Letters

Carol Breeze,* Caroline M de Costa,† Mark Jagusch‡ * Senior Registrar, † Professor, Department of Obstetrics and Gynaecology, James Cook University School of Medicine; ‡ Director of Pathology, Cairns Base Hospital, PO Box 902, Cairns QLD 4870. caroline.decostaATjcu.edu.au To the Editor: The incidence of cervical cancer in Far North Queensland (FNQ) is 10 times the national average and the mortality rate five times greater.1,2 Of the Australian states, Queensland has the lowest average rate of regular cervical screening (57% of eligible women), and in some FNQ communities rates of less than 40% have been reported. Cairns Base Hospital (CBH) provides all public colposcopy services in Cairns and throughout Cape York for a population that is largely rural, remote and transient. In 2004, through the outpatients department of CBH, 12 new cases of invasive cancer were diagnosed (with additional advanced cases admitted directly to the surgical services). None of these women had undergone cervical screening in the previous 4 years. We conducted a three-part study at CBH: a 3-month retrospective study (Feb–Apr 2004) and a 3-month prospective study (Oct–Dec 2004) comparing cytological reports with histological results, and a further study (Oct–Dec 2004) of women who were referred for colposcopy but failed to attend. In the retrospective study, of 43 new patients with a cytology report of low-grade epithelial abnormality (LGEA) who had histology performed, 19 (44%) had a histological diagnosis of a high-grade epithelial abnormality (HGEA). (“Low-grade cytology” was defined in the 1994 National Health and Medical Research Council [NHMRC] guidelines3 as two consecutive “atypical” smears or one smear reported as cervical intraepithelial neoplasia [CIN 1], with or without the presence of human papilloma virus. CIN 2 or CIN 3 were defined as “high-grade” abnormalities.) In the prospective study, of 40 women with a cytology report of LGEA, 13 (33%) had HGEA on histopathology. Although our numbers were small, the incidence of histologically confirmed HGEA in patients presenting with LGEA on cytology appeared to be higher than the 24.5% reported by the Queensland Pap Smear Registry in 2000 for Queensland as a whole.4 Our colposcopy attendance study showed that, of 341 women referred for colposcopy over a 3-month period, 106 (31%) failed to attend scheduled appointments. Non-attenders included 27 Indigenous women, 10 women living only transiently in the area and 40 women living in remote areas. Thirty per cent of newly referred women and 32% of follow-up patients failed to attend, despite prolonged efforts by doctors, nurses and social workers to persuade them to do so (Box). (These proportions are substantially higher than those reported in clinics in large urban centres.5) Under previous NHMRC guidelines, women with reports of CIN 1 were immediately referred for colposcopy.3 However, under the recently adopted guidelines, such women are required to have at least one further smear 12 months later and demonstrate ongoing abnormality before referral.6 This policy assumes a stable, informed, compliant population with well motivated patients able to return for long-term follow-up. It also requires a reliable, non-labour-intensive system to track down non-attenders. In the FNQ region, with limited health care personnel, a population scattered over a huge area and patients often non-compliant (for many reasons, including social, financial, geographic and educational factors), we feel that the latest NHMRC policy is likely to be counterproductive, with the women most at risk possibly slipping through the net. We believe that in FNQ, and possibly in other rural areas where the incidence of cervical cancer is high, it may be appropriate to adapt the new national guidelines and continue with policies for managing LGEA that are more akin to the former guidelines. Breakdown of patients who failed to attend for colposcopy, by last-recorded cytology/histopathology results LGEA or less Possible HGEA HGEA Total number of non-attenders Newly referred patients (n = 157) 27 3 17 47 (30%) Follow-up patients (n = 184) 44 0 15 59 (32%) HGEA = high-grade epithelial abnormality. LGEA = low-grade epithelial abnormality.

