Volume 194 Issue 9

Our health and medical research sector is under threat and needs the support of the clinical community Until quite recently, it was believed that peptic ulcers were caused by stress and lifestyle and that the most effective treatment was a bland diet and rest. However, in 1982, two Australian medical researchers (Barry J Marshall and J Robin Warren) discovered the bacterium Helicobacter pylori and demonstrated its role in gastritis and peptic ulcer disease.1 Thanks to this discovery, millions of people worldwide are now cured of peptic ulcer with a short regimen of antibiotics and acid secretion inhibitors. This is just one of hundreds of examples of effective translation of Australian health and medical research into clinical practice and, importantly, better outcomes for patients. Over the past 50 years, health and medical research has saved the Australian health care system trillions of dollars and delivered better quality of life for all Australians. It is estimated that between 1960 and 1999, medical research was responsible for a longevity gain of 8 years worth $2.9 trillion and gains in quality of life worth $2.5 trillion in avoided health expenses.2 Regrettably, these hard-won advances now stand to be undermined by potential cuts to National Health and Medical Research Council (NHMRC) funding in the May federal Budget. Over the past decade, the nation’s research community has achieved a level of critical mass, thanks to the vision and leadership of successive governments. But the sector was coming off a very low base and, compared with overseas competitors, Australian Government funding for research as a proportion of gross domestic product still remains low, at only 0.11%–0.12%.3 Over the same period, demand for medical research and the knowledge to cope with emerging disease patterns has grown with the inexorable rise in chronic disease, an ageing population and the impact of globalisation on health epidemics. In order to manage these new health challenges with the financial resources available, we will inevitably see more and more health care delivery taking place in the community and away from acute settings. In preparation for this seismic change, we need research breakthroughs and long-term, evidence-based solutions. A cut to the annual $775 million NHMRC budget will not just affect Australians today but will compromise the health outcomes of our children, grandchildren and great-grandchildren. Health and medical research is an essential component of the current health reform agenda and plays a vital role in providing better outcomes for a self-improving health system. A large proportion of Australian health and medical research is now focused on translational outcomes, such as disease prevention, improved clinical care, and new diagnostics, therapies and vaccines, which have a demonstrated capacity to reduce the nation’s health budget and deliver better patient care. Indeed, without such research, the impact of health reform on patient-relevant outcomes such as death and disability will remain substantially uncertain. Another illustrative example of Australia’s contribution to global health gains is the development by Professor Ian Frazer and colleagues, in collaboration with CSL Biotherapies, of the quadrivalent human papillomavirus vaccine (Gardasil; Merck Sharp & Dohme) for cervical cancer prevention. According to an Access Economics report, the vaccine is expected to prevent around 70% of cervical cancers and result in significant economic returns in averted health care costs in Australia.4 As well as making significant contributions to global health, it is crucial that we maintain a strong Australian health and medical research sector in order to identify solutions for unique local health problems. Last year, researchers at The George Institute launched a major international trial of a very low-cost, once-a-day “polypill” for the prevention of cardiovascular disease. This treatment is particularly promising for Australia’s Indigenous communities, for whom cardiovascular disease is the leading cause of death and disability. Compared with other Australians, Indigenous Australians suffer heart attacks at three times the rate, at an average of 10–15 years younger, and have 3–4 times higher rates of diabetes.5 We are unlikely to “close the gap” in Indigenous health by reading reports of research conducted in the United States or Europe. Moreover, cuts to research funding will seriously impair Australia’s ability to respond effectively to health crises, through delays in access to the latest and most effective vaccines and treatments. This applies equally to mobilising a rapid and successful response to acute emergencies such as severe acute respiratory syndrome, pandemic (H1N1) 2009 influenza or, in the context of the recent floods, outbreaks of Ross River fever. For all these reasons, a cut to the NHMRC budget will increase health care costs in the long term and harm the Australian economy, through the failure to use the capacity of existing and new state-of-the-art facilities, a downturn in productivity and lost intellectual property as we are forced to “buy back” health innovations from international pharmaceutical and device companies. There is also the very likely spectre of our brightest scientists and clinicians leaving Australia for rapidly growing biomedical research hubs in Asia and beyond, as well as a loss of future capacity through the failure to train an adequate research workforce. Interestingly, in the United Kingdom, medical research has been protected, despite wide and deep cuts in other public sectors, and in the US, biomedical research has been identified as a priority for government support by President Obama. India, China and Singapore are also making unprecedented investments in medical research and associated intellectual and capital infrastructure. Proposed funding cuts will place emerging Australian medical researchers in a particularly vulnerable position, given that their training extends over a 10–15-year period. The effects of reducing training places, even in the short term, through a reduction in any of the funding programs will be felt for more than a decade. It would only take a small cut to the NHMRC budget to have a serious impact on medical research outputs, denying Australians access to the best available preventive therapies, diagnostics and treatments, today and in the future. For this reason, the medical research sector has been forced to take its fight public in a bid to safeguard leading research programs that are a lifeline for children and adults suffering from heart disease, cancer, genetic diseases and many other forms of serious illness. The support of Australia’s clinical community will be crucial to ensuring that our research sector continues to deliver translational benefits to Australians. There are a number of ways clinicians can provide this support. Writing letters to and raising the issue with members of parliament and the Prime Minister is critical to maintaining the profile of this issue. Research Australia has developed an online petition to the federal government (http://researchaustralia.org/personal-stories/petition-to-federal-government.html), and concerned clinicians can vote for community advocacy organisation GetUp! to take on the campaign (http://suggest.getup.org.au/forums/60819-campaign-ideas/topics/61385-i-suggest-a-campaign-about-/filter/top). More information is available at the Discoveries Need Dollars website (http://www.discoveriesneeddollars.org).

Garry L R Jennings MD, FRACP · Stephen MacMahon DSc, PhD · Geoffrey A Donnan MD, FRACP

New results from an Australian collaborative randomised trial will change practice Every year in Australia, 1000 people are admitted to intensive care units with severe traumatic brain injury, mostly as a result of motor vehicle accidents.1 Despite high standards of prehospital and medical care, 50% of these people either die or survive with severe lifelong disability.2 Most of the survivors with severe disability are young men aged in their mid 20s;2 they cannot return to work and will never be able to live independently. The cost of severe traumatic brain injury in human terms is huge, and in economic terms has been recently independently calculated to be $4.8 billion every year in Australia.1 In the United States, the annual economic burden of traumatic brain injury is $60 billion.3 Half of patients with severe traumatic brain injury have haematomas that may require neurosurgical evacuation; management of these patients before and after surgery is not controversial. However, about 10% of patients have diffuse brain injury,4 and also have persistent brain swelling that cannot be effectively controlled in intensive care units by airway management, mechanical ventilation, intracranial pressure monitoring, heavy anaesthesia, resuscitation fluids, osmotherapy, and drainage of cerebrospinal fluid from ventricular catheters. Over the past decade, management of these patients has been shifting in many centres from barbiturate therapy, and sometimes hypothermia, to decompressive craniectomy5 — a well established neurosurgical procedure in which a large piece of skull bone is removed (stored for 1–2 months, and then replaced) to enable better control of intracranial pressure and a more rapid decrease of sedation, with the ultimate goal of improving patients’ long-term functional outcomes. About 20 case series of adult patients from many countries have reported mainly favourable results from this procedure.6 However, all suffer from a lack of prospective randomised control groups and of objective blinded outcome assessment at defined time points. To objectively assess decompressive craniectomy for the first time and to establish its true efficacy in adult patients with traumatic brain injury, intensivists and neurosurgeons in Australia, New Zealand and Saudi Arabia collaborated between 2003 and 2010 to conduct the Decompressive Craniectomy (DECRA) randomised trial. The results of the DECRA trial have recently been published.7 This was the first randomised trial of any neurosurgical technique to be completed in complex adult neurotrauma patients. Patients were randomly assigned to receive decompressive craniectomy plus standard care (maximised intensive care therapies, which could include barbiturate anaesthesia) or standard care alone. The study found that early decompressive craniectomy clearly and dramatically achieved its short-term goals: it decreased intracranial pressure, markedly decreased medical therapies required for intracranial pressure, shortened mechanical ventilation time, and shortened stay in the intensive care unit by 5 days compared with the standard care group. The dramatic short-term effects meant that the study was difficult to complete because neurosurgeons and intensivists were aware of group allocation, could see the early benefits, and increasingly preferred to conduct early surgery rather than recruit patients to the trial. However, despite these positive short-term effects, the findings in relation to patients’ eventual functional outcome, measured carefully at 6 months, were startling and the reverse of what had been expected. There were 19% more patients with poor functional outcomes (odds ratio, 2.21; 95% CI, 1.14–4.26; P = 0.02) and 23% more survivors with severe disability in the decompressive craniectomy group compared with patients who received standard care alone. The cause of these poor outcomes is speculative. They may have related to the surgery itself or to surgical complications (including hydrocephalus), but surgical complications seem an unlikely explanation given that the rates overall were less than those reported in published case series. A more likely explanation is that “axonal stretch” that occurred during swelling of the brain outside the skull through the craniectomy defect8 exacerbated brain injury in a way that has not previously been described in humans and was not anticipated. Multimodal magnetic resonance imaging may enable confirmation of this. We might now coin the term “brain volutrauma”, analogous to the “lung volutrauma” observed in mechanically ventilated patients with acute lung injury. A second ongoing randomised trial — the Randomised Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intracranial Pressure (RESCUEicp) — is addressing similar questions in the United Kingdom and Europe. The RESCUEicp trial also includes patients with brain haematomas and intervenes at a slightly higher intracranial pressure threshold,9 so the results will be complementary to the DECRA trial and are likely to be equally important. What is unequivocal is that functional outcomes of future patients with severe diffuse traumatic brain injury in Australia and New Zealand can be substantially improved by choosing best intensive care medical and surgical therapies, based on established guidelines,10 without early decompressive craniectomy, despite increases in intracranial pressure that may be concerning to clinicians. The role of decompressive craniectomy as a rescue therapy in the context of very high intracranial pressure has not been resolved by this study, but is now clearly uncertain. It is also unequivocal that the Australian health care system will save many tens of millions of dollars annually when the less invasive treatment regimen is chosen. Although careful cost–benefit analyses are urgently required (and can be done using existing databases), it is already clear from independent costing analyses, which confirmed that most of the traumatic brain injury cost burden relates to rehabilitation costs of survivors with severe disability,1 that the savings to Australia of choosing intensive medical therapies instead of craniectomy in appropriate patients will be greater than $100 million annually. Savings in the US and Europe are likely to be proportionately greater. Finally, the DECRA trial illustrates with new clarity that carefully designed randomised controlled trials are the only way to correctly advance clinical practice, even in complex, critically ill patients, and despite the clear inherent difficulties of such trials.11 Recent calls for “comparative effectiveness research” in neurosurgery,12 based on aggregations of non-randomised databases, do not represent a valid substitute. In the DECRA trial, a collaborative network of clinician-investigators (the Australian and New Zealand Intensive Care Society Clinical Trials Group), which was supported by the National Health and Medical Research Council (NHMRC) and co-funders, unfettered by industry, and motivated by a strong desire to improve the quality of outcomes in critically ill patients, enabled the trial to be supported to completion and to influence clinical practice for the better. These are the essential ingredients needed to make meaningful improvements in health care.

