Volume 184 Issue 5

Managing access block involves reducing hospital demand and optimising bed capacity Hospital overcrowding causing “access block” — a lack of available inpatient beds for emergency department patients — remains a major impediment to the delivery of good health care both in Australia and overseas. It is obvious that making elderly or disabled patients wait on uncomfortable emergency trolleys in corridors, with sleep deprivation and minimal privacy, is inhumane. Previous research has shown that hospital overcrowding is actually inefficient: it is associated with increased length of hospital stay,1,2 thus potentially reducing throughput. The number of adverse events has also been shown to increase with worsening access block.3,4 An overcrowded hospital should now be regarded as an unsafe hospital Two articles in this issue of the Journal have put pressure on efforts to solve this problem. Sprivulis and colleagues5 and Richardson,6 using different methods and different populations, have shown a strong association between access block and mortality rate. Their findings now make access block a patient safety issue for which all health care workers and the community must be responsible. It is incumbent on governments and administrators to prevent overcrowding by improving management of the health care system and, where necessary, providing increased resources. These two studies have certain methodological issues that require comment. Firstly, both studies used administrative databases. These are convenient and allow very large populations to be studied. Sprivulis et al, in their study, have also taken advantage of the linked databases in Western Australia and looked at outcomes beyond hospital admission, thus avoiding the potential bias of only studying outcomes in hospital. Unfortunately, many data elements are not available on administrative databases. Data on physiological variables, details of treatment and past medical history, for example, were not available to more accurately adjust for risk within patient groups. It is also likely that unknown confounders may have been present, such as changing referral patterns, patient choice, and non-seasonal changes to illness patterns. Despite this, the association between periods of overcrowding and increased mortality is quite strong. Both studies have attempted to adjust for obvious confounders such as age, type of illness, seasonal effect, and so on. What Sprivulis et al and Richardson have shown is that there is an association between overcrowding and mortality, not that overcrowding causes mortality. It is possible (but unlikely) that an influx of sick, elderly patients at high risk of death may actually cause overcrowding, thus resulting in the apparent association. Without a controlled intervention study, it is not possible to conclude that reducing overcrowding would reduce mortality. There are good reasons for assuming a causal relationship: known effects of overcrowding include delays in patient management, poor hospital processes, poor infection control, patients not being placed on the appropriate ward, and so forth. Given that it is logical that there is a causal relationship and that there is no known increased risk to patients under conditions of normal hospital bed occupancy, it is unacceptable to continue to allow hospital overcrowding to occur. There have been many attempts to ameliorate the problem of access block across Australia7 and internationally.8 The exacerbation of access block seen in the past few years is symptomatic of much larger changes occurring within the health system. Changes to workforce, working hours, aged care, and funding, as well as fewer hospital beds, and increasing demand for seemingly limitless new treatments and procedures, have all contributed to access block. Governments have responded to these challenges by increasing resources (health care now consumes 9.6 % of Australia’s gross domestic product9), improved monitoring of performance through various indicators, and myriad initiatives to improve efficiency within hospitals as well as divert some patients away from hospitals. This effort has alleviated access block in some jurisdictions,10 but there are still major difficulties across Australia. What should be done?There are two broad strategies for managing access block resulting from hospital overcrowding — reducing hospital demand and optimising hospital bed capacity. Reduce hospital demandDiversion/substitution: The major focus of this strategy has been to divert patients to community services and provide more services in the community that traditionally occur in hospital (eg, hospital outreach programs, hospital in the home, and improved after-hours general practice services). Reducing expectations: Reducing community expectations of what a public hospital system can provide is a politically sensitive strategy that has not been systematically addressed. Access block cannot be controlled without some limits being placed on the provision of services. Demand for health care is elastic and potentially unlimited, especially in an essentially free health care system. There must be public debate about what is essential versus what is desirable, and how much the community is willing to pay. Prevention: There is potential to reduce demand by disease prevention strategies, and improved management of patients with chronic ill health. Optimise hospital bed capacityImproved processes: There has been an enormous effort by health care workers to increase capacity by improved efficiency of health care delivery. Many initiatives with quick returns have already been implemented. Further significant improvements will need major investments in infrastructure, especially information technology. Workforce reform is necessary to increase the flexibility of the workforce and the capacity of the health care system. There is presently a shortage of virtually every type of skilled worker in the health care sector. Balancing elective and emergency workload: Contrary to popular opinion, the emergency workload is highly predictable across metropolitan areas. Elective treatment must be tailored to match the capacity allowed by predicted emergency work. Better discharge: Moving patients quickly from acute hospitals to more appropriate facilities increases hospital bed availability. Access to rehabilitation, residential aged care and community outreach programs is an essential component of an efficient and well managed health system. Addressing physical, social and psychological issues through care coordination in the emergency department and after hospital discharge can also help reduce hospital length of stay and readmission. Increased bed numbers: It is important to note that access block does not correlate well with the absolute number of hospital beds. Increasing the number of hospital beds temporarily alleviates access block, but does not solve the problem — the beds quickly fill and the problem recurs. Nevertheless, governments must fund an adequate number of beds to provide the health care that the community demands. An overcrowded hospital should now be regarded as an unsafe hospital. Health care workers should not have to provide services in an environment that potentially jeopardises patient safety. Government and communities must decide whether they want a well managed, adequately resourced health care system where demand is matched to available resources or to take their chances with the present system.

Peter A Cameron MB BS, FACEM, MD

Public trust depends on promoting good practice and protecting the public from poor practice Traditional medical professionalism derives from medical practice in the late 18th and early 19th centuries. In the past 10 years, the search has been on in the United Kingdom — and in other countries — for a “new professionalism” more in harmony with patients’ expectations and the nature of medical practice today.1-5 Last month, the Royal College of Physicians of London affirmed its commitment to professionalism as the foundation of good quality medical practice through a Working Party report titled “Doctors in society: medical professionalism in a changing world”.6 That commitment is important, and has relevance beyond the UK. It comes at a time when some consider the very notion of “profession” and “professionalism” to be outmoded. The report and a supplement of excellent evidence7 (underpinning the report) is seen as the starting point for further development. The case for rethinking medical professionalism is presented with conviction and passion. Located in the social context and environment of today’s practice, medical professionalism is defined as a “set of values, behaviours, and relationships that underpin the trust the public has in doctors”.6 Medicine is described as a “vocation in which a doctor’s knowledge, clinical skills, and judgement are put in the service of protecting and restoring human well-being. This purpose is realised through a partnership between patient and doctor, one based on mutual respect, individual responsibility, and appropriate accountability”.6 In their everyday practice, doctors are committed to integrity, compassion, altruism, continuous improvement, excellence and partnership in health care teams. These values should form the basis for a new “moral contract” between the medical profession and society. Professionalism, the report argues, is as important as ever today because it codifies the idea that a doctor’s responsibilities go beyond a “mere” contract of employment. It advocates a concept that “recognises the complexity and uncertainties within clinical practice and which is based on an indissoluble partnership between patient and doctor in a radically new social context”.6 To this end, notions of knowledge, skills, science, practice, profession, society, service, commitment and integrity are retained. The report discards notions of “mastery”, “autonomy”, “privilege”, and “self-regulation” as out-dated or inappropriate. Competence, which describes “mere” capability, is replaced by excellence reflecting abilities of an “eminent” degree. The long tradition of the “art” of medicine yields to “judgement” as a characteristic more in tune with the application of clinical reasoning. Altruism and the idea of vocation are still there, but only just. And accountability is valued provided that it is “appropriate”, that it avoids creating a culture of suspicion and blame. All these ideas, some deeply controversial, will give doctors and the public much food for thought. So far so good. Then we come to the implications and 19 recommendations for implementation. These cover six areas: leadership, teams, education, appraisal, careers, and research. Professional bodies in the UK are urged to create a common forum that would speak on behalf of medicine with a unified voice. The proposals are sensible but lack bite. They are full of gentle, permissive words like “review”, “revise” and “consider”. Moreover, the report shies away from areas where tough decisions are needed if public trust in the institutions of the UK medical profession is to be restored.8 For example, it is tentative about the profession’s responsibility for defining the boundaries of medical practice and the standards, both the acceptable and the unacceptable, which it will expect individual doctors to observe consistently. In rejecting self-regulation — without discussion — it says nothing about the regulatory framework within which the profession and its professionalism must function. Revalidation, the most important recent development in medical regulation likely to improve patient safety if done thoroughly, is scarcely mentioned. Similarly, there is nothing about the role of rigorous peer review in quality assurance of doctors’ professionalism. This may be no accident. The authors say that they are attempting to usher in a major philosophical shift in attitudes to medical practice in the UK. They believe that the regulatory pendulum has swung too far towards a new, rule-based orthodoxy in which good standards of medical practice are a matter of rigorously enforced dutiful conduct. They seek to revert to a “more balanced position” where there is an understanding that an environment that encourages a doctor’s “goodness” is one that will promote positive patient outcomes. This is a false dichotomy. Modern professionalism is about both the encouragement and celebration of good practice and the protection of patients and the public from suboptimal practice. They are one of a piece — indivisible. Public trust is dependent on both. Achieving that will require some hard, creative thinking and courageous leadership by doctors’ organisations if professionalism, medical education and professional regulation are to put — and be seen to put — the interests of patients unequivocally first.8,9 The College has made a good start. However, fine words are no substitute for a track record of decisive action. The General Medical Council has had to learn that the hard way.10 Dame Janet Smith, who conducted the Shipman Inquiry,10 said to the Working Party that the public ought not even have to think about whether they trust their doctors — it should be something they are able to take completely for granted. Quite so. Everyone expects to have a good doctor.

