into their studies of 134, 164 and 74 couples, respectively. We believe that a qualitative approach is needed, specifically seeking out and examining the experiences of a group of same-sex couples and comparing and contrasting their experiences with those of a group of male–female couples. This is an approach we are considering in future studies to help us develop and refine an effective but broadly applicable couple-focused psychosocial intervention for PCA.

Jeremy W Couper

To the Editor: We disagree with the recent recommendation of Graham and colleagues that all medical students should be offered BCG vaccination.1 In countries with a low prevalence of tuberculosis (TB), the side effects from the vaccine and losing the use of a Mantoux test to readily diagnose recent TB infection outweigh any benefits of a vaccine with relatively poor efficacy. The incidence of pulmonary TB in Australia is low (3.3 per 100 000 per year) and only 1.5% of isolates are multidrug-resistant.2,3 Thus, the likely exposure of medical students and doctors in Australia to pulmonary TB (let alone multidrug-resistant TB) will be low. In addition, most hospitalised patients with pulmonary TB would have been suspected of having TB before being sent to hospital, so adequate respiratory precautions should have been in place for most. This makes the risk of transmission to health care workers very small. Information from the Australian immunisation handbook is also very relevant to this debate.4 BCG can be effective, but mainly in preventing disseminated TB in children (> 80% efficacy). In adults, the overall protective efficacy is only about 50%,4 and the sole Australian study showed, at best, a protective efficacy of only 30%.5 The effect of BCG may not persist for more than 10 years but repeat vaccination is not recommended.4 Adverse events occur in about 5% of those vaccinated, with 2.5% being injection site abscesses and 1% lymphadenitis. About 1% of vaccinees may need medical attention as a result of the adverse event. Anaphylactoid reactions can occur, and keloid scarring can also occur (although rarely) at the injection site. The vaccine is “live”, and therefore contraindicated in anyone who might have HIV, other forms of immunosuppression, or generalised skin diseases.4 Graham and colleagues believe the problem of BCG vaccination interfering with the interpretation of Mantoux results can be overcome by using whole blood-based interferon assays, such as QuantiFERON-TB Gold, purportedly unaffected by BCG vaccination.1 However, the data for QuantiFERON-TB Gold need to be treated with some caution because it is a new test and there is no gold standard against which to compare it for diagnosing latent TB. The specificity of interferon assays in diagnosing latent TB has been estimated at 95% or more,6 but this will still result in a poor positive predictive value if the pretest probability of latent TB infection is low — and this is the case for health care workers in Australia. In summary, Australia is far more likely to protect its health care workers from TB through effective hospital infection control measures and migrant screening than through a vaccination program with a mediocre vaccine.

Sanjaya N Senanayake · Peter J Collignon

To the Editor: Graham and colleagues correctly assert that medical students are at increased risk of infection with Mycobacterium tuberculosis in settings where they are treating patient groups with a high prevalence of active pulmonary tuberculosis (TB).1 This is well illustrated by the increasing prevalence of latent TB infection among medical students in their later clinical years in countries where community TB incidence markedly exceeds that of Australia.2 Their case for a standard approach to screening of medical students at course entry has great merit, and their arguments in favour of using an interferon gamma release assay to screen for latent TB infection would bring Australia into line with current international best practice. However, the data presented do not substantiate a policy of offering BCG vaccination to all Australian medical students whose screening test result for latent TB infection, whether by interferon gamma or tuberculin skin testing (TST), is negative. Although BCG offers definite benefits in reducing the risk of life-threatening disseminated disease in children under 2 years of age, it does not offer dependable protection against pulmonary TB in adults.4 Medical students who are vaccinated with BCG may be lulled into a false sense of security, and neglect other more effective infection control measures that would reduce their risk of TB exposure and infection. Although BCG is a relatively safe vaccine, there is a small but well defined risk of local and systemic adverse events.5 We therefore support a standardised approach to screening medical students with TST or, preferably, interferon gamma at course entry and exit. Screening for latent TB infection should be offered whenever merited during the course of study, after exposure to active TB disease in Australia or abroad. The benefits of chemoprophylaxis on conversion outweigh the risks associated with isoniazid use, and the risks associated with BCG may not be acceptable where the risk of TB exposure for many Australian medical students is currently negligible.