D James Cooper MD, FRACP, FCICM · Jeffrey V Rosenfeld MD, MS, FRACS

Australian and US collaborators provide evidence on outcomes of mammographic screening in previously affected women Women with a personal history of breast cancer (PHBC) represent an increasing group of cancer survivors, and have a lifelong increased risk of developing a new or recurrent cancer in the conserved (ipsilateral) breast, or a contralateral cancer. The risk of a “second” breast cancer in women with PHBC has been estimated at 5.4 to 6.6/1000 woman-years.1 Evidence of screening benefit in PHBC women comes from observational studies2-4 and extrapolation of benefit from randomised mammographic screening trials; consensus-based recommendations include annual mammography in routine surveillance of PHBC women.5-7 Early detection may also minimise the physical and psychosocial burden and consequences of a second breast cancer. Evidence reviews have consistently acknowledged the lack of quality data on mammographic screening in PHBC women,4,8 and research into screening high-risk women has mostly focused on those with breast and ovarian cancer susceptibility genes; evaluation of screening in women with PHBC has received relatively little attention.4,8 Together with other collaborators from Australia and the United States, we recently reported the most comprehensive study to date of mammographic screening in women with a history of early-stage breast cancer.9 Based on data from mammography facilities affiliated with the US National Cancer Institute-funded Breast Cancer Surveillance Consortium for the years 1996–2007, we examined the accuracy and outcomes of screening in 58 870 mammograms from 19 078 women with PHBC. These were matched to 58 870 screening mammograms from 55 315 women without PHBC, to ensure that characteristics that affect mammography accuracy (such as age group and breast density) were similar in both cohorts.9 Key findings from the study are summarised in the Box. Although the cancer detection rate of screening was substantially higher in PHBC women relative to women without PHBC (6.8 v 4.4/1000 screens), screening detected a smaller proportion of the cancers occurring in PHBC women at 1-year follow-up (65.4% v 76.5%). Due to this lower sensitivity of mammographic screening, as well as the higher underlying breast cancer risk in PHBC women, the interval cancer rate in women with PHBC was more than twice the rate in women without PHBC (3.6 v 1.4/1000 screens). The lower sensitivity and higher interval cancer rate occurred despite more imaging work-up in PHBC women relative to women without PHBC (18.1% v 8.3%) and more recommendations for biopsy or surgical consultation (2.3% v 1.4%). Unique aspects of this study were characterisation of screening outcomes and underlying cancer risk according to characteristics of the women and their first cancer treatment, and ascertainment of ipsilateral and contralateral second cancers.9 The latter has not previously been possible because notification of recurrent cancer is not obligatory in most countries, but was achieved through the data-linkage processes of the Breast Cancer Surveillance Consortium. Hence, the twofold higher rate of breast cancer in women with PHBC relative to those without (Box) represents a reliable risk estimate. We found heterogeneity of both breast cancer risk and screening accuracy across subgroups of women and by the treatment received for the first cancer. The highest rates of second cancers (> 12 cancers/1000 screens) were in women younger than 50 years, women with extremely dense breasts, women who received breast-conserving surgery without radiation therapy or who did not receive any systemic therapy, and women with previous ductal carcinoma-in-situ (the latter probably reflects the infrequent use of adjuvant therapy in the treatment of ductal carcinoma-in-situ). Should these findings change our practice or recommendations for women with PHBC? Superficially, these results9 could be interpreted as casting doubt on the efficacy of mammographic screening in women with PHBC. However, careful consideration of the data shows that although mammographic screening was relatively less sensitive in PHBC women, it detected their second cancers at an early stage, with similar stage distributions to women without PHBC.9 The evidence from this study therefore supports consensus recommendations that advise mammographic screening in women with PHBC, and which also include clinical breast examination as part of annual surveillance.5-7 Many of the interval cancers were also early-stage, suggesting that cancers not detected at time of mammographic screening were detected through clinical examination or investigations prompted by symptoms, or possibly through ad-hoc adjunct screening (using breast ultrasound or magnetic resonance imaging). Currently, adjunct screening is not routinely recommended for women with PHBC (unless they are known to have breast cancer gene mutations), and our study did not evaluate adjunct imaging. Our data may, however, guide future evaluations of adjunct screening in subgroups of PHBC women who had high interval cancer rates; specifically, women younger than 50 years and/or with extremely dense breasts, and those who had breast conservation without radiation therapy for their first cancer. It is essential that evaluations of strategies integrating adjunct screening for PHBC women consider the impact this may have on false positives and overdetection, as well as whether enhanced screening sensitivity through adjunct imaging translates into a reduction in interval cancers. Recommendations from the BreastScreen Australia evaluation10 included the potential provision of annual screening through BreastScreen for women with PHBC, from 5 years after their first cancer diagnosis. Our study shows that screening sensitivity improves after 5 years from the first cancer diagnosis and supports the idea of allowing PHBC women access to screening in BreastScreen-accredited facilities, which undergo rigorous quality assurance, to ensure that they receive high-quality mammographic screening. BreastScreen may also be ideally placed to implement screening evaluations for PHBC women to provide insight into screening outcomes in these women in the Australian setting. Mammographic screening in women with a personal history of early-stage breast cancer (PHBC)9* Screening outcomes were significantly different (P < 0.001) for comparison of screening mammograms in women with PHBC relative to women without PHBC: Cancer rate: 10.5 (9.7–11.3) v 5.8 (5.2–6.4)/1000 screens Cancer detection rate: 6.8 (6.2–7.5) v 4.4 (3.9–5.0)/1000 screens Interval cancer rate: 3.6 (3.2–4.1) v 1.4 (1.1–1.7)/1000 screens Screening sensitivity: 65.4% (61.5%–69.0%) v 76.5% (71.7%–80.7%) Sensitivity for detection of invasive cancers: 61.1% (56.6%–65.4%) v 75.7% (70.4%–80.3%) Screening specificity: 98.3% (98.2%–98.4%) v 99.0% (98.9%–99.1%) Abnormal mammogram results (based on final imaging assessment): 2.3% (2.2%–2.5%) v 1.4% (1.3%–1.5%); this also reflects the percentages recommended for biopsy or surgical consultation. Screen-detected breast cancers in women with and without PHBC were predominantly early-stage cancers (ductal carcinoma-in-situ [DCIS] or stage I–II invasive cancer in > 90%, for both groups). In women with PHBC, screening sensitivity was similar for detection of ipsilateral cancer (66.3% [60.3%–71.8%])† and contralateral cancer (66.1% [60.9%–70.9%]); however, sensitivity differed significantly (P < 0.05) for the following: Higher for detection of DCIS (78.7% [71.4%–84.5%]) than invasive cancer (61.1% [56.6%–65.4%]) Higher in women with non-dense breasts (BI-RADS category 1–2: 69.6% [63.3%–75.3%]) than in women with dense breasts (BI-RADS category 3–4: 60.2% [54.0%–66.2%])‡ Higher after 5 years from first cancer (70.8% [65.4%–75.6%]) than within the initial 5 years (60.2% [54.7%–65.5%]) Lower in women who received any systemic therapy§ (54.1% [47.5%–60.6%]) than in those who had not received any systemic therapy (71.0% [66.0%–75.5%]) for first cancer. Low screening sensitivity (about 55% or lower) was observed in women younger than 50 years, women with extremely dense breasts, and women who received chemotherapy§ for first cancer. BI-RADS = Breast Imaging Reporting and Data System. * 95% confidence intervals are shown in parentheses. † Excludes ipsilateral relapse in women who had mastectomy. ‡ BI-RADS tissue density categories: 1 = almost entirely fatty; 2 = scattered fibroglandular tissue; 3 = heterogeneously dense; 4 = extremely dense. § After adjusting for age, breast density, stage and treatment of first cancer, only women who received chemotherapy were significantly less likely to have their second breast cancer detected by mammographic screening than women who had not received any systemic therapy.