Donald H Irvine CBE, MD, FRCGP

New tumour testing methods can improve the accuracy of diagnosis Although a strong genetic predisposition to colorectal cancer (CRC) is rare, it is important because of its large contribution to CRC diagnosed before the age of 50 years and because mortality from CRC can be reduced by appropriate management. There are currently limitations in determining whether a case of CRC is “sporadic” or whether it might be related to an inherited predisposition. However, Australian research that examines the utility of new diagnostic tools to help diagnose genetic tendency to CRC may be showing us a way forward.1,2 What is hereditary non-polyposis colorectal cancer?The two best-characterised high-risk inherited syndromes are familial adenomatous polyposis and hereditary non-polyposis colorectal cancer (HNPCC) — sometimes known as Lynch syndrome. Both are inherited as autosomal dominant traits. Familial adenomatous polyposis can usually be readily diagnosed on the basis of clinical findings alone, when an individual develops CRC at a relatively young age on a background of colorectal adenomatous polyposis (mostly with more than 100 adenomas). HNPCC cannot usually be readily diagnosed. HNPCC accounts for about 1%–4% of all CRC, but up to 10% in patients younger than 50 years at diagnosis. It is caused by a germline (heritable) mutation in one of a family of genes known as the DNA mismatch repair genes: hMLH1, hMSH2, hMSH6 and hPMS2.3 HNPCC is characterised clinically by an early age of onset of CRC, a predisposition for proximal colonic cancers, and a tendency to develop multiple CRC, along with an increased risk of some extra-colonic malignancies, including cancers of the uterus and ovary, stomach, small bowel, biliary tree, ureter, renal pelvis, pancreas and brain. The family history is often complex. What are the difficulties in diagnosing HNPCC?Traditionally, HNPCC has been suspected in families where the family history of cancer meets the modified Amsterdam criteria.4 These require a family to have at least three close relatives in two generations diagnosed with cancer of the colon, rectum, endometrium, small bowel, ureter or renal pelvis, with at least one diagnosed before age 50 years. One problem is that not all “Amsterdam positive” families will be proven to have HNPCC and, conversely, some families with proven HNPCC do not meet these criteria. Family history alone is not enough — a diagnosis of “suspected HNPCC” may be based on verified clinical and pathological information from the family pedigree, but the diagnosis of HNPCC is ultimately confirmed by the demonstration of a family germline mutation in one of the mismatch repair genes. This is done by taking blood from one of the affected family members and searching the mismatch repair genes to determine whether a causative mutation can be found. However, a mutation cannot be found in every family, as mutations may be missed or mutations may be present in other genes that are not yet identified. This means that if the family history is strong (Amsterdam positive) and the genetic test (mutation search) fails to identify a mutation in an affected family member, the test result should be considered “inconclusive” and all relatives remain at potentially high risk. Only when a causative mutation in one of the mismatch repair genes has been identified can other at-risk adult family members be offered “predictive” genetic testing to determine their risk. Importantly, those found not to carry the family mutation should be considered at the average population risk for cancer, and they (and their offspring) can be spared additional cancer screening and concern. At present, many families with a family history that meets or approaches the Amsterdam criteria are offered this expensive approach to germline genetic testing; few are found to have proven HNPCC. How are these difficulties being addressed?The accurate detection of HNPCC has improved recently for a number of reasons. The first is an increasing awareness of family history as a risk factor for CRC. Clinical practice guidelines assist in estimating CRC risk based on family history.5,6 For those with a more complex family history, referral to a family cancer clinic may be appropriate. These clinics have been developed to provide cancer risk assessment, surveillance, and prevention strategies, with genetic counselling and testing when appropriate. Finally, we now have improved diagnostic tools, including molecular testing of tumours for microsatellite instability and immunohistochemical staining of tumour tissue for mismatch repair proteins, which can be used to help investigate a history of “suspected HNPCC”. Additional molecular tumour tests are in development. Molecular testing for microsatellite instabilityMicrosatellite instability is one of the hallmarks of HNPCC-related cancers and is due to unrepaired mutations in repetitive sequences of DNA known as microsatellites. CRCs that occur in patients with HNPCC tend to be right-sided, mucinous, poorly differentiated and characterised by the presence of tumour infiltrating lymphocytes. On molecular testing, these tumours show high levels of microsatellite instability. The Bethesda guidelines7 were developed to provide criteria for testing tumours for microsatellite instability in an individual affected family member to assist in the diagnosis of HNPCC. These guidelines suggest that all people with CRC diagnosed before the age of 50 years should have microsatellite instability testing to look for possible HNPCC. However, another limitation presents itself. Although high levels of microsatellite instability are seen in most HNPCC-related tumours, microsatellite instability is not exclusive to HNPCC. Some people develop sporadic cancers with high levels of microsatellite instability, unrelated to an inherited defect in mismatch repair; around 10%–15% of sporadic colorectal cancers will exhibit high levels of microsatellite instability. This tends to occur in older women with right-sided cancers, often mucinous, with poor glandular differentiation (as per HNPCC), but with no associated HNPCC family history. In patients with sporadic CRC with high levels of microsatellite instability, the defect in mismatch repair is not heritable and occurs only in the tumour as a result epigenetic silencing of the promoter region of hMLH1. It does not alter the risk of CRC in offspring, so it is important to differentiate this from HNPCC. Tumour BRAF gene mutations occur in most of these sporadic cancers, but virtually never in HNPCC-associated cancers with high levels of microsatellite instability. The presence of a BRAF gene mutation in a tumour with high levels of microsatellite instability makes it more likely to be a sporadic CRC; however, the use of tumour testing for BRAF mutation is speculative at this stage and it is not yet readily available. Immunohistochemical stainingAnother approach used to improve the accuracy of diagnosis of HNPCC is the use of immunohistochemical staining in suspected cases. Immunohistochemical staining uses antibodies to the proteins encoded by the four relevant mismatch repair genes (hMLH1, hMSH2, hMSH6 and hPMS2) to test for the expression of these proteins in tumour tissue. Absence of mismatch repair proteins is often seen in HNPCC and may be specifically related to the gene in which a germline mutation may subsequently be found; that is, the absence of hMSH2 protein in cancer cells usually indicates a germline mutation in hMSH2. However, once again, this absence of staining is not specific to HNPCC — loss of expression of hMLH1 due to somatic inactivation of hMLH1 does occur in sporadic cancers. How is Australian research contributing in this field?Southey et al have recently conducted an analysis of the use of tumour testing to prioritise mismatch repair germline testing in an Australian population-based study of early onset (< 45 years old) CRC.1 In 131 patients, unselected for family history, they found 18 with germline mutations in one of the mismatch repair genes (indicating HNPCC). Based on family history alone (the Amsterdam criteria), only half of these would have been identified, indicating that tumour testing (specifically immunohistochemical staining) is a very useful adjunct to diagnosis, and more sensitive than family history. Ward et al, also Australian, have since published similar findings.2 Immunohistochemical staining has an advantage over microsatellite instability testing in that it is relatively inexpensive, can be conducted in a routine pathology laboratory (rather than a molecular laboratory), and the immunohistochemical staining test identifies the specific mismatch repair gene in which to search for a germline mutation, thereby saving money by directing the mutation search. However, although immunohistochemical staining is promising as a tool to increase diagnostic accuracy for HNPCC, it may be too early to apply this test routinely at diagnosis to all patients with CRC. There are still some problems with tumour testing. Some patients have loss of staining on immunohistochemical staining without a demonstrable mismatch repair germline mutation, indicating a lack of specificity, although this may change as germline testing improves. Immunohistochemical staining utilises antibodies that are not commonly used in pathology laboratories, and staining may be patchy and difficult to interpret for those who do not use these antibodies routinely. Moreover, there is generally a lack of understanding concerning the interpretation of loss of stain — loss of hMLH1 in a patient with an older onset CRC, without family history, usually indicates a sporadic cancer rather than HNPCC, but some of these families are now inappropriately being referred to family cancer clinics as “possible HNPCC”. Finally, some argue that tumour testing is a surrogate genetic test and so requires genetic counselling and fully informed consent. However, tumour testing should be simply viewed as a useful adjunct to HNPCC diagnosis, in that an abnormal finding on immunohistochemical staining raises the possibility, rather than the certainty, of a familial predisposition to CRC. Where to from here?Tumour testing could now be used as a “triage” measure to assist referral to a family cancer clinic for further assessment and germline testing, if appropriate. It is especially applicable when the family history approaches, but does not quite meet, the Amsterdam criteria for suspecting HNPCC or when CRC is diagnosed at an early age (younger than 50 years). However, before this can become routine, immunohistochemical staining testing for HNPCC may need to be standardised, and laboratories validated through the Royal College of Pathologists of Australia to ensure reliable results. Even so, for now, the best diagnostic precision is still achieved by a combined analysis of all the variables: family history, and clinical and pathological findings, as well as results of genetic tests.

Judy A Kirk MB BS, FRACP

Objective: To examine the relationship between hospital and emergency department (ED) occupancy, as indicators of hospital overcrowding, and mortality after emergency admission.Design: Retrospective analysis of 62 495 probabilistically linked emergency hospital admissions and death records.Setting: Three tertiary metropolitan hospitals between July 2000 and June 2003.Participants: All patients 18 years or older whose first ED attendance resulted in hospital admission during the study period.Main outcome measures: Deaths on days 2, 7 and 30 were evaluated against an Overcrowding Hazard Scale based on hospital and ED occupancy, after adjusting for age, diagnosis, referral source, urgency and mode of transport to hospital.Results: There was a linear relationship between the Overcrowding Hazard Scale and deaths on Day 7 (r = 0.98; 95% CI, 0.79–1.00). An Overcrowding Hazard Scale > 2 was associated with an increased Day 2, Day 7 and Day 30 hazard ratio for death of 1.3 (95% CI, 1.1–1.6), 1.3 (95% CI, 1.2–1.5) and 1.2 (95% CI, 1.1–1.3), respectively. Deaths at 30 days associated with an Overcrowding Hazard Scale > 2 compared with one of < 3 were undifferentiated with respect to age, diagnosis, urgency, transport mode, referral source or hospital length of stay, but had longer ED durations of stay (risk ratio per hour of ED stay, 1.1; 95% CI, 1.1–1.1; P < 0.001) and longer physician waiting times (risk ratio per hour of ED wait, 1.2; 95% CI, 1.1–1.3; P = 0.01).Conclusions: Hospital and ED overcrowding is associated with increased mortality. The Overcrowding Hazard Scale may be used to assess the hazard associated with hospital and ED overcrowding. Reducing overcrowding may improve outcomes for patients requiring emergency hospital admission.