Carol Breeze · Caroline M de Costa · Mark Jagusch

Simon R Brice,* Marie V Pirotta† * Honorary Research Fellow, † Senior Lecturer, Department of General Practice, University of Melbourne, 200 Berkeley Street, Carlton, VIC 3053. chiro_6AThotmail.com To the Editor: During a recent year-long Primary Health Care Research, Evaluation and Development (PHCRED) research fellowship, we encountered all the usual barriers to undertaking good research (funding, time, etc). While privacy legislation has been reported to adversely affect research,1,2 we were unprepared for the time and cost of dealing with the Health Insurance Commission (HIC — now “Medicare Australia”). Our research involved mailing a survey to Victorian general practitioners. For approved research, the HIC supplies a valuable service in providing representative datasets of randomly selected GPs. This was once a quick and relatively inexpensive process — a boon when conducting research with limited funding. Being the first within our department to use this service since the new privacy laws were introduced, we struck unexpected administrative and financial barriers. To maintain anonymity of potential respondents, research materials (ie, surveys and plain language statements) must be mailed by the HIC. So, all items must first be forwarded to the HIC, from where they are remailed to respondents. This process raises a number of hurdles: materials need to be approved (and altered if required) by the “Privacy” department at the HIC, despite prior approval from a duly constituted university ethics committee; there is a limit of two reminder mail-outs (usual protocols for maximising response rates require up to four mail-outs, and inadequate response rates may render research findings unrepresentative and therefore useless); and each mail-out is sent with the same HIC covering letter. Additional requirements lead to an increase in costs — sending envelopes, surveys and plain language statements in bulk to Canberra (numerous times), printing HIC covering letters, and charges for “preparing business rules, extraction specifications, project manage processes to completion . . .”. The list goes on. We were also charged for extraction of the same dataset again for mailing the reminder letter, as more than 2 weeks had elapsed since the original data extraction. Finally, there is the added time. We estimated this to be around 4 weeks, which is detrimental in a limited fellowship position. While the people we dealt with at the HIC were helpful and professional, the time and expense were almost overwhelming. We respect the need to protect the privacy of research participants. However, the “side effects” of applying the new privacy laws are having an adverse impact on primary health care research. Let this be a friendly warning to all those about to set off down the research path — excessive red tape is no longer the exclusive domain of practitioners.

Simon R Brice · Marie V Pirotta

Kari A J Jarvinen,* Bradley J McCall,† Clare B Nourse,‡ Joe G McCormack,§ Martyn H Tilse¶ * Senior Public Health Registrar, † Public Health Medical Officer, Communicable Disease Control, Brisbane Southside Public Health Unit, 39 Kessels Road, Coopers Plains, QLD 4108; ‡ Paediatric Infectious Diseases Physician, § Director of Infectious Diseases, ¶ Director of Microbiology, Mater Health Services, South Brisbane, QLD. kari_jarvinenAThealth.qld.gov.au To the Editor: Pertussis continues to be a significant public health problem in Australia. Children aged under 1 year are most at risk from severe, life-threatening complications from the disease.1 Traditionally, erythromycin has been the drug of choice for treatment of cases and prophylaxis in selected contacts. However, its use in neonates is known to carry a risk of infantile hypertrophic pyloric stenosis.1,2 Its propensity to cause QT prolongation and ventricular arrhythmias is also well described.2,3 Both azithromycin and clarithromycin have been recently recommended as suitable alternatives for management of pertussis.2,4 The US Centres for Disease Control now regard azithromycin as the agent of choice for neonates less than 1 month of age.1 There is evidence suggesting azithromycin has less pro-arrhythmic potential than erythromycin or clarithromycin.5,6 Azithromycin does not interact significantly with the hepatic cytochrome P450 system and has less potential for significant drug interactions than other macrolide antibiotics.3,5,6 Azithromycin and clarithromycin also require less frequent administration (1–2 doses per day) and shorter treatment regimens (5–7 days) than erythromycin. In Australia, roxithromycin is the most widely prescribed macrolide antibiotic. However, there are no clinical studies on its effectiveness in pertussis, and in-vitro sensitivity studies suggest it may be inferior to erythromycin. Thus, roxithromycin cannot be recommended in pertussis.4 Updated versions of Australian antibiotic guidelines to be released later this year will recommend azithromycin for pertussis treatment and prophylaxis. However, access to azithromycin for this purpose in Australia is currently limited by the restrictions placed on prescribing through the Pharmaceutical Benefits Scheme (PBS). Azithromycin is currently approved for Chlamydia trachomatis urethritis, cervicitis and trachoma. Pertussis is an approved indication only for the use of 500 mg tablets under the Repatriation PBS. This restriction has important implications for the effective and safe management of pertussis in Australia. Widespread use of newer macrolides in the community is not advisable because of the propensity of macrolides to induce antibiotic resistance, and their greater cost. However, for pertussis infection, Australians need to be able to access agents such as azithromycin. PBS restrictions for this indication need to be revised, for both tablet and liquid formulations.