Nehmat Houssami MB BS, FAFPHM, PhD · Diana L Miglioretti PhD

Upcoming large studies may shed light on why this technique was not rapidly widely adopted like certain other laparoscopically assisted procedures Laparoscopic “keyhole” surgery has been the gold standard for gall bladder surgery for a few decades. It has also been widely used for appendicectomies, a multitude of gynaecological procedures and, to various extents, for other procedures such as hernia repair, splenectomy and nephrectomy. However, the uptake of laparoscopically assisted resection in elective surgery for colorectal cancer (CRC) has been slow, both in Australia and overseas. This is the subject of the article by Thompson and colleagues in this issue of the Journal (→ National trends in the uptake of laparoscopic resection for colorectal cancer, 2000–2008).1 The authors searched the National Hospital Morbidity Database (NHMD), which uses codes based on Medicare Benefits Schedule item numbers, for elective laparoscopic resections for CRC. Their search was somewhat restricted and the internal validity was not tested, but Thompson and colleagues reported that, in about a quarter of elective CRC resections performed in Australia in the financial year 2007–08, an item number for a laparoscopy was included. Reliance on databases may overestimate or underestimate outcomes. Three studies from the United States reported percentages of laparoscopic resections for cancers of the colon ranging from 3.3% to 5.2%2-4 in the period July 2003 to June 2004, based on the National Cancer Data Base and Nationwide Inpatient Sample. However, a fourth US study that used the Perspective Rx Comparative Database (Premier Inc, Charlotte, NC), which relies on procedure codes, reported a percentage of 33.7% for the period July 2004 to June 2006.5 Such an increase is far greater than what would be expected to be the result of the publication of the Clinical Outcomes of Surgical Therapy trial.6 The adoption of laparoscopic surgery for CRC has been slow despite the proven short-term benefits of laparoscopic compared with open resection, which include a shorter hospital stay.7,8 In line with other published articles, the Australasian Laparoscopic Colon Cancer Study (ALCCaS) — the largest Australasian study to date of laparoscopic resection for CRC — showed that the laparoscopic method was associated with a smaller number of patients with complications and a shorter length of stay than open resection.9 However, the ALCCaS group also reported that reviews show that the short-term advantages for laparoscopic resection for CRC are arguably relatively minor and often subjective, and that patients who benefit most from improved outcomes are patients who are aged 70 years or older whose procedures were completed laparoscopically.10 The median length of stay for patients younger than 70 years of age undergoing laparoscopic resection in the ALCCaS trial was 7 days (range, 1–30 days) compared with 8 days (range, 4–49 days) for open resections in the same age group — a difference of only 1 day.10 The average hospital stay for conventional open resection has been reported to be about 10 days (range, 7–12 days).7,11-13 It seems likely that authors of large series, trials and reviews report more conservative (and perhaps more realistic) results than earlier series reporting a new surgical procedure or innovation. The first published series of laparoscopic colorectal surgery in 1991 reported achieving the aim of a 5-day hospital stay in 14 out of 20 patients undergoing sigmoid resections (70%).14 Most subsequent larger studies, reviews and meta-analyses report lengths of stay of around 8 days for laparoscopic resection.7-9,11,12 Thompson and colleagues (→ National trends in the uptake of laparoscopic resection for colorectal cancer, 2000–2008) recommend exploring whether the short-term benefits of laparoscopic resection are experienced outside of the clinical trial environment.1 If we accept the limitation of using secondary data, such as those from the NHMD, in exploring the uptake of laparoscopic surgery for CRC, then a quarter of elective resections for CRC performed in Australia in 2007–08 were laparoscopic. That represents an increase from zero to 25% in more than 17 years. There are no comparable studies that used similar methods to assess the uptake of laparoscopic cholecystectomy in the late 1980s. However, many of us experienced first-hand the rapid uptake of laparoscopic gall bladder surgery. The first laparoscopic cholecystectomy was probably performed in France by Phillippe Mouriat of Lyons in 1987.15 There are published data that show that laparoscopic surgery was well and truly the gold standard for gall bladder surgery in 1992.16 That represents an increase from zero to close to 100% in less than 5 years. The contrast is stark. In 1999, Kehlet and Mogensen introduced the concept of fast-track surgery to colorectal resections;17 this concept is now known as Enhanced Recovery After Surgery (ERAS). It involves a multimodal rehabilitation program that commences before surgery to optimise all aspects of care using evidence-based protocols that hasten recovery. Kehlet and Mogensen reported a median hospital stay of 2 days (range, 2–6 days) after 16 consecutive elective open sigmoid colectomies. Fifteen of the 16 patients resumed bowel function before discharge.17 The results of a systematic review of five studies comparing laparoscopic with open colorectal surgery using an ERAS rehabilitation program were inconclusive.18 Further, the authors of a meta-analysis of 11 studies (1021 patients) reported a 2.5-day shorter length of stay for patients on an ERAS rehabilitation program who had resections compared with those not on an ERAS program.19 These authors assumed an added benefit to the laparoscopic approach, but an advantage was not clearly demonstrated. They concluded that ERAS programs should become a mainstay of elective colorectal surgery.19 These later and larger series, trials and reviews have shown that an average length of stay of 5 days seems to be quite achievable within an ERAS protocol, regardless of whether the surgical approach is open or laparoscopic. Many of the aspects of the ERAS program are now included in “standard” care regardless of whether a structured protocol is in place or not. It seems that, on the whole, laparoscopic surgery for CRC has probably not been successful in delivering the outstanding benefits suggested by early reports. This may be partly responsible for its slow uptake. Attention to a multimodal approach such as an ERAS program may, in fact, produce more clinical benefits for patients and cost benefits for hospitals. Whether the laparoscopic approach “adds” to these benefits or not has not been established.20 The Australasian Laparoscopic Cancer of the Rectum Trial (A La CaRT), with a target sample size of 470 patients, is expected to shed more light on the safety and efficacy of laparoscopic compared with conventional open resection for rectal cancer.21 The Dutch Laparoscopy and/or Fast Track Multimodal Management (LAFA) trial, with a target sample size of 400 patients, will examine laparoscopic versus open CRC surgery with or without an ERAS rehabilitation program.22

Ned S Abraham MMed, FRACS, PhD

Objective: To examine the trends in the uptake of laparoscopic resection for colorectal cancer.Design and setting: Retrospective analysis of Australia-wide data on elective resections for colorectal cancer over the 8 financial years 2000–01 to 2007–08, obtained from the National Hospital Morbidity Database.Main outcome measures: National trends in annual percentage of colorectal resections for cancer that were conducted laparoscopically for each year, stratified by hospitals conducting a high volume of elective resections (40 or more/year) versus a low volume, and by public versus private hospitals.Results: For all Australian hospitals combined, the percentage of resections for colon cancer conducted laparoscopically increased from 2.4% in 2000–01 to 27.5% in 2007–08. For rectal cancer, this increase was from 1.1% to 21.5%. The largest increases were seen in high-volume private hospitals (colon cancer, 2.7% to 34.1%; rectal cancer, 1.5% to 26.2%), but increases also occurred in high-volume public hospitals (colon cancer, 2.7% to 32.2%; rectal cancer, 0.5% to 20.3%), low-volume private (colon cancer, 3.8% to 27.1%; rectal cancer, 2.4% to 25.5%) and low-volume public (colon cancer, 1.1% to 17.0%; rectal cancer, 0.5% to 13.8%) hospitals.Conclusions: The use of laparoscopic resection for colorectal cancer has increased throughout Australian hospitals. Our findings provide the data necessary to ensure adequate resource allocation by the appropriate medical bodies to achieve optimal success in the uptake of laparoscopic resection for colorectal cancer in Australia.

Bridie S Thompson BSc · Michael D Coory BSc(Applied), MB BS, PhD · John W Lumley MB BS, FRACS

Objective: To evaluate the effectiveness of redesigning and streamlining perioperative services.Design: A before-and-after evaluation, with retrospective analysis of de-identified administrative data.Setting: A major tertiary hospital, Melbourne, Australia.Participants: Patients undergoing elective surgery, February 2005 – February 2010.Intervention: Implementing a process redesign to streamline clinical pathways for elective surgery, with a focus on the patient journey from referral to discharge, and establishing a separate, dedicated elective surgery facility.Main outcome measures: Numbers of patients waiting beyond national recommended waiting times for elective surgery; hospital-initiated postponement (HIP) rates for elective surgery; and lengths of stay (LOS), both combined and for specific diagnostic-related groups.Results: The clinical process redesign resulted in a sustained downward trend in the number of elective surgery patients waiting longer than national recommended maximum waiting times. HIP rates were reduced to 1% in the dedicated elective surgery facility, and there was a significant reduction in the combined LOS, as well as the LOS for the most common surgical procedures (P < 0.001).Conclusions: Clinical process redesign of perioperative services and collocation of a separate elective surgery centre improved (i) timeliness of care for elective surgery patients and (ii) key indicators (LOS and HIP rates) for planned elective admissions.

Judy A Lowthian MPH, BAppSc(SpPath), LMusA · Andrea J Curtis BSc(Hons), PhD · Bernadette L Comitti DipAppSc(Nsg), GradDipBusinessAdmin · Peter A Cameron MB BS, MD, FACEM · Martin J Keogh GradDipCritCareNsg, GradDipManagement · William R Johnson MD, FRACS, FRCS · James Tomlinson MB BS, FRACP, FANZCA · Andrew M Stripp BBehavSc(Hons), MSc(ClinPsych)

Objectives: To describe professional discipline cases in Australia and New Zealand in which doctors were found guilty of professional misconduct, and to develop a typology for describing the misconduct.Design and setting: A retrospective analysis of disciplinary cases adjudicated in five jurisdictions (New South Wales, Victoria, Queensland, Western Australia and New Zealand) in 2000–2009.Main outcome measures: Characteristics of the cases (setting, misconduct type, patient outcomes, disciplinary measure imposed), characteristics of the doctors involved (sex, specialty, years since qualification) and population-level case rates (by doctor characteristics).Results: The tribunals studied disciplined 485 doctors. Male doctors were disciplined for misconduct at four times the rate of their female colleagues (91 versus 22 cases per 100 000 doctor-years). Obstetrics and gynaecology and psychiatry were the specialties with the highest rates (224 and 178 cases per 100 000 doctor-years). The mean age of disciplined doctors did not differ from that of the general doctor population. The most common types of offences considered as the primary issue were sexual misconduct (24% of cases), illegal or unethical prescribing (21%) and inappropriate medical care (20%). In 78% of cases, the tribunal made no mention of any patient having experienced physical or mental harm as a result of the misconduct. Penalties were severe, with 43% of cases resulting in removal from practice and 37% in restrictions on practice.Conclusions: Disciplinary cases in Australia and New Zealand have features distinct from those studied internationally. The recent nationalisation of Australia’s medical boards offers new possibilities for tracking and analysing disciplinary cases to improve the safety and quality of health care.