Peter C Sprivulis MB BS, PhD, FACEM · Julie-Ann Da Silva BPsych · Ian G Jacobs RN, PhD · George A Jelinek MD, FACEM · Amanda R L Frazer MB BS, LLB

Objective: To quantify any relationship between emergency department (ED) overcrowding and 10-day patient mortality.Design and setting: Retrospective stratified cohort analysis of three 48-week periods in a tertiary mixed ED in 2002–2004. Mean “occupancy” (a measure of overcrowding based on number of patients receiving treatment) was calculated for 8-hour shifts and for 12-week periods. The shifts of each type in the highest quartile of occupancy were classified as overcrowded.Participants: All presentations of patients (except those arriving by interstate ambulance) during “overcrowded” (OC) shifts and during an equivalent number of “not overcrowded” (NOC) shifts (same shift, weekday and period).Main outcome measure: In-hospital death of a patient recorded within 10 days of the most recent ED presentation.Results: There were 34 377 OC and 32 231 NOC presentations (736 shifts each); the presenting patients were well matched for age and sex. Mean occupancy was 21.6 on OC shifts and 16.4 on NOC shifts. There were 144 deaths in the OC cohort and 101 in the NOC cohort (0.42% and 0.31%, respectively; P = 0.025). The relative risk of death at 10 days was 1.34 (95% CI, 1.04–1.72). Subgroup analysis showed that, in the OC cohort, there were more presentations in more urgent triage categories, decreased treatment performance by standard measures, and a higher mortality rate by triage category.Conclusions: In this hospital, presentation during high ED occupancy was associated with increased in-hospital mortality at 10 days, after controlling for seasonal, shift, and day of the week effects. The magnitude of the effect is about 13 deaths per year. Further studies are warranted.

Drew B Richardson MB BS(Hons), FACEM, GradCertHE

Objectives: To compare the injury profiles of the Indigenous population in New South Wales with that of the non-Indigenous population.Design and setting: Descriptive analysis of NSW Health data obtained from the Health Outcomes Information and Statistical Toolkit (HOIST) database. Hospitalisation data were collected for the period 1 July 1999 to 30 June 2003. Mortality data were collected for the period 1 January 1999 to 31 December 2002.Main outcome measures: Hospitalisation and death rates due to injury by age, sex, injury mechanism and Indigenous status. Rate ratios for comparison between Indigenous and non-Indigenous populations.Results: Rates of death from injury were higher for all age groups in the Indigenous population, except people older than 65 years. Indigenous people aged 25–44 years were twice as likely to be hospitalised as their non-Indigenous counterparts (rate ratio [RR], 2.09; 95% CI, 2.03–2.14), and five times as likely to be hospitalised for interpersonal violence (RR, 5.19; 95% CI, 4.98–5.40).Conclusion: The higher rates of injury-related hospitalisation and death in the Indigenous population in NSW are consistent with data reported for other parts of Australia. Of particular concern is the number of Indigenous deaths and hospitalisations due to interpersonal violence.

Kathleen F Clapham PhD · Mark R Stevenson PhD · Sing Kai Lo PhD

Objective: To determine whether pancreatic islet transplantation can control diabetes and prevent severe life-threatening hypoglycaemia.Design, setting and participants: A single-arm observation study of six patients undergoing islet transplantation. All patients had had type 1 diabetes mellitus for over 5 years and documented episodes of repeated severe hypoglycaemia. Islets were isolated from donor pancreases digested by Liberase. Separated islets were infused into the recipient’s liver via the portal vein. Patients were immunosuppressed with daclizumab, sirolimus and tacrolimus. The transplants were performed at Westmead Hospital, NSW, between October 2002 and February 2005.Main outcome measures: Normal blood glucose control without administration of exogenous insulin; demonstration of islet function and abolition of hypoglycaemia.Results: Five of the patients received two islet infusions, and the sixth was withdrawn after one infusion following a portal vein thrombosis. Three patients became insulin-independent, with excellent glycaemic control. Two had islet function with circulating C-peptide, improved glycaemic control, reduced insulin requirement and abolition of severe hypoglycaemia. However, over a 2-year period, graft function deteriorated. Recipients who were initially insulin free remained C-peptide positive but required supplemental insulin. Complications included one postoperative bleed, two portal vein thromboses (which resolved completely), presumed recurrence of tuberculosis in one patient, and deterioration in renal function in one patient.Conclusions: Islet transplantation is effective at improving glycaemic control and hypoglycaemia unawareness in the short to medium term. However, problems with long-term safety of immunosuppression, islet-induced thrombosis and early detection of loss of islet function remain to be addressed.

Philip J O’Connell MB BS, FRACP, PhD · Wayne J Hawthorne MHSc, MD · Brian J Nankivell MD, PhD, FRACP · Anita T Patel BSc · Stacey N Walters DipAppSci · Henry C C Pleass MD, FRCS, FRACS · Richard D M Allen MB BS, FRACS · Jeremy R Chapman MD, FRACP, FRCP · D Jane Holmes-Walker MB BS, FRACP, PhD · Jenny E Gunton MB BS, FRACP, PhD

Objectives: To examine changes in asthma prevalence in the context of other population changes between 1990 and 2003, for specific age and sex groups.Design: Cross-sectional survey based on household interviews, repeated annually.Setting and participants: Representative samples of the South Australian population between 1990 and 2003 (around 3000 people per year).Main outcome measures: Current prevalence of doctor-diagnosed asthma and other health and demographic variables potentially associated with asthma, and asthma management.Results: Response rate was over 71%. Between 1990 and 2003, asthma prevalence increased significantly, doubling in females (from 7.3% in 1990 to 14.6% in 2003), with a smaller increase in males (from 7.8% to 9.4%). Asthma also increased in all age groups, but the largest relative increases occurred in people aged 55 years and older. Logistic regression analyses showed that obesity was a major predictive variable for every age group studied. The prevalence of asthma morbidity (waking at night and days lost from usual activities because of asthma) among those with asthma showed no significant changes between 1990 and 2003. Asthma action plans (introduced on a population basis in 1992) peaked in their distribution at 42% in 1994, and then declined to half that percentage in 2003. The increase in asthma prevalence occurred at the same time as increases in population prevalence of obesity (10.3% to 18.7%) and diabetes (3.1% to 6.9%), and decline in recent vigorous exercise (42.4% to 32.7%).Conclusions: The increase in asthma prevalence over a decade was large, but concentrated among specific sex and age groups. The increase accompanied population increases in obesity and diabetes and a decline in vigorous exercise.

David H Wilson PhD, MPH, BEd, AdvDipEd · Robert J Adams MD · Richard E Ruffin MD · Graeme Tucker BSc · Anne W Taylor MPH · Sarah Appleton BA

The reduction in the incidence of contralateral breast cancer in women treated with adjuvant tamoxifen provided a model for prevention using endocrine agents. Oestrogen-receptor-positive cancer can be prevented with tamoxifen, but side effects limit its clinical utility, and the risk–benefit ratio is not sufficiently high to routinely recommend tamoxifen as a preventive agent. Agents being evaluated in prevention trials include raloxifene and the aromatase inhibitors; these are expected to be at least as effective as tamoxifen and to have fewer side effects. Core needle biopsy (providing histological information) and high-resolution breast ultrasound enhance preoperative assessment of breast cancer. Mammography remains the only screening test shown to reduce breast cancer deaths in randomised trials. Magnetic resonance imaging may have a role in screening women with inherited mutations of the breast cancer genes. Sentinel lymph node biopsy accurately assesses lymph node status and is associated with less morbidity than axillary dissection. Where the biopsy is negative (no histologic evidence of metastases), no further axillary treatment is necessary. Breast reconstruction after mastectomy can produce good cosmetic results, especially where autologous tissue is used. Myocutaneous flaps using latissimus dorsi or transverse rectus abdominus muscles are increasingly popular. Adjuvant trastuzumab therapy in patients whose tumours overexpress HER2 (growth factor receptor) can reduce recurrence rates and improve survival. Neoadjuvant endocrine therapy (as an initial treatment before surgery) is an underutilised treatment in postmenopausal women with oestrogen-receptor-positive large operable or locally advanced cancers. It makes more patients suitable for surgery and offers others the choice of breast conservation.

Nehmat Houssami PhD, FAFPHM, FASBP · Jack Cuzick PhD · J Michael Dixon MD, FRCS, FRCP

Individual values sometimes lead patients to make lifestyle choices that have negative effects on their health. Doctors tend to feel responsible for delivering best-practice health outcomes to such patients, but also feel inclined to respect their patients’ values. The adoption of a harm reduction model may provide a strategy for delivering the best care that is compatible with each patient’s chosen lifestyle.