David N Durrheim · Michael J Hensley

In reply: The intention of our article was to highlight inconsistent approaches to tuberculosis (TB) prevention in Australian medical schools and stimulate a new informed debate. We therefore welcome the responses from Senanayake and Collignon, and Durrheim and Hensley. Interference with interpretation of tuberculin skin testing (TST) is one argument cited against the use of BCG vaccination for health care workers. While we agree that the new blood-based tests need further evaluation, unlike TST, they are not affected by BCG because they employ TB-specific antigens. The lack of a gold standard for diagnosis of latent TB affects both TST and the blood-based tests. Recent reviews of these new tests have been favourable — including one that states that, compared with TST, these new assays seem to have “better correlation with surrogate measures of exposure to M. tuberculosis” and that “because of their higher specificity they may be helpful in low-prevalence, resource-rich settings where cross-reactivity due to BCG may pose difficulty in BCG interpretation”.1 In fact, this article summarised the specificity of these new tests as between 95% and 100%. Other authors found a specificity of 98.1%.2 We agree that infection control is crucial in preventing nosocomial TB transmission, but every infection control practitioner has seen patients with unrecognised TB admitted to an open ward. One missed patient can mean contact-tracing and testing of dozens of staff. The Melbourne Mantoux study (involving 14 Melbourne hospitals) found that health care work and years of hospital employment were significantly associated with a positive Mantoux result — indicating the risk to Australian health care workers is not “negligible” as Durrheim and Hensley state. Nosocomial outbreaks of TB are well documented in low-prevalence countries.1,3 BCG is by no means a perfect vaccine. However, while BCG efficacy was once thought to only last 10 years, a recent large study suggested that it persists for 50–60 years,4 and there is new evidence that BCG vaccination may prevent some primary infections.5 While the risk of health care-associated tuberculosis in Australia is currently low, it would be unwise to assume this will remain the case, or that doctors will only work in safe environments. What will be the effects of HIV, further immigration from high-risk countries, drug resistance and the increasing use of immunosuppressant medications on the incidence of TB? We stand by the recommendations in our article, although we acknowledge they are controversial. There should, however, be no controversy about the need for a consistent policy concerning TB prevention in our medical schools.

Maryza Graham · Tanya M Howley · Robert J Pierce · Paul D R Johnson

To the Editor: In a recent observational study, Krum et al concluded that the treatment of heart failure after myocardial infarction in Australian teaching hospitals is suboptimal because angiotensin-converting enzyme (ACE) inhibitors, β-blockers and aldosterone antagonists are underutilised.1 We believe that another explanation, mentioned by the study’s authors, is worth exploring further — for valid clinical reasons, it was not appropriate for certain patients to start or continue taking some of these medications. An understanding of the enrolment criteria of relevant clinical trials is informative. The large, long-term ACE inhibitor trials quoted by Krum et al — SAVE,2 TRACE and AIRE4 — between them screened 34 037 patients with myocardial infarction and left ventricular dysfunction. Only 5986 patients (18%) met the inclusion/exclusion criteria to be enrolled in one of the trials. Unfortunately, the CAPRICORN5 (β-blocker) and EPHESUS (aldosterone antagonist) trials did not publish the number of patients screened versus the number randomised, but a glance at their exclusion criteria explains why, for some patients, it may not have been appropriate to start these medications during their hospital stay. Some of the exclusion criteria for CAPRICORN were: unstable angina, ongoing therapy with antiarrhythmics (except amiodarone), secondary or tertiary heart block or sick sinus syndrome unless paced, uncontrolled hypertension (> 160/95 mmHg), bradycardia (heart rate, < 60 beats/min), hypotension (systolic blood pressure, < 80 mmHg), requirement for intravenous diuretics or inotropes, chronic obstructive pulmonary disease with ongoing inhaled β2-agonist or steroid therapy, and unstable insulin-dependent diabetes. Is there any harm in prescribing outside the inclusion/exclusion criteria for clinical trials? A population-based, time-series analysis linking prescription-claims data and hospital admission records of 1.3 million adults in Canada6 showed that hyperkalaemia-related deaths in hospital doubled after the RALES trial (spironolactone) was published in 1999. There was no reduction in re-hospitalisation for heart failure or all-cause mortality. The authors speculated that part of the reason for this was prescription of spironolactone to patients who would have been excluded from the RALES trial. While we would not advocate prescribing strictly within the boundaries of the inclusion/exclusion criteria of clinical trials, it is important to understand these criteria, so that prescribing in “real world” patients is done with care. We are reassured that Krum et al’s study suggests there is discretion in the prescribing of drug therapy. Presumably, during ongoing medical assessment, it will be appropriate for some patients to commence some of these medications (potential benefit outweighs potential harm), while others may need to have their medications reviewed because of adverse events.