Kari A J Jarvinen · Bradley J McCall · Clare B Nourse · Joe G McCormack · Martyn H Tilse

Michael Guy Duke Psychiatrist, Family Counselling Service, Victorian Aboriginal Health Service, 279 High Street, Northcote, VIC 3070. mmgdukeATbigpond.net.au To the Editor: Rey seems to me to have struck upon the ideal solution for the 20% of Australians who suffer from the various mental illnesses.1 Daniel Defoe (The shortest way with dissenters) would doubtless have approved. There is ample European precedent in the idea of a “ship of fools”. The solution, as Rey says, is to ship everyone diagnosed with a mental illness to a Pacific island. This would solve many problems at a stroke. The population of Australia would be reduced by 20% (and this would be continually improved as more cases develop), thus freeing resources for proper healthy Australians. Thoroughly screened (for mental illnesses) refugees and asylum seekers would easily enter the depleted urban centres. General practices would have a reduction of more than 40% of patients, as we all know this is roughly the percentage of people presenting with primarily mental health problems. No more crisis with general practitioner numbers. Hospitals would have a similar reduction of cases. No more shortages of hospital beds. Single vehicle traffic fatalities would surely reduce, if alcohol and other drug-dependent people were to be included under the umbrella of one of the mental illnesses. I envisage a whole fleet of Tampas flowing back and forth to the Pacific nations, ferrying more than 4 million psychiatric emigrants to their proper places in the world.

Michael Guy Duke

Andrew J A Holland,* Frank I Ross,† Patricia Manglick,‡ Fiona E Fahy,§ Daniel T Cass¶ * Associate Professor of Paediatric Surgery and Urology, † Clinical Nurse Consultant, ‡ Scientific Officer, § Clinical Nurse Consultant, ¶ William Dunlop Professor of Paediatric Surgery and Director of Trauma, Department of Academic Surgery, The Children's Hospital at Westmead, University of Sydney, Locked Bay 4001, Westmead, NSW 2145. andrewh3ATchw.edu.au To the Editor: Several studies from Australasia and North America have identified that in up to 24% of children with pedestrian motor vehicle injuries (MVIs) the event occurred in a driveway.1-4 Earlier work from our centre in Sydney and others in Auckland, New Zealand, highlighted prevention as the most effective method for reducing the morbidity and mortality associated with this unique mechanism of injury.2,3,5 With ethics committee approval, we prospectively reviewed injury circumstances in children under 16 years of age presenting with a driveway MVI to our institution over a 3-year period between June 2002 and May 2005. Of 36 children injured in 35 separate driveway MVIs, 26 caregivers agreed to an interview and scene visit. Fifteen patients (58%) were male, with a mean age of 48 months. The majority of events occurred in western and south-western Sydney — a paediatric population centre — in the afternoon (18; 69%) and on a weekday (19; 73%), with a trend for greater frequency at the beginning and end of the working week. In all but two cases, the injury occurred at the child’s home, which was owned by the parents in 13 cases (50%; with a mean occupation period, 47 months) and rented in 10 (38%; mean occupation period, 22 months). The majority of homes (22; 85%) had no separation between the dwelling, external play areas and the driveway. Even when a separation was present, this had been circumvented. Sedans were the most common vehicle involved (18; 69%), with the remainder four-wheel drives (4WDs) or light commercial vehicles, and 22 (85%) were reversing. The vehicle was driven by an adult known to the child in 21 cases, but in four the vehicle was inadvertently set in motion by another child. Box 1 reports parental perception of contributing factors and Box 2 lists injuries sustained, with 23 (89%) children receiving injuries severe enough to warrant hospital admission. There were no deaths. This review indicates that driveway MVIs persist as a common and potentially fatal problem for children in New South Wales, with at least one child injured every month.2 Following our previous study published in 2000, and findings of the NSW Child Death Review Team, campaigns by the Motor Accidents Authority of NSW and others have focused on driveway safety, particularly for young children. This review suggests that further intervention is needed to reduce the frequency of these injuries, either through enhanced application of present strategies or the development of more effective, novel approaches. 1 Parental perception of factors contributing to their child sustaining pedestrian motor vehicle injuries in the driveway Lack of supervision 15 Child playing in parked car 5 Children’s behaviour around cars 5 Negligent driving 2 Excessive speed 2 Hand brake not applied 1 Front house door left open 1 Hurrying when leaving home 1 2 Injuries identified in children sustaining pedestrian motor vehicle injuries in the driveway Head and neck Skull fracture 1 Intracranial haematoma 1 Concussion 2 Retropharyngeal haematoma 1 Torso Hepatic contusion 1 Adrenal haematoma 1 Haemopneumothorax 1 Multiple rib fractures 1 Pelvic fracture 1 Major soft tissue injury 1 Limb Fractures 2 Burns Full thickness 4 Partial thickness 3 Major soft tissue injury 1 Minor soft tissue injury 17

Andrew J A Holland · Frank I Ross · Patricia Manglick · Fiona E Fahy · Daniel T Cass