Bradleigh D Hayhow BA(Hons), BM BS · Michael Peter Lowe BMed, FRACP

Setting The new junior medical officer is arriving next week. You have just been to a workshop about planning for JMO learning during clinical attachments and feel enthused about applying what you learned to her 3-month attachment with you. This also means you will be well prepared for the accreditation visit. A term working in a clinical unit, whether in the community or in a hospital, is a great learning opportunity for junior medical officers (JMOs). Increasing the amount of teaching in the clinical setting, improving teaching methods and providing feedback can improve a JMO’s experience.1,2 Previous “teaching on the run” tips have focused on single teaching episodes,3-5 but it is also important to have an overall plan for what should be achieved during the attachment.2 Planning learning during a clinical attachment (Box)OutcomesWhat will the JMO learn? Define what you want him or her to know or be able to do by the end of the attachment.6 Writing outcomes isn’t about narrowing down learning and ignoring unexpected topics that may arise, but rather about organising learning.6,7 Outcomes need to be: Specific. Each outcome should be clearly defined, important and relevant; Achievable. Outcomes should involve areas JMOs are likely to be exposed to, at a level appropriate for their training. Avoid listing too many outcomes; Measurable. By observing or testing, you should be able to determine at the end of term whether the JMO has achieved specific outcomes. Outcomes should cover all areas important to being a doctor, such as knowledge, skills, communication and professional behaviour.3 Ensure that trainees have input into topics, and include any areas of particular interest or areas in which they are deficient.8 Take-home message When planning learning for a clinical attachment: Use a framework that defines outcomes; methods of teaching and learning; appraisal (with feedback) and assessment. Ensure the desired outcomes are specific, achievable and measurable. Use all available resources and settings. Set aside a formal time for teaching. MethodsHow will the JMO learn? Learning on the job means that teachers should be teaching and giving feedback on a continual basis. One of the biggest complaints from JMOs is the lack of formal teaching, so some time should be set aside to provide this on a regular basis.9 Use a variety of methods and encourage input from JMOs themselves. Ensure your program complements rather than duplicates hospital tutorials. Appraisal and assessmentRemember to give feedback to JMOs at the time they complete a task, such as after a case presentation.5 Assessment may be a formal requirement of your hospital or the medical colleges. Remember the criteria on which JMOs are being assessed and find “assessable moments” to observe their performance. Much of this may be happening now — but is it organised? Strategies to make it workGordon et al2 advise that a strategic approach is needed to implement a learning plan in the clinical environment. (“Strategy” comes from the Greek strategos — an approach to battle!) OrientationMeet the JMO within the first few days and inform him or her of the learning plan during the attachment. Also issue written material. A good orientation covers: The JMO’s clinical duties; The plan for appraisal and assessment during the attachment; Administrative information (rosters, key contact people, meetings); A summary of how you expect the JMO to contribute to the teaching program; and An outline of how you and other staff will help the JMO with service work and learning. Seizing the momentYour regular contact with the JMO and opportunities for teaching usually revolve around cases in the practice, clinics or ward. Relate these cases to training outcomes, using cases notes, discharge summaries, letters and drug charts as the basis for discussion. Debriefing after recent challenges can be a powerful learning exercise. Remember to give feedback at these times and gather information for the end-of-term assessment. Sharing the workRecruit others with expertise relevant to the learning outcomes (eg, nurse educators, laboratory staff, radiologists). Involve the JMO in any program by allocating topics for him or her to present. There is an increasing amount of relevant Internet-based material that you could use. Evaluate the teaching at the end of the term. Ask JMOs what was useful for their learning and what could be improved. Illustrative plan for a postgraduate Year 2 doctor attached to a respiratory unit for 3 months. The trainee’s interest is to work in general practice OUTCOMES (should be specific, achievable and measurable) Methods (what you or your colleagues will do; what your trainee will do; resources to be used) APPRAISAL AND ASSESSMENT (should be matched to outcomes) Clinical (knowledge) Causes and investigation of common respiratory presentations (shortness of breath, chest pain, cough with or without sputum, haemoptysis) Ward work Departmental tutorials (JMO-led, case-based) Check JMO hospital tutorial program for relevant topics (eg, respiratory failure and pulmonary embolism) Data: inpatient presentations, outpatient cases Feedback: Regular (with each case) Mid-term appraisal End-of-term assessment Clinical (practical skill) Aerosol therapy (techniques, educating patients on use) Demonstrations by asthma nurse educator Giving instructions to a patient (observed by asthma nurse educator) Communication (with patients or colleagues) Ability to write concise and accurate discharge summaries Hospital orientation session Departmental manual Review of summaries Copies to consultant for review and regular feedback JMO to bring summaries to mid-term appraisal Professional Attendance to duties, punctuality, time management Departmental orientation Data: observation and feedback from registrar Feedback: mid-term appraisal (more often if required) Individual learning needs Interpretation of basic lung function test reports Internet-based tutorials, texts and guides (eg, <www.woolcock.org.au/teaching/teaching3.htm>) Session with respiratory technician measuring own lung function and performing spirometry Reporting lung function tests on current inpatients Participation in weekly reporting sessions with registrar when possible Consultant feedback on inpatient reports Technician feedback on spirometry measurements JMO = junior medical officer.