Lauren J Bailey · Vasi Naganathan

In reply: We thank Bailey and Naganathan for their thoughtful viewpoint regarding prescribing according to clinical trial criteria. We agree that prescribing in the real world often involves complex decision making, taking into account age, comorbidities, concomitant medications and other factors, whereby guidance regarding individual patients cannot readily be extracted from clinical trial literature. This may certainly contribute to underutilisation of evidence-based drug treatment.1 Nevertheless, several analyses support the contention that physicians who more closely adhere to evidence-based guidelines (which in turn are derived from randomised clinical trials) produce better outcomes for their patients.2,3 Therefore, we would still advocate prescribing as closely as possible to guideline recommendations, while acknowledging that these recommendations may not always be readily applicable to every patient.

Henry Krum

To the Editor: The guidelines for managing acute coronary syndromes, published in a supplement to the Journal in 2006, provide a readily accessible tool for clinicians to enhance patient care.1 However, unfortunately the recommendations concerning adjunctive anticoagulation in patients with acute coronary syndromes (ACS) are suboptimal. The 2006 guidelines recommend that high-risk patients with non-ST-segment-elevation ACS should be treated with aggressive medical management, including unfractionated heparin or the low molecular weight heparin (LMWH) enoxaparin, based on evidence from randomised trials showing that these agents reduce the risk of non-fatal myocardial infarction (MI).1 However, neither unfractionated heparin nor enoxaparin have been shown to reduce mortality in patients with non-ST-segment-elevation ACS, even when compared against placebo, and enoxaparin increases the risk of bleeding when compared with unfractionated heparin.2-4 By contrast, the OASIS-5 study, presented at the European Society of Cardiology Meeting in September 2005 and published in early 2006, showed that fondaparinux (a pentasaccharide inhibitor of factor Xa) compared with enoxaparin reduced death and stroke rates, and reduced the risk of bleeding by one half.5 Updating the recommendation so that enoxaparin was replaced with fondaparinux for patients with non-ST-segment-elevation ACS would save six Australian lives at 30 days for every 1000 patients treated, and would cause 19 fewer bleeds. The recommendations of the 2006 ACS guidelines concerning the management of patients with ST-segment-elevation MI are similarly suboptimal. There are now convincing data from randomised trials that enoxaparin is more effective than unfractionated heparin for preventing recurrent MI in patients with ST-segment-elevation MI who have been treated with fibrinolytic therapy.4,6 However, as in the case with non-ST-segment-elevation ACS, enoxaparin has never been shown to reduce mortality in ST-segment-elevation MI. By contrast, both the LMWH reviparin, and fondaparinux, reduce mortality,7,8 and fondaparinux does so without increasing the risk of bleeding.8 We appreciate that rapid advances in the management of ACS make it increasingly difficult for evidence-based guidelines to reflect the best evidence from clinical trials. However, when new evidence becomes available that is clinically relevant at the individual and population level, we believe the guidelines working group and the Journal have a responsibility to update the readers.