Katie J Elkin LLB(Hons), BSc, GDipMedHlthLaw · Matthew J Spittal PhD, BSc(Hons) · David J Elkin MA, BSc(Hons), BA · David M Studdert ScD, MPH, LLB

Psychiatrist Diana McKay explains why she chose the public hospital system PUBLIC: There’s nothing like surprising your medical colleagues. Almost a year ago, I announced to some colleagues that, after 6 or so years primarily in private practice as a psychiatrist, I was shutting up shop and returning to work as a staff specialist in a busy public hospital. There was a notable pause before the congratulations ensued. Friends and private patients asked me why was I going to work in the public sector? I gave a mixture of responses, such as wanting to improve “the system”, becoming more involved in teaching, and a desire to use my skills with those unable to pay privately for them. Personally, with my children getting older, I felt I had more energy — and hopefully more wisdom and patience — to invest in an often demanding health system. I’m now not quite at my first anniversary of being fully back in the public sector. Professionally, it has been both challenging and rewarding. I’m lucky enough to work in a teaching hospital small enough to enable personal relationships to be the key currency of professional connections. My immediate colleagues are a small but cohesive group, who meet regularly to discuss service and clinical difficulties (there are always several to raise) in a thoughtful manner. Our management team is happy to listen to new ideas, although (it goes without saying) innovation must always involve innovation with the budget as well. Relationships between professions are respectful, and the “us” and “them” dynamics that I have experienced elsewhere seem little apparent. The passion and commitment of staff are evident throughout the hospital. The clinical variety is considerable, with the need for further study and reflection much in evidence. I am often reminded of Hippocrates’ aphorism “ars longa, vita brevis” (the craft is long, life is short) as I search online for the latest information on treatments and complications to discuss with my patients. The work can be difficult, but it is a privilege to work with people often at their most vulnerable — frequently people I would not have seen in private practice because they could not have paid for my services there. A sense of contributing to social justice has been one reward of my return to the public sector. It is not, however, all a land of milk and honey. Being on-call is tiring, and can be stressful at times when there is demand for inpatient services but access block preventing patients from being admitted. Somehow, the hospital and I have found a path through these occasions, again, with the goodwill of many staff who work together to ensure a bed is found for someone who needs it. Other challenges include the stark realities of the gaps in our system generally, with care provided to those with intellectual disability being one example. It’s hard not to feel guilty when a person is sent away because their needs are not part of our purview, particularly when I’m aware of what limited options are available anywhere. Although it feels a bit infra dig to mention remuneration, it is true that a staff specialist earns less than someone in the same specialty in private practice. This difference is less stark in my non-procedural specialty than in others, but must be acknowledged. There are the benefits of being an employee: paid holidays, study leave, a training allowance (with some irritations attached — just ask me about the interpretation that a computer does not constitute study “equipment”) and no late-night chat sessions with my accountant discussing the benefits of cash versus accrual accounting. The money — even if it is less than I could earn elsewhere — arrives with pleasing regularity in my bank account, with the needful done. The inexplicable delays in organising some basic things like email access has provided ample opportunity for me to revise the serenity prayer (http://en.wikipedia.org/wiki/Serenity_Prayer). I suggest all staff specialists keep a copy near their elderly computers to assist them in times of bureaucratic or information technology crisis. Another challenge can be the freedom to join in public debate, even in a forum such as this. The New South Wales Health code of conduct reminds me of many very pertinent and sensible things, but also that I must not use my job title when engaging in sociopolitical debate; hence my vanilla listing in this article. I have watched a few colleagues thoughtfully ignore this stipulation and speak out on issues they feel are in the public interest, and I wonder how I would manage if (or when) I were in the same situation. I have spoken about my own outcomes in this debate, but little about the outcomes of those who matter most in any health care debate — the patients. It seems to me that the jury is out on whether the public or private sector provides the best outcomes, with lack of access to data limiting the confidence with which conclusions can be drawn.1 From my personal viewpoint, it matters less to me how health care is delivered than how it can be accessed. At present the rather fragmented Australian health care system allows only some people access to private health care, and this seems inequitable. If we want private and public good for ourselves and our patients, we need to consider how the principle of universal access can more effectively integrate both sectors. This would be truly innovative.

Diana R McKay MB BS, BSc(Med), FRANZCP

Neurosurgeon Terry Coyne explains why he left the public hospital system PRIVATE: After completing my specialist training and overseas fellowship, I spent 11 years working between five and six sessions a week as a visiting medical officer (VMO) in neurosurgery at adult and paediatric public hospitals. The remainder of my working week, I worked in private practice. Several years ago, I resigned from my public appointments. There were a number of reasons for this. I accept that things may be different now, that my circumstances may have been unique to me or to my specialty, or that I was too sensitive. Nonetheless, my reasons for leaving the public system are outlined, in no particular order, below. A feeling of constant combat with administration: I had the feeling that, as a clinician, I was essentially a cost generator, and needed to be kept in check. That I was there to help ill people get better seemed to be beside the point. Negative interaction with administrators ranged from the petty (our department secretary was forbidden from sending letters related to a College exam I was organising — this was my personal responsibility because it “didn’t relate directly to patient care”) to the outright hostile (being told the views of VMOs at a departmental meeting were of no interest because “in this hospital, the tail doesn’t wag the dog”). I was once at a hospital meeting where we VMOs were told that if we didn’t like the way the hospital worked, there were many South African doctors “just waiting to take your place”. While I initially enjoyed the jousting, over time, the constant antagonism began to grind me down, and coming to work was just no longer enjoyable. Lack of guaranteed indemnity: This is an important issue in my specialty, in which compensation settlements can be large. Private medical defence organisation contracts generally exclude public hospital work. While there were verbal assurances from administrators that “VMOs would be covered”, this was never put in writing, and all the written documentation I ever saw allowed the state government to exercise discretion as to whether a VMO would be indemnified in the event of a claim. Two of my colleagues were denied indemnity before my resignation because, although surgery was undertaken in public hospitals, the alleged negligent action was deemed by health department administrators to have occurred outside the hospital grounds and was therefore the surgeon’s personal responsibility. Difficulty reconciling different standards of care: This was manifest in several ways. I found it difficult to see enough outpatients in my weekly clinic to keep the outpatient waiting time acceptable. Taking a reasonably complete history, examining patients and reviewing the findings of investigations takes a certain time, particularly if this is also combined with teaching registrars, residents and medical students. The number of patients that would occupy an entire day of consulting in private practice would be scheduled for a 2–3-hour public clinic. When I tried to reduce the clinic appointments to a more manageable number, the waiting time to attend the clinic quickly blew out to more than a year. Frequent cancellation of my weekly operating list: This was largely because most of my patients require postoperative care in the intensive care unit (ICU) or high-dependency unit (HDU). My weekly operating day was a Monday, and the ICU and HDU were frequently full of patients with problems like trauma and drug overdose after the weekend, which meant my patients could not have their surgery. In addition, a number of public holidays fall on a Monday and, while surgery considered reasonably necessary can generally be negotiated in a private hospital, only absolutely urgent cases could be done in the public hospital. This is understandable, but I was still left with the problem of having patients needing surgery some time that week, but now with no time allocated to perform it. Better operating theatre equipment in the private sector: This was the case during my 11 years in the public system. Examples included higher quality operating microscopes and image guidance technology. Financial aspects: No VMO attends a public hospital to become rich. However, it shouldn’t be the case that a VMO all but pays to work there. I was spending a third of my time at the public hospital, but the costs of running my private practice continued 100% of the time. When I left the public system, based on practice costs spread over a nominal 45-hour week, my net rate as a VMO was $30 an hour. I therefore had to either accept that my family would live on what I could earn during the remainder of the week, reduce my VMO hours (not easy to do in my specialty while still providing a reasonable service), or just work more hours in private practice and abandon any hope of a balanced lifestyle. Ultimately there was no single reason why I left the public system. It may have been possible to tackle some or all of my issues, but, at the time, I felt the chances of achieving any meaningful change were poor. There are many good aspects of a public appointment, including the chance to help those who are less well off, the sense of giving something back to the system that provided much of one’s training, and more opportunity to teach and mentor the next generation of surgeons. However, over time, the negative aspects came to outweigh the positive. I take some comfort in the fact that I wasn’t the only one feeling this way; 12 months before my resignation, my public hospital department had two full-time staff and three VMOs. Two years later, of those five, only one full-timer remained; the others had moved into full-time private practice.

Terry J Coyne MB BS, FRACS

Demographic changes among junior doctors are driving demand for increased flexibility in advanced physician training, but flexible training posts are lacking. Suitable flexible training models include flexible full-time, job-share and part-time positions. Major barriers to establishing flexible training positions include difficulty in finding job-share partners, lack of funding for creating supernumerary positions, and concern over equivalence of educational quality compared with full-time training. Pilot flexible training positions should be introduced across the medical specialties and educational outcomes examined prospectively.

Suzanne E Mahady MB BS, BMedSci

Trainee surgeons must acquire expert status in the context of reduced hours, reduced operating room time and the need to learn complex skills involving screen-mediated techniques, computers and robotics. Ever more sophisticated surgical simulation strategies have been helpful in providing surgeons with the opportunity to practise, but not all of these strategies are widely available. Similarities in the motor skills required in skilled musical performance and surgery suggest that models of music learning, and particularly skilled motor development, may be applicable in training surgeons. More attention should be paid to factors associated with optimal arousal and optimal performance in surgical training — lessons learned from helping anxious musicians optimise performance and manage anxiety may also be transferable to trainee surgeons. The ways in which the trainee surgeon moves from novice to expert need to be better understood so that this process can be expedited using current knowledge in other disciplines requiring the performance of complex fine motor tasks with high cognitive load under pressure.