Fiona R Lake MB BS, FRACP, MD · Gerard Ryan MB BS, FRACP

Clinical records Patient 1 A 75-year-old woman, who was born in Greece and migrated to Australia 50 years ago, presented with acute shortness of breath secondary to cardiac failure due to valvular heart disease. Her only cardiovascular risk factor was hypertension. A transthoracic echocardiogram 1 month earlier had shown moderate aortic regurgitation, moderate left ventricular dysfunction, and a markedly dilated ascending aorta measuring 5.8 cm (normal, < 3.4 cm). Her symptoms were alleviated with diuresis and medication to treat cardiac failure. She underwent cardiac catheterisation, which revealed a dilated aortic root and ascending aorta, measuring 4.3 cm and 6 cm, respectively, with normal coronary arteries. Syphilis serology, requested because of the dilated aortic root, was positive with a rapid plasma reagin titre of 1 : 2 and a reactive Treponema pallidum particle agglutination test. Because of penicillin allergy, intravenous ceftriaxone 1 g daily was given for 21 days. No lumbar puncture was performed. She had an aortic valve replacement, and replacement of the ascending aorta with a synthetic graft. Macroscopically, the aortic wall was extremely thick. Histological sections showed features consistent with syphilitic aortitis (Figure 1). Her recovery was slow, but she is now living independently 15 months after surgery. 1 Aortic wall of Patient 1 A: Aortic wall (2 x objective) with thickened media (m) and intima (i). B: Aortic media with inflammatory infiltrate of plasma cells (arrowhead) and lymphocytes (arrow) (40 x objective). C: Aortic adventitia with narrowed vasa vasorum (endarteritis obliterans) (20 x objective). Patient 2 A 40-year-old Indonesian man who had lived in Australia for 14 years presented with acute onset severe central chest pain, on a background of similar but less severe pain over the previous 2 months. He smoked one packet of cigarettes per day, but had no other risk factors for coronary artery disease. He was in a monogamous heterosexual relationship of 18 months. His electrocardiogram revealed 3 mm ST elevation in the anterior leads (V1–3) and reciprocal ST depression in the inferior leads (II, III, aVF). His serum troponin level was 4.9 μg/L (reference range, 0–0.4 μg/L). A coronary angiogram revealed a completely occluded left main coronary artery at the ostium, and a 90% ostial lesion of his right coronary artery; the remainder of his right coronary system was clear of disease (Figure 2). He underwent emergency coronary artery bypass grafting. The operative notes do not comment on the appearance of the native coronary arteries, nor were these sent for histological examination. An aortic wall biopsy showed mild degenerative changes only — syphilis could not be excluded as causing these changes. In view of the bilateral coronary ostial lesions, syphilis serology was performed. His rapid plasma reagin titre was 1 : 64, together with a reactive Treponema pallidum particle agglutination test. Treatment with intravenous penicillin 1.8 g every 4 hours was given for 15 days, and prednisolone 25 mg twice daily for 2 days to prevent a Jarisch–Herxheimer reaction. The patient declined a lumbar puncture. 2 Coronary angiograms of Patient 2 \ A: Tapering of the aortic root (thin arrows) and left main coronary stump (arrowhead). B: 90% occlusion of right coronary ostium with no distal disease. Details of five patients The details of these two patients and another three patients seen between 1998 and 2004 are summarised in the Box. Although confirmatory histology of cardiovascular syphilis was not available for four of the five patients, this was considered the most likely diagnosis. All patients were born outside Australia. None of the three men reported having sex with men. No patients reported a history of syphilis. Syphilis has become a rare disease, although peaks of syphilis notifications occurred in Australia in the mid 1970s to mid 1980s and again more recently.1 Clinicians need to be aware of the manifestations of syphilis, and to consider the diagnosis outside the groups considered at risk of this infection in the modern era, such as men who have unprotected sex with other men. The five patients in our series ranged in age from 40 to 77 years. Notably, all were born overseas, and none belonged to a group considered at high risk of syphilis in the contemporary Australian context. Serology was consistent with acquisition of infection in the distant past in four of the five patients. Among patients with untreated syphilis, aortitis occurs in up to 70%–80%, and the clinically apparent manifestations of aortic regurgitation, coronary ostial stenosis and aortic aneurysms are seen in 10%–15%.2 Although aortic regurgitation is rarely caused by syphilis, it occurs in 20%–30% of patients with syphilitic aortitis.3 Coronary ostial lesions may be seen in 20%–25% of patients with syphilitic aortitis,3 but it is uncommon for such coronary ostial lesions to lead to acute myocardial infarction.4 In contrast, ostial lesions are only seen in 0.1% of patients with coronary artery disease, and bilateral lesions are even less common.5 The high plasma reagin titre seen in Patient 2 is also unusual in cardiovascular syphilis, but has been previously noted.6 Lessons from practice Cardiovascular syphilis may occur in patients outside of the usual risk groups for syphilis. Testing for syphilis serology should be considered in patients with aortic regurgitation, and particularly bilateral coronary ostial lesions or aortic aneurysms. Cerebrospinal fluid should be examined in patients with cardiovascular syphilis to exclude neurosyphilis. Patients with bilateral coronary ostial lesions but no distal coronary artery disease and those with ascending aortic aneurysms should be screened for syphilis. Screening should be considered for people with aortic regurgitation, especially those with risk factors, including birth in a country where syphilis has been or continues to be common. Although rates of neurosyphilis are low in patients with cardiovascular syphilis,3,7 a cerebrospinal fluid examination is recommended to exclude neurosyphilis. In addition, screening for other sexually transmitted infections, including HIV, should be considered, and appropriate contact tracing instituted. Sexual transmission of syphilis occurs only when mucocutaneous lesions are present, but long-term sexual partners of patients with late latent or tertiary syphilis should be screened serologically. The duration and route of penicillin therapy for cardiovascular syphilis are controversial. Each of our five patients received a different therapy. Penicillin has never been formally evaluated as treatment for cardiovascular syphilis, but a study from the 1950s showed that few patients had progressive disease after penicillin therapy, and up to 60% reported symptomatic relief.8,9 The Australian Therapeutic guidelines: antibiotic suggest intravenous benzylpenicillin for 15 days,10 the Australian National management guidelines for sexually transmissible infections suggest intramuscular procaine penicillin for 20 days,11 and the World Health Organization, European and United States guidelines suggest intramuscular benzathine penicillin 2.4 million units once weekly for three doses.12-14 These variations reflect the paucity of good clinical data comparing the different regimens. Although definitive evidence of the efficacy of benzathine penicillin is lacking, there is also no evidence to the contrary. There is little evidence that Jarisch–Herxheimer reactions complicate treatment of cardiovascular syphilis.8,9,15 Cardiovascular syphilis: one proven and four presumptive cases Age, sex and country of origin Indications for syphilis testing Syphilis serology and cardiovascular risk factors Management and follow-up 75 years, female, Greece Aortic regurgitation; dilated aortic root RPR: 1 : 2 TPPA: reactive Hypertension Aortic valve and aortic root replacement. Histological confirmation of syphilitic aortitis. Treated for cardiovascular syphilis with intravenous ceftriaxone 1 g daily for 3 weeks. No evidence of a Jarisch–Herxheimer reaction. Lumbar puncture not performed. Follow-up 15 months after therapy: mild exertional shortness of breath. Follow-up syphilis serology has not been requested. 40 years, male, Indonesia Acute myocardial infarction; bilateral ostial lesions and no visible disease in the right coronary artery RPR: 1 : 64 TPPA: reactive Smoker CABG. Histology from aortic wall biopsy was inconclusive for cardiovascular syphilis; no biopsy of the coronary arteries. Presumptively treated for cardiovascular syphilis with intravenous penicillin 1.8 g every 4 hours for 15 days. Oral prednisolone 25 mg twice daily for 2 days was given to prevent a Jarisch–Herxheimer reaction. No evidence of a Jarisch–Herxheimer reaction. CSF normal (lumbar puncture performed after treatment completed). Follow-up 2 years after therapy: symptom-free with RPR 1 : 8. 56 years, female, Vietnam Angina; bilateral ostial lesions; minor irregularities of the left circumflex artery, but no visible disease in the left anterior descending and right coronary arteries RPR: 1 : 1 TPPA: reactive Type 2 diabetes mellitus Hypercholesterolaemia Ostial lesions were not sufficiently severe to require revascularisation procedures, so no biopsies were taken of the aortic wall or coronary arteries. Presumptively treated for cardiovascular syphilis with intramuscular procaine penicillin 1 g daily for 15 days. No evidence of a Jarisch–Herxheimer reaction. CSF normal (lumbar puncture performed after treatment completed). Follow-up 1 year after therapy: symptom-free with RPR 1 : 1. Cardiovascular MRI revealed no further evidence of ostial coronary disease. 77 years, male, Hong Kong Aortic regurgitation; dilated aortic root RPR: 1 : 2 TPPA: reactive Hypertension Type 2 diabetes mellitus Aortic regurgitation was not sufficiently severe to warrant valve replacement, so no aortic wall biopsy was obtained. Presumptively treated for cardiovascular syphilis with intramuscular benzathine penicillin 2.4 g weekly for 3 doses. No evidence of a Jarisch–Herxheimer reaction. CSF normal. Follow-up: returned to Hong Kong and lost to follow-up. Follow-up syphilis serology has not been requested. 72 years, male, Timor Wife had been found to have positive syphilis serology. Following positive syphilis serology, aortic regurgitation was noted on clinical examination and then echocardiographically RPR: Non-reactive TPPA: reactive No cardiovascular risk factors present Aortic regurgitation was not sufficiently severe to warrant valve replacement, so no aortic wall biopsy was obtained. Presumptively treated for cardiovascular syphilis with intravenous penicillin 1.8 g 4 hourly for 14 days. Intravenous hydrocortisone 50 mg four times a day given for 48 hours because of concern about a Jarisch–Herxheimer reaction when atrial fibrillation occurred on antibiotic therapy. No other manifestations of a possible Jarisch–Herxheimer reaction. Atrial fibrillation reverted to sinus rhythm with amiodarone and sotalol therapy. CSF normal. Follow-up: ongoing medical management for cardiac failure. Repeat syphilis serology 3 years after therapy, showed RPR non-reactive. CABG = coronary artery bypass graft. CSF = cerebrospinal fluid. MRI = magnetic resonance imaging. RPR = rapid plasma reagin titre. TPPA = Treponema pallidum particle agglutination test.

Steven Y C Tong MB BS · Alan C Street MB BS, FRACP · Haris Haqqani MB BS

Effectively managing on-field emergencies is the most important role of the doctor on the sidelines. Pre-event preparation is essential and should include a formulated plan for dealing with emergencies and access to emergency equipment such as a stretcher and a bag and mask. Game day injuries should be assessed by adhering as closely as possible to a normal clinical consultation, with a proper history and examination being performed for all injuries. The athlete with an on-field head injury should be treated as having a concomitant cervical spine injury until proven otherwise. Athletes with any symptoms after head injury should be comprehensively and continuously assessed. Return-to-play decisions are made by balancing the risk of injury recurrence, the potential severity of injury recurrence and the benefits of returning to the field (which are higher at elite than amateur level). There is currently a shortage of doctors willing to cover sports events in Australia, which is partially explained by inadequate remuneration, inadequate facilities provided at venues, inadequate training opportunities in sports medicine, and fear of the medicolegal consequences in taking on the role as a team doctor.

Geoffrey M Verrall MB BS, FACSP · Peter D Brukner MB BS, FACSP · Hugh G Seward MB BS, FACSP, FASMF

Heather E Robinson,* Ellen L Maxwell,† H Miles Prince,‡ Mary A O'Reilly,§ Andrew Jakobovits¶ * Haematology Registrar, ‡ Chair of Haematology Service, Peter MacCallum Cancer Centre, Locked Bag 1, A'Beckett Street, East Melbourne, VIC 8006; † Haematologist, Melbourne Pathology, Melbourne, VIC; § Infectious Diseases Physician, ¶ Physician, Cabrini Health, Melbourne, VIC. Miles. PrinceATpetermac.org To the Editor: A 32-year-old woman presented with fatigue and jaundice 12 days after an uncomplicated elective caesarean delivery. She had a haemoglobin level of 76 g/L (reference range [RR], 110–160 g/L), reticulocytosis (202 × 109/L, 12.6%; RR, 20–100 × 109/L) and hyperbilirubinaemia (139 μmol/L, 97% unconjugated; RR, < 20 μmol/L). Within 24 hours, her haemoglobin level fell to 37 g/L, and a blood film showed spherocytes and polychromasia consistent with haemolysis (Box). A direct antiglobulin test was strongly positive for IgG and complement. The patient’s obstetric case notes revealed administration of a single intravenous dose of cefotetan at the time of delivery. Donor red cells treated in vitro with this antibiotic reacted dramatically with the patient’s serum, indicating the presence of antibody to the drug–red cell combination. The patient was admitted to the intensive care unit and received 6 units of red cells over 24 hours, until the haemolysis resolved. Cefotetan disodium is a broad-spectrum second-generation cephalosporin commonly used as prophylaxis in abdominal and pelvic surgery. It is given as a single intravenous dose at the start of the operation, and 50%–80% of the dose is excreted within 24 hours.1-3 A positive direct antiglobulin test is seen in one in 250 patients treated with cefotetan, although this in itself does not always imply active haemolysis. The true incidence of symptomatic haemolysis is difficult to determine for several reasons: the severity of haemolysis varies between patients, and, if mild, may go undiagnosed; the process is self-limiting; and, when the drug has been used perinatally, symptoms may not be distinguished from the fatigue and anaemia expected (and therefore accepted) by most new mothers. Furthermore, as in our case of caesarean delivery, the obstetrician is not always aware of drugs administered by the anaesthetist, making the link between the antibiotic and haemolysis easy to miss. The Adverse Drug Reactions Advisory Committee has 15 listings of haemolytic anaemia caused by cefotetan in Australia, which probably represents significant under-reporting. Indeed, the recognition of cefotetan-induced haemolysis prompted a US Food and Drug Administration review of its incidence in 2002, which revealed more than 85 reports worldwide, including 15 fatal cases.4 Cephalosporins are the most common group of drugs to cause haemolytic anaemia (93% of all cases), with cefotetan alone accounting for 83%.5 A patient with haemolytic anaemia induced by one cephalosporin carries a 10% risk of cross-reactivity with other cephalosporins and consequently should avoid further exposure if possible. First-generation cephalosporins are less likely to cause significant haemolysis than second- and third-generation cephalosporins, yet are equally efficacious in surgical prophylaxis.1,3 We therefore recommend the use of cefazolin as an alternative to cefotetan. Blood film in a woman with drug-induced haemolytic anaemia Blood film taken on Day 1 of admission shows features of immune-mediated haemolysis, with polychromasia (vertical arrow) and spherocytosis (horizontal arrow).