John W Eikelboom · Graeme J Hankey · Paul E Langton

In reply: We thank Eikelboom et al for presenting new data on acute coronary syndrome (ACS) management. In this field of rapid advances, another recent study, ACUITY, has also been published, which examined bivalirudin in ACS.1 The Australian guidelines2 are based on peer reviewed published reports, and neither OASIS-53 nor ACUITY1 were released at the conclusion of the formulation of the guidelines. Also, fondaparinux is only available on the Pharmaceutical Benefits Scheme (PBS) in Australia for thromboembolic prophylaxis, and bivalirudin is currently only approved by the PBS for therapy during percutaneous coronary interventions. The Australian guidelines are consistent with international guidelines for both unfractionated heparin and low molecular weight heparin considered as Grade A recommendations for treating non-ST-segment-elevation ACS, based on Level 1 evidence (American College of Cardiology/American Heart Association guidelines). For example, the FRISC trial showed a significant reduction in mortality and myocardial infarction with dalteparin (compared with placebo; 1.8% v 4.8%; P = 0.001) at 6 days, which persisted at 40 days.4 The Australian ACS guidelines are a living document, and new evidence, such as the OASIS-5 (fondaparinux)3 and ACUITY (bivalirudin)1 findings, will be considered on their relative merits in future updates of the guidelines (available on the National Heart Foundation Australia website at http://www.heartfoundation.com.au).

Constantine N Aroney · Philip Aylward

To the Editor: A seminal 1997 article by Fine et al described the pneumonia severity score from the Pneumonia Patient Outcomes Research Team study and raised the role for Hospital in the Home (HIH): For the remaining patients in [risk] classes II and III for whom treatment at home with oral antimicrobial therapy is judged to be unsuitable, there are alternatives to traditional inpatient care. These include parenteral antimicrobial therapy at home or a short stay . . . in a hospital observation unit.1 A recent article in the Journal by Charles et al2 omitted a role for HIH in managing community-acquired pneumonia (CAP). Where their protocol mentions outpatient care, readers are led to interpret this as oral therapy only, managed by a general practitioner. Similarly, it is implied that inpatient therapy relates to traditional treatment in a hospital ward. No further clarification is given. This is a surprising omission, given that one of the authors has written extensively in support of HIH in the past.3 HIH administers hospital-level therapy (intravenous antibiotics, oximetry, rehydration, medical and nursing attendance, with 24-hour cover) to a clinical subgroup of CAP patients who can be defined and included within any protocol. Evidence suggests that HIH can offer effective and safe treatment of patients with acute CAP referred directly from hospital emergency departments after diagnosis.4-6 Many patients with pneumonia appreciate the option of well organised, acute, home-based care. An important and growing subgroup of patients living in residential nursing care facilities can also receive acute CAP treatment in facilities with HIH involvement.7 A significant proportion of patients receiving HIH care have failed oral therapy.4-7 Why the omission of HIH? Protocols are tools of influence to be tussled over. This sometimes conflicts with their general aim of organising science into process and progress. Fine and colleagues’ intent in investigating the use of pneumonia severity scores was to help address the question of where and how to treat acute pneumonia. One of the aims of developing scores was to broaden the treatment options, not to narrow them.

Michael Montalto

To the Editor: The recent editorial on community-acquired pneumonia (CAP) stated that “even in an era in which penicillin resistance appears to be increasing among some Streptococcus pneumoniae isolates, there have been no documented failures of high-dose penicillin in treating pneumococcal pneumonia or bacteraemia”.1 The medical literature suggests otherwise. Firstly, North American guidelines do not mention penicillin at all, and, in one analysis of 25 996 hospitalised patients who received monotherapy, mortality was about 50% higher with penicillin monotherapy than with monotherapy with ceftriaxone, another cephalosporin, a macrolide or a quinolone.2 More importantly, however, the same study found that the mortality rate in patients (even low-risk patients) treated with two antibiotics, one of which was a macrolide, was half the mortality rate of patients treated with one antibiotic. Dual therapies used were a macrolide agent in combination with ceftriaxone, another cephalosporin, a penicillin or a quinolone. Best outcomes were achieved with a ceftriaxone–macrolide combination. In a review of seven studies, Waterer3 found that patients with severe pneumococcal pneumonia or bacteraemic pneumococcal disease who were treated with two antibiotics had a significantly lower mortality rate than patients treated with a single antibiotic. This was despite the fact that the patients treated with a single antibiotic were not as ill initially as those treated with two antibiotics. Research by Waterer and colleagues4 showed that the benefit of taking two antibiotics was most apparent in the highest risk hospitalised patients, in whom mortality was five times higher in those receiving one antibiotic than in those receiving two. Thus, it is imperative that all patients with severe pneumococcal CAP be treated with two antibiotics, one of which should be a macrolide.

Patrick J Bradley