Andrew W McCaskie MMus, MD, FRCS · Dianna T Kenny ATCL, MA, PhD · Sandeep Deshmukh MB BChir, MA

Despite “safe-hours” campaigns and doctors health programs, “at-risk” behaviour and suicides still occur in junior doctors. A recent national survey found that 46% of junior doctors believed that their hospital administration was not supportive. The Royal Melbourne Hospital has developed a comprehensive program for preventing and identifying at-risk behaviour and supporting junior doctors, tailored to the individual’s needs. Patient and individual doctor safety is paramount, and confidential collaboration between medical workforce and medical education structures, clinical supervisors and the Victorian Doctors Health Program is required. The boundaries of the hospital’s “duty of care” for those who do not want assistance is unclear, and balancing increased supervision within a limited workforce is challenging.

Alison J Dwyer MB BS, MBA, FRACMA · Peter Morley MB BS, FCICM, FRACP · Esther Reid BEd · Cassandra Angelatos BBus

We report a case of compassionate use of a haemoglobin-based oxygen carrier in a severely injured Jehovah’s Witness patient, for whom survival was considered unlikely. Severe anaemia and cardiac hypoxia were reversed after slow infusion of this agent. No vasoactive side effects were associated with the treatment, possibly due to the slow infusion, and the patient survived. (MJA 2011; 194: 471-473) Clinical recordA healthy 32-year-old woman was a passenger in a vehicle involved in a high-speed collision with a truck, and she was entrapped for 2 hours. Initially, her heart rate was 100 beats/min, blood pressure was 90/50 mmHg, respiratory rate was 28 breaths/min and oxygen saturation measured by pulse oximetry (SpO2) was 92% on air. Her Glasgow Coma Scale score was 9 (eye opening, 2; verbal response, 1; motor response, 6) and her pupils were equal and reactive to light. Her family indicated that she was a Jehovah’s Witness and would not accept the units of blood that had been transported to the accident site. Paramedics performed endotracheal intubation, immobilisation, left femoral splinting and resuscitation with a 7000 mL crystalloid infusion, and applied dressings to wounds. The patient was transported by helicopter to The Alfred’s trauma centre. On arrival at the trauma centre, she was ventilated, her heart rate was 120 beats/min, blood pressure was 62/26 mmHg and SpO2 was 79% on 100% fraction of inspired oxygen (FiO2). Following discussions with the family, the trauma team agreed not to treat the patient with packed red cells, platelets or fresh frozen plasma. Thoracostomies for a right tension pneumothorax and a left pneumothorax were performed, which increased her blood pressure to 105/65 mmHg and SpO2 to 100% on FiO2 100%. Intercostal drains were inserted and connected to a cell salvage device. She was administered 1400 mL of succinylated gelatin, 10 units of cryoprecipitate and 5 mg of recombinant factor VIIa. Bleeding was controlled with direct pressure, and a scalp wound was closed. Ultrasonography demonstrated a moderate pericardial effusion with systolic right ventricular collapse and free intraperitoneal fluid. Electrocardiography demonstrated sinus tachycardia with no ST segment changes. Initial blood tests showed a haemoglobin (Hb) level of 67 g/L (reference range [RR], 113–159 g/L), activated partial thromboplastin time of 44.3 s (RR, 26–38 s), international normalised ratio of 1.9 (RR, 1.0–1.3), serum fibrinogen level of 3.2 μmol/L (RR, 5.9–11.8 μmol/L, lactate level of 3.9 mmol/L (RR, 0.6–2.2 mmol/L) and serum creatinine level of 55 μmol/L (RR, 60–105 μmol/L). Imaging showed a fractured right orbit and maxilla, bilateral rib fractures, a grade 4 splenic laceration, a likely jejunal injury with intramural haematoma, a left distal humerus fracture, a comminuted open left femoral shaft fracture, an unstable T12/L1 fracture dislocation (60% off-ended), and multilevel spinous process and transverse process fractures. Laparotomy and fixation of the patient’s thoracolumbar injury were deferred because of the likelihood of associated bleeding. Instead, she underwent splenic embolisation, external fixation of her open left femoral shaft fracture and debridement of her left humerus injury. She received 1000 mL of 4% albumin and 1000 mL of crystalloid fluid during these procedures, and 10 mg of intravenous vitamin K afterwards. On postoperative admission to the intensive care unit, her Hb level was 36 g/L and her coagulation profile was normal. Low-dose noradrenaline was required to support her blood pressure until Day 2. Her urine output over the first 24 hours was 4500 mL. A follow-up transthoracic ultrasound showed abatement of the pericardial effusion. An abdominal computed tomography (CT) scan with oral contrast excluded jejunal injury. To protect renal function, intravenous contrast was not used. Placement of an inferior vena cava filter was deferred because of anatomical distortion secondary to the thoracolumbar injury. Several strategies were used to manage the patient’s anaemia. Sedation minimised metabolic demand. A ventilation cycle of 2 hours of 90% FiO2, followed by 2 hours of 90% SpO2 and then 20 hours of 95% SpO2 was used. This was employed to maximise oxygen delivery while minimising shunt from absorption atelectasis and to promote erythropoiesis. Recombinant erythropoietin (36 000 units daily for 6 days), folic acid (5 mg daily continued until discharge), vitamin B12 (1 mg daily for 6 days) and a single iron infusion of 500 mg were administered to maximise haematopoiesis. Menses was inhibited with progesterone. Blood testing was performed using paediatric-sized samples. Pneumatic calf compressors were applied and regular lower-limb sonography was performed to exclude venous thrombosis. The trauma team considered using a synthetic haemoglobin-based oxygen carrier (HBOC) to increase oxygen delivery to the patient’s tissues. On Day 3, OPK Biotech (Cambridge, Mass, USA), the Therapeutic Goods Administration (TGA), the Australian Quarantine and Inspection Service and airline carriers were contacted to determine availability and import permissions. HBOC-201 was supplied by OPK Biotech without charge. Informed consent for use of HBOC-201 was obtained from the patient’s family. Approval for emergency compassionate use of HBOC-201 was obtained from The Alfred Ethics Committee on Day 4. The published and unpublished in-vivo and in-vitro research into HBOC-201 was reviewed at a multidisciplinary meeting, and its use was agreed to. Ten 250 mL units of HBOC-201 were imported under Category A of the TGA’s Special Access Scheme. By Day 5, the patient’s Hb level had dropped to 29 g/L and her serum troponin I level was 0.33 μg/L (RR, < 0.10 μg/L), indicating cardiac hypoxia (Box). An electrocardiogram showed widespread ST depression and an episode of non-sustained ventricular tachycardia was documented. Survival with this degree of metabolic demand, the associated anaemia, and resultant end-organ hypoxia was considered unlikely. Following advice from experienced United States physicians, 3 units of HBOC-201 were administered on Day 5, and a further 2 units were administered on Day 6 with ascorbic acid (1 g twice daily continued until discharge). Each unit of HBOC-201 was infused over 8 hours to minimise any adverse effects related to volume overload, vasoactivity or methaemoglobin. Intravenous glyceryl trinitrate was the agreed treatment in the event of hypertension,1 but this was not necessary. After the slow administration of 5 units of HBOC-201, the patient’s Hb level increased from 35 g/L to 62 g/L (Box). Echocardiography performed before and after HBOC-201 treatment showed a reduction in cardiac output from 6.8 L/min to 5.0 L/min. Electrocardiography findings and troponin I levels returned to normal and no further arrhythmias were noted. Somatosensory evoked potentials revealed intact lower-limb neurological pathways. On Day 7, closed reduction was performed and a body cast was applied to treat the T12/L1 fracture dislocation. Imaging showed improved alignment, and an inferior vena cava filter was placed. From Day 6, the patient’s temperature began spiking, secondary to femoral pin site infections and pneumonia. Despite treatment with antibiotics, temperature spiking continued. Cooling was commenced to minimise metabolic demand. A transoesophageal echocardiogram on Day 11 showed right ventricular regional wall motion abnormality but no evidence of endocarditis. A CT scan showed persistent bilateral pneumothoraces, a left pleural effusion and an epidural haematoma at L1 level. Bilateral tube thoracostomies were re-performed and an antifungal was added to the anti-infective regimen. A percutaneous tracheostomy was performed on Day 12. Low-dose heparin therapy for thromboprophylaxis was deferred until Day 17. By Day 21, the infections had resolved and the tracheostomy tube was removed. The femoral and humeral fractures were internally fixed on Day 20 with minimal blood loss. On Day 30, the patient’s Hb level was 107 g/L and operative reduction and internal fixation of her thoracolumbar spine was performed. She was well when discharged to a rehabilitation facility on Day 43 — her cognition was formally assessed as normal, lower-limb neurological pathways were intact and Hb level was 101 g/L. DiscussionWe have described compassionate use of HBOC-201 in a severely injured Jehovah’s Witness patient. To our knowledge, this is the first report to describe reversal of documented cardiac hypoxia secondary to anaemia following trauma. Haemorrhagic shock is responsible for one-third of deaths following high-energy trauma.2 Integrated trauma care systems coordinate rapid haemorrhage control, shock recognition and surgical interventions to minimise blood loss and coagulopathy.3 Healthy volunteers can tolerate Hb levels of 50 g/L without evidence of end-organ hypoxia.4 However, it is estimated that the median Hb concentration associated with mortality is about 25 g/L.5 During the phase of increased metabolic demand in our patient, there was evidence of cardiac hypoxia when her Hb level reached 29 g/L. This prevented further operative interventions and placed her at high risk of cardiac dysrhythmias and death. HBOC-201 is a modified lactated Ringer’s solution containing 130 g/L of polymerised Hb of bovine origin. It is compatible with all blood types, stable for 3 years when stored at 2–30°C and stable for 2 years when stored at 40°C. When fully saturated, HBOC-201 has the same oxygen-carrying capacity as whole blood with the same Hb concentration. The partial pressure of oxygen at which HBOC-201 is 50% saturated (40 mmHg) is higher than that for cellular Hb (27 mmHg), which facilitates oxygen delivery to tissues. The half-life of HBOC-201 is approximately 20 hours.6 Polymerisation of the Hb reduces its glomerular diffusion and nephrotoxicity. A potential complication of HBOC-201 administration is hypertension and increased left ventricular afterload. Infusing each unit slowly (over 8 hours) in our patient may have diminished any vasoactive side effects. Two case reports of using HBOC-201 to treat severe anaemia following blunt trauma have been published. The first described improved cerebral oxygen delivery, but not survival, in a patient with head injuries.7 The second described successful reversal of haemorrhagic shock in a patient whose Hb level dropped to 45 g/L before HBOC-201 administration.8 However, the lack of clear HBOC-201 transfusion indications and end points, as well as the lack of data to support widespread use of HBOCs, has been criticised.9 A meta-analysis of data from HBOC trials has demonstrated an increased incidence of myocardial infarction and death in anaemic patients without life-threatening haemorrhagic shock.10 However, the analysis did not address the issue of “risk versus benefit” for use of these agents, including HBOC-201, in cases where blood transfusion for severely anaemic patients is not possible. A subsequent series of 54 consenting non-trauma patients with a median Hb level of 40 g/L demonstrated improved chances of survival with no serious adverse events following HBOC-201 administration.11 When blood transfusion is not possible, HBOCs can sustain oxygen delivery to hypoxic tissues.12 Such treatment may represent a life-saving intervention for patients with acute anaemia.13 Interest in safe and effective red blood cell substitutes for oxygen transport is increasing. Agents such as HBOC-201 show particular promise and could make a large difference to survival of trauma patients when blood is not accessible, available or acceptable. Haemoglobin and troponin I levels of a woman who was treated with a haemoglobin-based oxygen carrier (HBOC) following severe trauma * Troponin I levels were measured using the Architect i2000 immunoassay analyser (Abbott Diagnostics, Abbott Park, Ill, USA).