Heather E Robinson · Ellen L Maxwell · H Miles Prince · Mary A O'Reilly · Andrew Jakobovits

Russell Stitz,* Michael R Kidd,† Liz M Kenny,‡ Anne M Howard§ * President, Royal Australasian College of Surgeons, Spring Street, Melbourne, VIC 3000; † President, Royal Australian College of General Practitioners, Melbourne, VIC; ‡ President, Royal Australian and New Zealand College of Radiologists, Sydney, NSW; § President, Australasian College of Dermatologists, Sydney, NSW. college.presidentATsurgeons.org To the Editor: The MJA is to be congratulated on promoting the debate related to the significant increase in the number of “skin clinics”.1 Standards are important in both the maintenance of the facilities and the formal training of the practitioners undertaking the assessment and care of patients. The four medical Colleges actively involved in treating skin conditions, who have their training programs accredited by the Australian Medical Council and their selection and assessment processes authorised by the Australian Competition and Consumer Commission, are the Royal Australian College of General Practitioners (RACGP), the Royal Australian and New Zealand College of Radiologists (Faculty of Radiation Oncology), the Royal Australasian College of Surgeons (RACS), and the Australasian College of Dermatologists. The Colleges already have established standards for accreditation of facilities (eg, Guidelines and standards for day surgery in Australia <http://www.surgeons.org/Content/NavigationMenu/FellowshipandStandards/ AustraliaDaySurgeryCouncil/Guidelines_and_Stand.htm>, or the RACGP Standards for general practice <http://www.racgp.org.au/document.asp?id=17623>) and have well established programs for training medical practitioners in the treatment of skin conditions. The Colleges base these programs on high standard “holistic” care that is not influenced by entrepreneurial medicine. Our Colleges encourage the development of improved training programs at all times. It is important that we maximise the benefit of the structures and standards that currently exist. Our Colleges have already begun discussion about the ways we can build on our work to date. Our members, and the Australian public, expect specialist medical Colleges to take a lead in ensuring the quality of health care, and we will continue to do so.

Russell Stitz · Michael R Kidd · Liz M Kenny · Anne M Howard

Graham Simpson,* Paul Clark,† Trevor Knight‡ * Director of Thoracic Medicine and Regional TB Control Unit, † Resident Medical Officer, ‡ Nurse Unit Manager, Department of Thoracic Medicine, Cairns Base Hospital, Cairns, QLD 4870. fgsimpsonATiig.com.au To the Editor: Australia has a low incidence of tuberculosis (TB), which has remained constant for over a decade.1 However, the incidence is not uniform across the population; immigrants and Indigenous Australians have higher rates. An audit of all cases of TB in Far North Queensland over 5 years showed an incidence of 35.9/100 000 per annum in Indigenous Australians, and poor outcomes in this group.2 This finding led to a number of policy changes, including an increase in directly observed therapy (DOT), made possible by increased use of Aboriginal health care workers in remote communities, and more aggressive and prolonged treatment of relapses. A follow-up audit was undertaken to assess the effect of these changes. The results are shown in the Box for both time periods. New cases of TB in Indigenous Australians were significantly reduced (P < 0.0001 by Fisher’s exact test), and DOT had increased significantly (P < 0.0001). The number of deaths from TB had declined, as had relapses, but these falls were not statistically significant. There were no deaths among Indigenous Australians during the second 5-year period. Of the people who died in this period, three were elderly men suspected of having cancer, and one was a patient from Papua New Guinea (PNG) who had HIV co-infection with TB. The most striking finding was the dramatic increase in cases in people from PNG (P < 0.0001). The outer Australian islands in the Torres Strait are only 3 kilometres from the PNG coast, and there is free movement of people across the border under a treaty arrangement. Although there are no precise figures,3 it is clear that there are epidemics of both TB and HIV in PNG, and that these have extended to rural areas. Specialist outreach clinics with x-ray facilities have been established on the outer islands, but numbers have continued to rise. In 2005, of 38 cases of TB in Far North Queensland, 26 were from the Torres Strait including seven cases of multidrug resistant TB. This represents a significant public health threat and highlights the importance of local audits of TB control, as state and national data may not be adequate to identify emerging local problems. Findings of two 5-year audits on tuberculosis in Far North Queensland Findings 1993–1997 1998–2002 Total cases 87 92 Indigenous Australians 50 22 Non-Indigenous 30 26 Papua New Guineans 7 44 Pulmonary tuberculosis 54 57 Sputum smear positive 67% 47%* Directly observed therapy 18 (21%) 67 (73%) Death from tuberculosis 10 4 Deaths in Indigenous Australians 7 0 Total early relapses 7 2 Indigenous Australians 7 0 Drug resistance 6 7 Multidrug resistant tuberculosis 1† 3‡ HIV co-infection 0 2‡ * Queensland average, 48%. † Patient from the Philippines. ‡ All in Papua New Guineans.

Graham Simpson · Paul Clark · Trevor Knight

Roslyn G Poulos,* Anthony B Zwi† * Lecturer, † Professor and Head, School of Public Health and Community Medicine, University of New South Wales, Sydney, NSW 2052. r.poulosATunsw.edu.au To the Editor: We support the suggestion in the recent editorial on modernising the National Health and Medical Research Council (NHMRC)1 that the Council assess the outputs and value of sponsored research by going beyond considering primarily published articles and granted patents. More attention to mechanisms that improve the translation of research into policy and practice is required. As part of an NHMRC Capacity Building Grant in Population Health in Injury, Trauma and Rehabilitation, we have interviewed a number of Australian injury researchers to identify the facilitators of, and barriers to, enhancing the interface of research with policy and practice. Researchers readily reported peer-reviewed journals and conference presentations as measurable indicators of research success, but found policy and practice outcomes more difficult to identify. This may be because research utilisation often occurs through a slow and indirect process of “enlightenment”;2 however, it may also reflect minimal opportunities available, or taken, to disseminate research directly to policy makers and practitioners, and thereby encourage uptake. Some researchers perceived that funding bodies, such as the NHMRC, do not explicitly fund the person-time necessary for researchers to work with relevant stakeholders to disseminate their research. Without such funding, researchers must move onto the next funded project, without the opportunity to “value-add” to their research by facilitating uptake. Further, there may be little incentive from academia to develop relationships with policy makers, industry or practitioners.3 Such interactions should be considered as “part of the ‘real’ work of research”4 and should attract funding. The Canadian Health Services Research Foundation has identified the job of a knowledge broker as someone “to bring people — researchers, decision makers, practitioners and policy makers — together and build relationships among them that make knowledge transfer more effective” and has recommended that the task of brokering be acknowledged and rewarded.5 The Sax Institute in New South Wales is exploring a similar concept. In considering new approaches to assessing sponsored research, consideration should be given to ensuring the legitimate funding of research dissemination (however, and by whom, that is to be undertaken), and appropriate, objective measurements that reflect dissemination, with the potential to improve uptake. Those familiar with program evaluation will recognise the importance of measuring effective dissemination as a prerequisite to outcome evaluation, and as being highly relevant to the assessment of research output and influence.

Roslyn G Poulos · Anthony B Zwi

To the Editor: Johnson et al detailed an intensive hand hygiene program planned to reduce the burden of nosocomial methicillin-resistant Staphylococcus aureus (MRSA) infections.1 The results were based on observations before and after the program. Hand hygiene compliance rates reached only 42% despite the program, and there was no effect on patient MRSA colonisation or environmental colonisation or contamination. Outside the intensive care unit, there was no effect on health care worker colonisation. Despite this evidence of ineffectiveness, the program was held responsible for a reduction in hospital-wide rates of clinically important MRSA infections. The literature on hand hygiene is inadequate. The recent edition of Clinical evidence contains no randomised controlled trials of hand hygiene.2 In fact, the only published randomised trial is the Mortimer study,3 which is now more than 40 years old. Huynh and Commens made the point that hand hygiene procedures involving application of chemical agents or scrubbing are hazardous for staff and suggested using mechanical barriers (ie, gloves) on clean unscrubbed hands.4 The hand hygiene bandwagon rolls on despite the absence of evidence of benefit for patients and its hazardous nature for staff. Mechanical barriers together with reduced contamination opportunities (hand-shaking, touching telephone handsets and computer key boards) may be better options. We need properly conducted studies to find an effective means of protecting patients from nosocomial infections by MRSA and other agents.