Mark C Fitzgerald MB BS, FACEM · Julie Y Chan MB BS(Hons), BMedSci · Andrew W Ross MB BS, FANZCA · Susan M Liew MB BS(Hons), FRACS(Orth) · Warwick W Butt MB BS, FCICM, FRACP · David Baguley MB ChB, BSc(Hons) · Hatem H Salem MB BS, FRACP · Matthias K Russ Orthopaedic and Trauma Surgeon (Germany) · Conor Deasy FACEM, FCEM, MB BCh BAO · Katherine E Martin MB BS, BMedSci, FRACS · Joseph K Mathew MB BS, MS · Jeffrey V Rosenfeld FRACS, FRCS(Edin), FACS

Women’s health in general practice. 2nd edition. Danielle Mazza. Sydney: Elsevier, 2011 (ix+346 pp, $94.95). ISBN 9780729538718. DANIELLE MAZZA, an associate professor at the School of Primary Health Care, Monash University, is a general practitioner with broad experience in women’s health and evidence-based research. She was previously medical director of Family Planning Victoria and is currently a member of the Royal Australian College of General Practitioners National Standing Committee on Quality Care. Her credibility is reflected in this comprehensive text on women’s sexual and reproductive health issues, with particular relevance to Australian general practice. This second edition has been fully revised to include developments in the field, such as the latest guides to taking “the pill”, the contraceptive vaginal ring, human papillomavirus epidemiology and polycystic ovary syndrome. The chapter on contraception provides practical and definitive information on all methods in current use — a mandatory knowledge base for all GPs providing such advice. The inclusion of chapters on violence against women, unplanned pregnancy and sexual problems is to be commended. Mazza’s style of frank discussion of the issues, legalities and practicalities presents these difficult subjects in an informative, non-judgemental manner. Registrars starting in practice and studying for their exams ignore this text at their peril! The layout is educationally sound, with learning objectives, case studies and key points. The chapters are extensively referenced. Mazza also uses many tables, photographs and helpful diagrams (although some of these could be larger). Mazza is to be commended for strongly presenting the evidence, or lack thereof, for treatments. Mostly, the evidence is cleverly mixed with practical approaches for the clinician. At times, however, evidence overwhelms practicality, discouraging some harmless treatments (eg, for mastalgia and premenstrual syndrome) and leaving options of reassurance only, or active drugs. Purchase of the softcover book includes online access to the complete book. In summary, this is an authoritative and comprehensive reference for new GPs as well as experienced practitioners wanting to update or check the latest evidence.

Karen M Flegg

This article critically analyses the prospects for introducing United States anti-fraud (or anti-false claims) laws in the Australian health care setting. Australian governments spend billions of dollars each year on medicines and health care. A recent report estimates that the money lost to corporate fraud in Australia is growing at an annual rate of 7%, but that only a third of the losses are currently being detected. In the US, qui tam provisions — the component of anti-fraud or anti-false claims laws involving payments to whistleblowers — have been particularly successful in providing critical evidence allowing public prosecutors to recover damages for fraud and false claims made by corporations in relation to federal and state health care programs. The US continues to strengthen such anti-fraud measures and to successfully apply them to a widening range of areas involving large public investment. Australia still suffers from the absence of any comprehensive scheme that not only allows treble damages recovery for fraud on the public purse, but crucially supports such actions by providing financial encouragement for whistleblowing corporate insiders to expose evidence of fraud. Potential areas of application could include direct and indirect government expenditure on health care service provision, pharmaceuticals, medical devices, defence, carbon emissions compensation and tobacco-related illness. The creation in Australia of an equivalent to US anti-false claims legislation should be a policy priority, particularly in a period of financial stringency.

Thomas A Faunce LLB(Hons), BMed, PhD · Gregor Urbas BA, LLB (Hons), PhD · Lesley Skillen BA(Hons), LLB(Hons), LLM

The Cancer Council Australia (CCA) Alcohol Working Group has prepared a position statement on alcohol use and cancer. The statement has been reviewed by external experts and endorsed by the CCA Board. Alcohol use is a cause of cancer. Any level of alcohol consumption increases the risk of developing an alcohol-related cancer; the level of risk increases in line with the level of consumption. It is estimated that 5070 cases of cancer (or 5% of all cancers) are attributable to long-term chronic use of alcohol each year in Australia. Together, smoking and alcohol have a synergistic effect on cancer risk, meaning the combined effects of use are significantly greater than the sum of individual risks. Alcohol use may contribute to weight (fat) gain, and greater body fatness is a convincing cause of cancers of the oesophagus, pancreas, bowel, endometrium, kidney and breast (in postmenopausal women). The existing evidence does not justify the promotion of alcohol use to prevent coronary heart disease, as the previously reported role of alcohol in reducing heart disease risk in light-to-moderate drinkers appears to have been overestimated. CCA recommends that to reduce their risk of cancer, people limit their consumption of alcohol, or better still avoid alcohol altogether. For individuals who choose to drink alcohol, CCA recommends that they drink only within the National Health and Medical Research Council guidelines for alcohol consumption.

Margaret H Winstanley BA · Iain S Pratt GradDip(Diet), APD, AEP · Kathryn Chapman BSc, MNutrDiet · Hayley J Griffin BMedSc, MNutrDiet, PhD · Emma J Croager PhD, MBA · Ian N Olver MD, PhD, FRACP · Craig Sinclair MPubPolMgt, GradDipOrgBehav, BEd(Sec) · Terry J Slevin MPH, FPHAA