Keith V Woollard

To the Editor: We congratulate Johnson et al on their article, which illustrates a successful hand hygiene program associated with a fall in transmission of multidrug-resistant organisms.1 Their publication is significant for three reasons: It is only the second article2 to demonstrate the anticipated relationship between increased hand hygiene and a fall in multidrug-resistant organism transmission; It again indicates that 100% compliance in hand hygiene is not necessary to significantly improve outcomes;2,3 and It suggests that environmental contamination with MRSA has little relationship to patient colonisation. However, the specific aspects of their program that led to success are not obvious, and may not relate to a sustained response to either education or the provision of alcohol/chlorhexidine hand hygiene solution. Alternative explanations include: The education program and/or overt observation induced a Hawthorne effect on hand hygiene practice; The screening and treatment program induced the same effect on hand hygiene behaviour; or The treatment of MRSA carriers reduced the size of the MRSA reservoir and thus the probability of transmission and subsequent colonisation. Although we agree that the approach of Johnson et al is laudable, without teasing out those causal factors that induce the improvement in hand hygiene in health care workers, it remains expensive to implement and maintain. Moreover, there is no evidence that improved hand hygiene would continue if the alcoholic gel alone remained, without all other aspects of the program. This was recognised in the successful Geneva program on which the protocol used by Johnson et al was modelled. In that study, the authors remained so uncertain as to what elements of the program were causal that they stated: Whether improved hand-hygiene practice will outlast the intervention remains uncertain; we decided to refrain from testing this issue by maintaining a permanent component of the intervention.2 Evidence currently available4 and soon to be amplified5 suggests that hand hygiene practice in health care workers is simply an extrapolation of their community behaviour. Unfortunately, community hand washing behaviour is not microbiologically founded, being developed on the basis of emotion not science. Both the Austin and Geneva protocols supported the introduction of alcoholic hand gel with strong promotion of specific behavioural elements to induce change in hand hygiene practice. Our findings suggest that alcoholic gel is not pivotal to the improvement of hand hygiene, in that behavioural modelling suggests its effect is relatively small and very dependent on concomitant behavioural change.4,5 The World Health Organization World Alliance for Patient Safety has recently advocated the introduction of alcoholic gel into all hospitals.6 While not denying that this is a step toward improvement, we strongly caution against unrealistic expectations of this single intervention. The hand hygiene practices of health care workers are learned behaviours of childhood, continued as professionals, and reinforced in everyone’s daily lives.4,5 Entrenched, longstanding behaviour patterns will not be changed in a sustained fashion by the introduction of a new hand hygiene product.

R Michael Whitby · Mary-Louise McLaws

In reply: Woollard is critical of the lack of randomised controlled data to support the use of alcohol/chlorhexidine hand rub solution (ACHRS). Although a placebo-controlled study would be ideal, it is doubtful whether one could be performed. Apart from the complexity of design and cost, there would be the requirement to ask patients to consent to being treated in a hospital where there was a substantial risk of nosocomial sepsis, but where half the health care workers would not have clean hands when attending them. Woollard argues that our failure to reduce colonisation or contamination with MRSA shows that our project failed. However, he offers no alternative explanation for the reduction in MRSA bacteraemia, clinical MRSA isolates and resistant gram-negative bacteria that we reported. Our project was a multimodal quality intervention, and we cannot know which component of the project resulted in the benefit, or whether the improvement should be attributed to other confounders, as suggested by Whitby and McLaws. However, we have presented all our data so that readers can draw their own conclusions. It seems unlikely to us that the intervention on which we concentrated our major effort, the progressive introduction and promotion of ACHRS, would be the one component that failed to contribute to the improvement. Woollard also mentions the potential toxicity of asking health care workers to scrub with a chemical agent, and proposes the use of gloves instead. Our ACHRS is a quick to apply, self-drying solution. It is rubbed on the hands, but scrubbing is not required. We actively monitored rates of cutaneous reactions and found it to be extremely well tolerated.1 Gloves must be changed between patients or when moving from a dirty to a clean site.2 We know that busy health care workers often do not have time to do this, and that hands can become contaminated despite the use of gloves.3 We agree with Whitby and McLaws that simply providing ACHRS, without an active campaign to support its use, is pointless. The provision and promotion of ACHRS is a tool to assist health care workers improve hand hygiene, and is just one component in a web of interventions needed to control nosocomial sepsis. Whether it is cost-effective depends on the largely unknown costs to Australian hospitals of preventable infections. At our institution, we believe that it is worth the money, and continue to require all clinical staff and students to know where to find and when to use ACHRS before they start work.

Paul D R Johnson · M Lindsay Grayson

To the Editor: Last year was the 60th anniversary of the liberation of the Nazi concentration camps. We would like to draw your attention to an anatomy textbook, Atlas of topographical and applied human anatomy, authored by a Nazi physician, Eduard Pernkopf, and the alarming evidence which has emerged about the source of subjects used for the illustrations of this book. The context of raising this issue is that this text is listed as available for loan in a general collection on the catalogue of several university libraries around Australia, including the University of Sydney, the University of New South Wales, the University of Adelaide, the University of South Australia, La Trobe University, the University of Western Australia, the Queensland University of Technology and the University of Tasmania, often with multiple copies, which suggests that it may be held as teaching material. Evidence overwhelmingly suggests that the Pernkopf anatomical atlas contains pictures of victims of the Nazi regime. An investigation into this issue by the University of Vienna in the mid 1990s revealed that at least 1377 bodies of murdered victims, including children, were accepted by the Institute of Anatomy.1 The bodies of the victims were used, without the victims’ or their families’ consent, for research and teaching, including by Pernkopf for his atlas.1,2 Pernkopf, an enthusiastic Nazi, took over as Dean of the Vienna Medical School after the annexation of Austria by Nazi Germany, and led the expulsion of the then majority Jewish faculty, including several Nobel laureates.3 He is known to have willingly accepted specimens from murdered children and adults. Original editions, even as recently as 15 years ago, contained swastikas painted at the bottom of the pictures. These have been airbrushed out in more recent editions.4,5 Internationally, there have been a number of different approaches to managing this item within library collections. Some have asked their libraries to remove this book from their general collections. For example, a US physician, upon finding the book in his centre’s library, convinced them to expunge it from their collection. He also resigned from editorial responsibilities to the publisher of the atlas, and cancelled his subscriptions to their journals.1 Another approach has been placing a summary of the report from the University of Vienna’s investigation inside the front cover of the book, so that library patrons are given the context for the drawings and can make an informed choice.1 While acknowledging the need to preserve freedom of access to information, the unethical use of executed victims for this atlas leads us to believe that it has no place as a general anatomy text in an academic setting. The atlas may have a role as a reminder of the atrocities committed in the name of medical science during the Nazi era, and could remain available for researchers examining abuse of human rights, medical ethics and history. We have contacted our library (the University of Sydney library) about this atlas and asked them to take appropriate action. They have elected to move copies held in high usage collections to special collections. We urge others whose institutions hold this text to do the same.

C Raina MacIntyre · Catherine L King · David Isaacs

To the Editor: Music is often played in operating theatres, for a variety of reasons. It has been shown to decrease the anaesthetic requirements of patients1 and the autonomic reactivity of surgeons,2 and not to interfere with laparoscopic task performance under non-clinical conditions.3 However, I have witnessed several events that have “pushed back the boundaries” of this common practice. In one case, a surgeon requested that a videocassette player and monitor be moved into the operating suite before a major operation. Thinking that this might be for educational purposes before use of a new technique, the nursing staff obliged. After the operation was under way, the surgeon directed that a commercial videocassette of an opera be taken from his briefcase and played during the operation. The anaesthetic team were concerned about this, and the video player was turned off when the operation became more difficult. In another case, a surgeon undertook an operation while listening through ear-bud headphones to low-level music from his digital music player. Before the operation began, the anaesthetist questioned the surgeon about the wisdom of this practice and asked several times if it might interfere with communication or concentration. The operation proceeded without incident with the surgeon listening to his music. These examples may represent extremes of practice, but they do remind us that we should remain vigilant and not allow developments in entertainment technology to interfere with patient care. Further studies are required to determine the effect of these practices on technical performance and decision-making of surgeons and also communication between staff in the operating suite.

Richard H Riley

Comment: Ask most surgeons about their operating theatres, and they will describe them as havens from the stresses and pressures of a busy clinical practice. The theatre protects them from the interruptions of telephone calls, the demands of patients and their relatives, and the politics of medicine. It is a microcosm where a surgeon may rule autocratically. Within reason, most theatre personnel would gladly accommodate any means that might diminish the stress or enhance the smooth running of an operation. Techniques such as dimming the lights, decreasing human traffic, eating lollies and playing music are common practices in operating theatres. As a surgeon, I find background music essential during surgery. It masks the chatter of the scout nurse, the telephone conversation of the anaesthetist, and the beeping of the diathermy machine and the electrocardiograph monitor. Without the pleasant background sound of ABBA or the love songs of Elvis, my stress levels would be compounded by every other audible distraction. The question of whether surgeons should be able to use whatever means necessary to achieve the best outcome, even if the anaesthetic and nursing staff perceive it as inappropriate, could only be answered with a prospective study using patients’ clinical outcomes as the end-point. With so many variables, a study of this nature would be impossible. Personally, I have no objection to the scenario in Riley’s second case if the surgeon can maintain adequate communication with the scrub nurse. However, I cannot accept that a person would not be distracted by watching a video while operating. Even if the surgeon was simply listening to the music, the video playing on the monitor would be a distraction to other theatre personnel. I agree with Riley that we must continually re-evaluate technology in the workplace. Patient care is paramount, and, unless audiovisual technology is helping us achieve this end, we would be wise to return to simpler times.

Charles Teo

Ivan Cher Retired Ophthalmologist, 54 Aroona Road, Caulfield North, VIC 3161. ursivanATbigpond.net.au To the Editor: McCallum and Smith’s1 quest for pathology in children’s literature took me back 50 years, to a memorable weekend in New Zealand. News had reached Wellington on the previous day that Hilary and Tenzing had climbed Everest — a coronation gift to Princess Elizabeth, who was to be crowned on the following Tuesday. On the morning of Sunday, 31 June 1953, I was on paediatric call at Wellington Public Hospital. I had been told of the admission of a boy of 11 months, who was neither short of breath nor otherwise ill, despite being very blue. As I approached the ward I could hear him crying at the top of his clarion lungs. He was, as it were, “blowing his horn”, upset at being abandoned by his parents, who would have to wait four more hours for visiting time. (Such was the cruel practice in those days.) He was standing in his cot bellowing energetically. Apart from his dramatic discolouration, he looked well. I expected a cardiac tetralogy, but he had turned blue only the previous day and there was no evidence of a heart or lung problem. I was bewildered with no idea of a diagnosis. I called my boss, John Harding, and met him in the corridor. Even before entering the ward, the paediatrician sniffed and said, “There’s a child here with diabetes.” Of course he was right, and sure enough, it was my little boy blue. I learned a lot that day: A child with diabetes mellitus can be acutely keto-acidotic; Our patient’s distressed cries probably disguised hyperventilation; In some people, acidosis can lead to methaemoglobinaemia; and I am unable to detect acetone from diabetics, although I can recognise its smell from a bottle. My little boy blue was too young for agricultural responsibilities and was not somnolent, so couldn’t have been the prototype for the rhyme.