Clinical record A 64-year-old woman who had never consumed alcohol presented to hospital with a several-day history of vomiting and severe diarrhoea, secondary to Clostridium difficile colitis. She had suffered a similar episode 3 months earlier. Her symptoms settled after 7 days’ treatment with vancomycin and metronidazole, but her admission was complicated by nosocomial pneumonia and her oral intake was poor. Fifteen days into her stay, she became drowsy and less communicative and developed generalised weakness. Clinical examination revealed signs of encephalopathy. She had slowed mentation, paucity of facial expression and slow limb movements. She could follow one-stage commands but only slowly and with significant prompting. Her eye movements were normal. She had mild generalised weakness in all four limbs, but her deep tendon reflexes were intact and plantar responses were downgoing. Ataxia could not be assessed reliably due to impaired consciousness. Electroencephalography showed generalised slowing without focal features. Magnetic resonance imaging (MRI) of the patient’s brain revealed symmetrical changes of high signal in the periaqueductal grey matter, superior colliculi and medial thalami, most evident on the fluid-attenuated inversion recovery (FLAIR) sequences (Box 1, A–C). These symmetrical periventricular changes were consistent with typical findings recently described for Wernicke’s encephalopathy.1 Given the clinical history of dietary deprivation and colitis, together with the typical radiological changes, a diagnosis of Wernicke’s encephalopathy was strongly suspected. Hence, intravenous thiamine 500 mg three times a day was administered, after which the patient made a dramatic clinical and radiological recovery (Box 1, D–F) over a period of about 7 days. Despite this, her pretreatment (Day 15) blood thiamine pyrophosphate level, measured using high-performance liquid chromatography, was eventually reported as being normal (136 nmol/L [reference range, 67–200 nmol/L]). However, given her clinical history, the changes noted on MRI and the dramatic improvement in her condition with thiamine, the diagnosis of Wernicke’s encephalopathy remained the most likely explanation. Wernicke’s encephalopathy is caused by thiamine deficiency and is most commonly associated with heavy alcohol intake paired with poor nutrition.2 However, the same phenomenon can occur in non-alcoholic patients with a very low dietary thiamine intake — for example, in patients who undergo prolonged therapeutic fasting or gastrointestinal (particularly bariatric) surgery, and in patients with recurrent vomiting or diarrhoea.3 It has also been reported after prolonged febrile illnesses, where thiamine requirements may be increased and where there is also inadequate oral intake.3 If not recognised, Wernicke’s encephalopathy can progress to Korsakoff syndrome, resulting in profound working memory deficits, or may even be fatal.4 In a healthy person, reserves of thiamine are estimated to be exhausted after only 2–3 weeks of dietary deprivation.3 In this case, we hypothesise that nutritional deficiency developed due to the patient’s ongoing vomiting and diarrhoea, combined with a catabolic state from her severe pneumonia, and that thiamine stores may already have been depleted from her previous bout of Clostridium difficile infection. Clinically, patients with Wernicke’s encephalopathy classically present with the triad of global cognitive deficits, eye signs (nystagmus and/or ophthalmoplegia) and ataxia,4 although there are also less common clinical features (Box 2). However, autopsy reports of pathologically confirmed cases of Wernicke’s encephalopathy indicate that only 16% of patients have the triad, 19% have no clinical signs at all, and the most common presentation is isolated cognitive changes (eg, impaired consciousness or disorientation).4,5 This is consistent with the clinical findings in our patient and emphasises the need to consider Wernicke’s encephalopathy as a diagnostic possibility even when the classic triad is absent. In the past decade, magnetic resonance imaging (MRI) has been recognised as a useful adjunct in Wernicke’s encephalopathy diagnosis.6 Wernicke’s encephalopathy typically causes symmetrical alterations in MRI signal intensity (increased on fluid-attenuated inversion recovery [FLAIR] images) in the periventricular regions of the brain, including the medial thalami, periaqueductal grey matter, tectal plate (inferior and superior colliculi), and mamillary bodies.1,7 It has been suggested that MRI changes which occur in alcoholic and non-alcoholic patients with Wernicke’s encephalopathy may differ, with contrast enhancement of the mamillary bodies and thalami occurring more frequently in the alcoholic patients, suggesting that these areas may be selectively susceptible to alcohol toxicity.7 Our patient’s normal thiamine level is also of interest. Thiamine functions as a coenzyme in the metabolism of carbohydrates, lipids and some amino acids and is involved in myelin sheath maintenance and neurotransmitter production.2 One would, by definition, expect a low thiamine level in Wernicke’s encephalopathy. However, thiamine assays have well recognised limitations. Serum thiamine levels are a poor measure of thiamine status.2 Until recently, many laboratories have used thiamine transketolase activation assays; however, these have also been reported to lack specificity, as well as being technically difficult.3 Many laboratories in Australia have moved to using high-performance liquid chromatography with fluorescent detection to measure thiamine pyrophosphate — the physiologically active form of thiamine — in whole blood, as done for our patient. This assay is thought to have improved reproducibility,2 but has also been noted to have weaknesses relating to the standardisation process of its complicated chromatographic methods (Ronda Greaves, Chair, Vitamins Working Party, Australasian Association of Clinical Biochemists, personal communication). In addition, although these assays give an estimate of whole-blood thiamine levels, they do not necessarily reflect intracerebral thiamine levels. Thiamine is predominantly transported across the blood–brain barrier by a slow, carrier-mediated process,8 hence Wernicke’s encephalopathy cannot be diagnosed simply by measuring the circulating thiamine level.9 In our case, the patient’s clinical presentation, MRI changes and rapid clinical and radiological recovery in response to administration of thiamine provide support for the diagnosis of Wernicke’s encephalopathy, despite the normal thiamine level. Further, it is critical to remember that while thiamine assays usually take several days, early initiation of thiamine is vital to prognosis9 and clinical response to thiamine is the most reliable diagnostic test.3 In conclusion, this case highlights the challenges of recognising Wernicke’s encephalopathy and the importance of prompt diagnosis. Given the underdiagnosis of Wernicke’s encephalopathy,4 the often incomplete clinical presentation of the condition, and the low toxicity of thiamine,2 a low clinical threshold is warranted for initiating thiamine therapy in patients with cognitive changes and significant predisposing factors for dietary thiamine deficiency. Clinicians should maintain a high index of suspicion when such risk factors are present. The characteristic MRI changes should also be looked for. Thiamine assays may help confirm suspicions but a normal thiamine level does not exclude the diagnosis. As this case demonstrates, early thiamine replacement can fully reverse the clinical and radiological features of this potentially devastating condition. 1 Magnetic resonance imaging scans of the patient’s brain before and after thiamine administration Axial fluid-attenuated inversion recovery (FLAIR) sequence images from when the patient was encephalopathic (A–C) show symmetrical changes of abnormal high signal in the periaqueductal area (arrows, A), superior colliculi (arrows, B) and posterior medial thalami (arrows, C). These changes resolved completely following thiamine administration (D–F). 2 Less common clinical features of Wernicke’s encephalopathy2,3 Autonomic: hypotension and tachycardia; hypothermia; bradycardia Ocular: sluggish pupillary reactivity; light–near dissociation; bilateral visual disturbances due to papilloedema and retinal haemorrhages Aural, vestibular: hearing loss; vestibular dysfunction; tinnitus Seizures: generalised tonic–clonic seizures Movement disorders: myoclonus; orthostatic tremor; choreic dyskinesias Motor system: acute peripheral neuropathy; increased muscular tone and spastic quadriparesis Mental status: hallucinations and behavioural disturbances; psychosis; coma Lessons from practice Wernicke’s encephalopathy can occur in non-alcoholic patients with other risk factors (eg, dietary deprivation of thiamine). In a previously healthy individual, thiamine stores can be depleted by 2–3 weeks of dietary deprivation. Although Wernicke’s encephalopathy is classically described as the clinical triad of cognitive deficits, eye signs and ataxia, this triad is much less common in practice than presentation with cognitive deficits alone. Magnetic resonance imaging is a useful diagnostic aid, showing symmetrical increased signal on fluid-attenuated inversion recovery (FLAIR) images in the periventricular regions of the brain. A normal thiamine level does not exclude a diagnosis of Wernicke’s encephalopathy.

Sarah B Davies BSc(Med)Hons · Fredrick F Joshua MB BS, FRACP, PhD · Alessandro S Zagami MB BS, FRACP, MD

To the Editor: Frei and colleagues recently drew our attention to combination analgesic misuse-related morbidity.1 The same phenomenon has also been reported in New Zealand.2 About 50 years ago, analgesic misuse was widespread in Australia and commonly involved chronic, excessive use of combination analgesics (including the aspirin–phenacetin–caffeine [APC] products, Bex and Vincent’s Powders). After many years, some people who used APC developed “analgesic nephropathy”, which made up 12%–15% of dialysis cases.3 I recently performed a retrospective chart review of patients who were referred to the Drug and Alcohol Services at the Western Hospital (Melbourne) for excessive compound analgesic use between September 2005 and September 2010. There were 32 patients (18% of all referrals; median age, 38 years; 23 were women). All had some form of chronic pain, had initiated compound analgesic use for acute pain (eg, headache) and all described progressive use of analgesics because of psychogenic effects (eg, “gave me energy”, “helped me forget”). All 32 patients were diagnosed with opioid dependence and had medical and psychiatric problems correlating with their compound analgesic misuse. One patient, a 34-year-old man, reported taking more than 70 codeine–ibuprofen tablets daily and sustained recurrent gastric ulceration, which eventually required surgery. Despite this, he continued to misuse the analgesics until he undertook opioid replacement pharmacotherapy. A 24-year-old man misusing the same analgesic, despite completing a detoxification program, also relapsed and died after bleeding from gastric ulceration.4 Overall, the patient profiles were remarkably similar to those described by Frei and colleagues.1 Combination analgesic misuse appears largely correlated with products containing drugs of dependence (eg, codeine) and the phenomenon of “rebound pain” (ie, pain that recurs after a short-acting analgesic effect wanes, or “medication overuse headache”). Most morbidity and mortality risks associated with combination analgesic misuse are a consequence of chronic overdose of the non-steroidal anti-inflammatory drug and/or paracetamol components. Paracetamol (mostly when in combination with an opioid analgesic) is reported as the commonest cause of acute liver failure in the United States and United Kingdom.5 Another long-term complication can be hearing loss.6 Two patients in my clinic group had hearing loss, and the ear, nose and throat specialist’s opinion was that it was related to analgesic misuse. Dextropropoxyphene–paracetamol combination products are still available in Australia but are no longer available in the UK. I question the need for opioids in combination analgesic products and, if used, they should be restricted to prescription.

Michael A McDonough

To the Editor: We read with interest the recent letter by He and colleagues.1 The authors described a case of ischaemic stroke in a patient with scurvy and considered whether there was a connection between the two conditions. They referred to evidence that vitamin C deficiency may be a risk factor for cerebrovascular disease, but acknowledged that a direct causal link is unlikely to be established. We propose adiponectin as the causal link between vitamin C deficiency and stroke. Adiponectin is an adipokine, secreted in multimers by adipose tissue, with insulin-sensitising, antiatherogenic and cardioprotective properties.2 A decrease in adiponectin levels — particularly the more biologically active, high molecular weight (HMW) multimers — is implicated in a number of disease states, such as obesity, type 2 diabetes, heart disease and some cancers. Adiponectin has also been reported to have cerebroprotective properties,3 and there is some evidence that levels may be reduced in patients with cerebrovascular disease.4 A recent study demonstrated that vitamin C supplementation increases the proportion of HMW adiponectin secreted from human adipocytes.5 Vitamin C levels are lower in obese and diabetic patients, and the patient reported by He et al had also been recently diagnosed with type 2 diabetes. While scurvy is admittedly rare, He and colleagues noted that subclinical vitamin C deficiency is not uncommon in the general population (about 10%). We suggest that it would be worthwhile to assay plasma vitamin C levels and total and HMW adiponectin levels in patients presenting with cerebrovascular events, and to undertake prospective studies to determine whether vitamin C supplementation improves patients’ adiponectin levels. Increased HMW adiponectin levels could be explained, at least in part, by the role of vitamin C in the multimerisation of adiponectin. Adiponectin levels are also reduced in other vascular conditions, such as ischaemic heart disease and peripheral vascular disease.4 As plasma vitamin C levels of patients with these diseases are also reduced, it is tempting to posit that vitamin C supplementation could have a role as a treatment, or even a prophylactic, in populations at risk of a range of adiponectin-related vascular diseases.

Felicity J Rose · Jonathan P Whitehead

To the Editor: The juxtaposition of articles by Braithwaite and colleagues1 and Ho and Maddern2 (a description of a trial of physician assistants [PAs] in Adelaide) provides an interesting contrast between what should be happening in health care and what is happening. While Braithwaite and colleagues argue for a value-driven change, the type of change that is occurring at the moment is that of role substitution. This is exemplified by Ho and Maddern’s assertion that “PAs ... would ... improve the quality and quantity of medical service”. The intent is to provide a substitute doctor. This is referred to as “task” substitution or transference, with the inference that those under discussion, whether PAs or nurse practitioners (NPs), will only perform a limited role — some of the tasks of a doctor. In South Australia, PAs are able to order investigations and prescribe. The former editor of this journal, Martin Van Der Weyden, discussed this issue in 2008,3 labelling it “doctor displacement”, a term that Brooks and Mitchell disputed.4 They said “[PAs] will never be able to practise independently; they will always have to practise under supervision and within the scope of practice of their supervisor”. The Health Legislation Amendment (Midwives and Nurse Practitioners) Act 2010 (Cwlth), however, provided NPs with access to the Pharmaceutical Benefits Scheme and the ability to prescribe. Any supervision by doctors seems nominal, with independent practices being set up, some attached to pharmacies. There is less supervision of NPs by the medical profession than that given to trainees in teaching hospitals, and they are effectively independent practitioners. It could be argued that United States-trained PAs are even better trained than Australian-trained NPs, and Brooks and Mitchell’s statement that they will “never” practise alone is hardly reassuring. Proponents of NPs and PAs justify their use4 by reference to a shortage of health professionals. It isn’t reasonable to take from one area of need (nursing) to bolster another area of need (medicine), and the rapid increase in medical undergraduates and increase in immigration of overseas-trained doctors renders medical workforce projections unreliable. Role substitution by PAs and NPs will only perpetuate the problems we now face, while introducing new problems related to limited training and skills and fragmentation of care. Australian GPs, traditionally well trained and highly skilled, and with the ability to manage complex problems, are the core of our health system. Proposed changes devalue their contribution by making the inevitably fatal assumption that the sick patient is easy to recognise and triage.

Patrick S Hanrahan

To the Editor: Eight Australian medical deans recently called for academic health science centres (AHSCs) — where a leading university joins with a major tertiary health care provider in a tripartite mission of excellence in clinical service, research and education.1 However, there are obstacles to their proposal due to the misalignment in purpose of universities and teaching hospitals. Why do they call for change, given that many of our public hospitals are already affiliated with universities, have academic units of the university, and are funded by governments to educate doctors? Many private hospitals are also involved in university and college education. The Garling report was commissioned in response to a crisis in the quality of acute care offered in New South Wales public hospitals.2 However, none of its 139 recommendations refer to striving to achieve excellence. While excellence must be the aim of our public hospitals, their immediate response should be patient-centred, ensuring an acceptable minimum standard of care. Other targets, such as research and concentrating limited resources on aiming for excellence in specified areas, could prove to be a distraction from this core purpose. Education was mentioned in the Garling report but in no sense was achieving excellence in clinical service or research implied to be its purpose, unless excellence is to be understood to mean the minimally acceptable level of care. Medical education and research need to fit within a public hospital system that has funding limits and is struggling to deliver its core goal of clinical care. Given the current misalignment of purpose between hospitals and universities, it is no surprise that the combined deans have expressed a tone of dissatisfaction. Mayo Clinic in the United States has a logo of three interlocking shields,3 representing a “tripartite mission of excellence in clinical service, research and education”. Mayo Clinic’s key to achieving excellence — the aspirational aim of the deans’ “world-class AHSCs” — is alignment of purpose of the hospital and the academic institution. Similarly, in Australia, the barriers highlighted by the deans1 were dealt with in the planning of Macquarie University’s medical school and hospital. A common purpose and a greenfield site, where a new culture could be introduced, were a core part of Macquarie’s approach.4 As Macquarie’s Vice Chancellor, Professor Schwartz, was reported to say in 2010: “By owning and running the hospital we can ensure that we put medical teaching and research at the forefront”.5 Macquarie knows that simply owning and running its own hospital does not necessarily assure success, but it is an important step.

Michael K Morgan · Janet D Greeley

To the Editor: The editorial on academic health science centres (AHSCs) in Australia by the deans of medicine in all eight research-intensive universities1 is an important platform for discussing fundamental issues to be considered in developing these centres. The essential basis of an AHSC is a combination of two major initiatives: Seamlessly integrating research done in laboratories and clinical trials with multidisciplinary patient care. Building a centre of innovation where questions are asked based on actual clinical problems and can be resolved by the collective efforts of on-site “knowledge workers”. It is timely and necessary to investigate this option of health care delivery, as politicians negotiate at state and federal levels on appropriate models, and is in keeping with the National Health and Medical Research Council’s objectives in its latest strategic plan for broadening and building Australia’s capacity for research.2 It is crucial that any AHSCs created justify their status. They could be national centres of excellence, funded by an agreed federal and state government contribution model, together with endowments and competitive research funds. They should not merely be cosmetic makeovers for current university hospitals, with their idiosyncratic selection of staff and clinical practice models. Their governance needs to be standardised, based on agreed principles. A competitive national selection process should include identifying submissions that define employment of specific personnel and implementation of interventions to address the challenges of health care delivery in a timely and efficient manner.3 A suggested list of required attributes of staff employed in AHSCs is shown in the Box. A single academic chief executive officer who is a proven educator and researcher and cognisant of local and regional issues of health care delivery can facilitate the development of the centre, with the assistance of similar professionals on the board of management. The knowledge workers in an AHSC should include knowledge leaders (who incorporate knowledge into clinical protocols and management plans), creators (who generate new knowledge from research data), users (clinicians and researchers who incorporate therapies and skills into the clinical arena) and learners (students training to be health professionals and researchers). Direct interaction between the financial regulators and leading researchers and clinicians in an AHSC can lead to implementation of state-of the-art clinical practice, with patient care consistently being evaluated so that clinical and financial inefficiencies can be eliminated. The interaction of knowledge workers within the AHSC can result in sharing innovative and ethical translational research with bedside clinical practice. Required attributes of academic health science centre (AHSC) staff Staff employed at AHSCs should have all these attributes: Ability — high-quality knowledge and skills Accountability — responsibility, being up to date with current evidence-based practice Availability — to the community of practice within the AHSC Accessibility — to patients and colleagues Affability — teamwork, cooperation, collaboration Affordability — social responsibility to the community and country Adaptability — dedicated to continuous professional development and ongoing research

David A Kandiah

Puffing on a delusion Although the public health announcements state that “every cigarette is doing you damage”, many smokers believe that the amount of damage depends on the colour of the cigarette packet. Researchers used data from the International Tobacco Control Four Country Survey, which polled more than 8000 smokers from Australia, Canada, the United Kingdom and the United States. The study found that 20% of smokers incorrectly believed that “some cigarette brands could be less harmful than others”. Compared with smokers from other countries, Australian smokers were more likely to believe that their own brand of cigarette “might be a little less harmful than others”, with 47% of Australian smokers agreeing with this statement. Smokers of silver, gold, purple or blue brands were much more likely to agree with this statement than those who smoked red or black brands. Researchers said that the study shows that smokers believe certain colours are associated with lower harm, highlighting the importance of plain packaging, as proposed in Australia. Addiction 12 April 2011 (Online first) Acne + antibiotics ≠ Drug resistance Acne is sometimes treated with the same antibiotics used to treat methicillin-resistant Staphylococcus aureus (MRSA) infections. Colonisation with S. aureus is common in the general population, raising concerns that acne patients using long-term antibiotic therapy could become a source of antibiotic-resistant S. aureus. Researchers tested 83 consecutive acne patients for S. aureus using cultures from oropharyngeal and nasal swabs, at an American dermatology clinic. Overall, 43% were colonised with S. aureus and two had MRSA. Patients using oral or topical antibiotics were less likely to be colonised than other acne patients. Researchers hypothesised that rates of S. aureus colonisation would be higher among long-term oral antibiotic users, due to antibiotic resistance; however, no statistically significant difference was found. Arch Dermatol 11 April 2011 (Online first) Combo drug fights obesity Using a new two-drug combination, overweight and obese patients lost an average of 8%-10% of their body weight, depending on the dose taken, during a 1-year Phase 3 trial. The CONQUER study examined a combination of phentermine, a central norepinephrine-releasing drug, and topiramate, a drug licensed for treating epilepsy and migraine. Almost 2500 patients — who had a body mass index of 27- 45 kg/m2 and at least two comorbidities such as diabetes or hypertension — were randomly assigned to receive placebo, a lower-dose combination of the two drugs, or a higher-dose combination. After 56 weeks of treatment, average weight loss compared favourably with existing and emerging obesity drugs. Patients lost an average of 1.4 kg in the placebo group, 8.1 kg in the lower-dose group and 10.2 kg in the higher- dose group. Lancet 11 April 2011 (Online) Superbugs win again Expanding the use of barrier precautions should reduce the spread of so-called superbugs in hospitals, right? Perhaps not, according to American research on the transmission of methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococcus (VRE) in 18 intensive care units (ICUs). The ICUs were randomly assigned to either an intervention group, in which the use of gloves and gowns was expanded, or to a control group in which existing practice was maintained. Gloves, gowns and hand hygiene were used more frequently in intervention ICUs. But surprisingly, the incidence of MRSA or VRE colonisation or infection did not differ significantly between the two groups. Researchers speculated that improved compliance by health care providers and improved turnaround times for confirming the results of surveillance cultures may have reduced transmission more effectively. N Engl J Med 2011; 364: 1407-1418 Fix the basics for AMD Age-related macular degeneration (AMD) is the leading cause of adult irreversible vision loss in developed countries. But two new studies based on data from the Carotenoids in Age-Related Eye Disease Study (CAREDS) build on our understanding that modifiable lifestyle factors play a huge role in the development of the condition. In the first paper, researchers found that changing lifestyle factors such as diet, exercise and smoking could reduce the risk of early AMD as much as threefold.1 A second study showed that for women aged 50-75 years, having high levels of serum vitamin D was significantly associated with a 48% decreased risk of early AMD; however, researchers called for further study to verify the association.2 1 Arch Ophthalmol 2011; 129: 470-480 2 Arch Ophthalmol 2011; 129: 481-489

Sophie McNamara