Ivan Cher

Alan Jennings was a pioneer in the field of child psychiatry whose visions were realised in his own lifetime. He was born on 10 June 1923 in Hull, UK, and completed his schooling there. At the outbreak of war in 1939, his mother migrated to Sydney with her three children. Alan graduated in medicine from the University of Sydney in 1945. After working for a short period in the NSW Department of Health, he went to Manchester to do a Diploma in Psychological Medicine. Returning to Australia in 1950, Alan worked at Yasmar Child Guidance Clinic in Sydney until 1954, when he became Director of the Brisbane Street child guidance clinics. These were teaching and training clinics for students in psychiatry and social work linked to the University of Sydney’s Department of Psychiatry. Alan soon realised that some children needed treatment in a residential unit. He was awarded a travelling grant to study residential care for emotionally disturbed children in the United States and the United Kingdom. In 1959, he established Australia’s first unit for emotionally disturbed children at North Ryde Psychiatric Centre. In a twin ward, he opened the first demonstration unit for 20 mentally retarded boys to show the advantages of having a much higher than usual ratio of nursing staff to patients. He also opened a ward for severely to grossly mentally handicapped children aged under 2 years, many of whom were also physically handicapped. He imbued all staff with a positive, caring philosophy. Alan was the first Director for the Mentally Handicapped in the NSW Department of Health (1964–1973), during which time he persuaded the Department to buy Renwick Children’s Hospital in Summer Hill to establish the first diagnostic unit for retarded children. Alan was Director of Marsden Hospital, Westmead (the first purpose-built institution for mentally retarded children), from 1969 to 1978. The Department of Health also bought the old King’s School, Parramatta, as a hostel for mentally retarded young men and women transferred from the old “mental retardation hospitals”. Later, group homes were established for selected children and residents from Marsden Rehabilitation Unit. Alan travelled and studied many times overseas, notably in Denmark and The Netherlands. He lectured at the University of Sydney, Macquarie University, the University of NSW and the NSW Institute of Psychiatry. He was the first President of the Australian Group for the Scientific Study of Mental Deficiency and served on many committees, including the Minister of Health’s Committee in Regard to Mental Defectives and the World Health Organization’s Policy Committee on Mental Retardation. After retirement in 1979, Alan studied Italian and lectured in art and religion at Adelaide University. Despite being blind in his later years, he had a very focused, enquiring mind and continued to explore many avenues of intellectual learning, including religion, philosophy, ecology and neuropathology. He died in Adelaide on 19 April 2005 after emergency heart surgery. He is survived by his wife Roleena and children Ian and Susan.

Millie Mills DipSocStud, AAPSW

CorrectionRe: “Challenges, conflict and change”, by David G Penington, in the 5/19 December issue of the Journal (Med J Aust 2005; 183: 585-589). On page 587, the article states that Australia became the first country in the world to test every single blood donation for HIV in May 1995. This should have read May 1985. The html and pdf versions of this article were corrected on 7 February 2006.

David G Penington AC

CorrectionRe: “Hospital in the home: what next?”, by Stephen F Wilson and Nicholas Collins, in the 6 February issue of the Journal (Med J Aust 2006; 184: 141-142). One author’s name was omitted from the byline. The letter’s authors are Stephen F Wilson, Program Director Population Health, Sacred Heart Rehabilitation Centre, St Vincent’s Hospital, Darlinghurst, NSW 2010; and Nicholas Collins, Ambulatory Care Specialist, Macarthur Health Service, Sydney, NSW. The html and pdf versions of this article were corrected on 7 February 2006.

Stephen F Wilson MB BS, FRACGP, FAFRM(RACP) · Nicholas Collins MB BS, FRACGP

The placebo effect and health. Combining science and compassionate care. W Grant Thompson. New York: Prometheus Books, 2005 (350 pp). ISBN 1 59102 275 4. The placebo effect, surrounded by myths resistant to time and research, fascinates researchers and clinicians alike. It has been said that the placebo effect is the only action which all medical treatment has in common, and, in some instances, it is the only useful action. Therefore, we all should have a keen interest in it. Understanding the placebo effect is difficult. There are, it seems, more definitions on offer than research groups investigating it — and all are unsatisfactory in one way or another. Difficulties increase when trying to answer some of the many questions that placebos pose. Do we need placebos to generate a placebo effect? What elements constitute a placebo response? Are placebo effects always beneficial? Are some situations more placebo-prone than others? What ethical implication does the use of a placebo have in research or clinical practice? Grant Thompson, a clinician, researcher and science writer, addresses these and other questions with analytical clarity. Well read and up-to-date on recent developments, he makes complex things understandable without oversimplifying them. His book is extensively referenced and helped by a detailed index — a text that can be used for reference as well as for reading. The “story” that Thompson develops before his readers’ eyes is coherent and exciting. There are of course many books on placebo, but this one is among the better ones in its class. It is not aimed at the specialist researcher nor at the uninformed layperson. For the many people who find themselves between these two extremes The placebo effect and health will be useful. Its strength lies in that it is easy to read, even when the subject matter is complex. As the placebo effect is responsible for so much of the success of medical interventions, it seems a good idea to know what it is about. Edzard ErnstDirector, Complementary Medicine Peninsula Medical School, Exeter, UK

Edzard Ernst

Flu drugs for epidemics only Have we been guilty of over-estimating the ability of anti-flu drugs to prevent illness and infection? A recent systematic review of 53 randomised controlled trials has revealed various shortcomings of available agents. The M2 ion-channel blocking drugs amantadine and rimantadine had a mainly symptomatic effect on influenza virus infections; however, they did not prevent infection or nasal shedding. The reviewers said their use should be discouraged. The neuraminidase inhibitors oseltamivir and zanamivir were also useful symptomatically. They also did not appear to prevent asymptomatic infection; however, they did decrease nasal shedding, possibly interrupting viral transmission in households. Because of this relatively low effectiveness, the reviewers advised against the use of neuraminidase inhibitors in seasonal influenza control; they said these agents should only be used in serious epidemics or pandemics — together with other public health measures. Lancet 2006; 367: 303-313 Amputation heights Being of taller height may be a disadvantage, in at least one respect, for patients with diabetes — their height is linked with lower-extremity amputation, according to Taiwanese research. Phone interviews with more than 93 000 patients with diabetes found that lower-extremity amputation has been performed in 1.7% of those with type 1 diabetes and 0.8% of those with type 2 diabetes. Further, in this large group of patients, for each 10-cm increase in height there was a 16% increase in risk of amputation. The report says it may be wise to pay particular attention to the early detection and treatment of leg ulcers in taller patients with diabetes. CMAJ 2006; 174: 319-323 With this bone I thee wed . . . A company called Biojewellery has proposed to take a sample of bone tissue from a betrothed couple and grow their samples into wedding rings, reports a UK ethicist. Brassington argues that the perceived ethical problem with such surgery — that is, when it implies surgery without any medical need — may not be a problem at all. He says that while surgery as a means to get jewellery might not be medically justified, this did not mean that it is not justified at all; he sees no reason why surgical skills might not be put to use in at least some non-medical projects. In this circumstance, a couple may believe that the exchange of bone-grown rings is a better one than the exchange of mere gold ones. J Med Ethics 2006; 32: 13-16 Clearing the lungs Sydney researchers have found that hypertonic saline can reduce pulmonary exacerbations in patients with cystic fibrosis.1 They randomised 164 patients with stable disease to receive 4 mL of either 7% hypertonic saline or 0.9% saline, preceded by a bronchodilator, twice daily for 48 weeks. Patients who received hypertonic saline were more likely to have no or fewer pulmonary exacerbations during the treatment period. A smaller, complementary US study of 24 patients with cystic fibrosis found that inhalation of hypertonic saline produced a sustained acceleration of mucus clearance.2 1. N Engl J Med 2006; 354: 229-240 2. N Engl J Med 2006; 354: 241-250 Scarlet fever outbreak A Western Australian report has raised the question of whether scarlet fever should be a notifiable disease in all of Australia and not, as is currently the situation, in just Western Australia. Although scarlet fever only occurs sporadically now, and infection is readily treated with antibiotics, an outbreak in a Perth primary school was successfully curtailed after notification of a cluster of cases led to the identification, and subsequent treatment, of asymptomatic pharyngeal carriers of group A streptococci. Commun Dis Intell 2005; 29: 386-390 What’s my prognosis? Euro Heart Survey Investigators have developed a heart angina score to help doctors determine very high risk and very low risk patients with stable angina. They followed 3031 patients with newly diagnosed stable angina for 1 year after first presentation or re-referral to a cardiologist. Six of the seven factors they found most predictive of death or myocardial infarction during this follow-up were subsequently included in the Euro heart angina score — comorbidity, diabetes, recent onset of symptoms, increasing severity of symptoms, abnormal ventricular changes, and ST or T wave abnormalities on the resting ECG. The seventh factor not included in the score was not having had any kind of stress test done; this also indicates high risk. BMJ Online First, 13 Jan 2006 Dr Ann Gregory, MJA

Ann Gregory