Neville R Blomeley President, Sports Doctors Australia, and Medical Director, Optima Sports Medicine, 6/66 Station Road, Indooroopilly, QLD 4068. drnbauscareindATbigpond.com Comment: I would like to draw readers’ attention to a very enthusiastic and active group of sports medicine practitioners that was not mentioned in the editorial by Orchard and Brukner,1 which introduced the Sports Medicine Practice Essentials series. Sports Doctors Australia comprises general practitioners and others from areas such as orthopaedics, rehabilitation, accident and emergency, and sports dentistry. Virtually all fellows of Sports Doctors Australia (SDrA) have obtained a postgraduate degree in sports medicine from an Australian university (most commonly a masters degree from the University of New South Wales). We are committed to delivering excellent care in all areas of sports medicine to the general public as well as to elite athletes. Because of our wider background in general medicine, we are in an ideal position to provide overall care to teams and individual athletes. Many of our fellows are, or have been, very successful team doctors for national teams. A number of fellows are active in clinical research and have academic appointments with university medical schools. Our main aim is not to obtain specialist status (as it is for members of the Australasian College of Sports Physicians), but to provide excellence in sports medicine care for athletes at all levels, and to provide sports medicine education to other doctors, medical students and the general public.

Neville R Blomeley

Garry J Walter Professor of Child and Adolescent Psychiatry, Coral Tree Family Service, University of Sydney, PO Box 142, North Ryde, NSW 1670. gwalterATmail.usyd.edu.au To the Editor: I read with interest Brooks’ letter on the value of professorial titles.1 It is not only in academic circles that the subject sometimes arouses passions. A short while ago, my wife had reason to speak sternly to our two young children. Losing the plot, my daughter replied, “What would you know, mum? You’re not a professor.” At that moment in this household, as I found myself slinking towards my study, the status of a professorial title — at least in my wife’s eyes — amounted to very little.

Garry J Walter

Christina V T Ng Specialist and Lecturer — Medical Oncology, Department of Medicine, University Malaya Medical Centre, Jalan Universiti, Lembah Pantai, Kuala Lumpur, 59100, Malaysia. christinavtngAThotmail.com To the Editor: I would like to clarify several issues pertaining to the case report published in the 7 February 2005 issue of the Journal.1 The patient reported was under the care of Dr Craig Underhill and Dr Kerrie Clarke, who are medical oncologists at Albury Base Hospital, Albury, New South Wales. Their contribution to the reporting of this rare and interesting case must be acknowledged. I regret any misconceptions arising from this article, and I would like to thank Dr Underhill and Dr Clarke for their support and professionalism.

Christina V T Ng

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

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

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

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

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

Graham Simpson · Paul Clark · Trevor Knight

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

Roslyn G Poulos · Anthony B Zwi

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

Keith V Woollard

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

R Michael Whitby · Mary-Louise McLaws

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

Paul D R Johnson · M Lindsay Grayson

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

C Raina MacIntyre · Catherine L King · David Isaacs

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

Richard H Riley

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

Charles Teo

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

Ivan Cher

Elizabeth May Pepper,* Dominique A Cadilhac,† Dora C Pearce,‡ James Burrow,§ Tarun S Weeramanthri¶ * Neurology Registrar, John Hunter Hospital, Newcastle, NSW. † Manager, Public Health Division; ‡ Biostatistician; National Stroke Research Institute, Melbourne, VIC. § Neurologist; ¶ Physician, Royal Darwin Hospital, NT. hornblowerATinternode.on.net To the Editor: Although the age-standardised stroke mortality rates among Australia’s Indigenous people is more than twice that of the non-Indigenous population,1 the medical literature contains only one audit of Indigenous stroke patients in Perth metropolitan hospitals.2 No review of hospital care has been reported. Royal Darwin Hospital (RDH) is the referral centre for Australia’s “Top End”, where 8.7% of Indigenous Australians reside; 40% of RDH inpatients are Indigenous. In 2002, while planning for the RDH stroke service, we audited stroke admissions from the previous year. Among 121 eligible patients admitted between 1 July 2001 and 31 June 2002 with International classification of diseases, 10th revision, Australian modification (ICD-10-AM) codes 160–164 (haemorrhages [subarachnoid, intracerebral, other non-traumatic intracranial] and cerebral infarction), records for 116 (96%) were available, but six patients were excluded because of incorrect coding. Box 1 outlines patient characteristics, while Box 2 examines risk factors and medication use for ischaemic stroke (because haemorrhages were few). Despite the observed differences between subgroups, there were no significant differences in mortality (4/36 for Indigenous v 7/42 for non-Indigenous; P = 0.204) or stroke severity at admission or discharge. Box 3 highlights differences in risk factors between Indigenous males and females. Retrospective data, particularly from a sample identified by medical record coding, should be interpreted with caution. In addition, the potential for random error due to small numbers, and the referral bias inherent in tertiary hospital admissions, mean our results may not truly represent the “Top End” Indigenous population. However, our data corroborate findings that Indigenous Australians suffer premature cerebrovascular disease, and have higher rates of vascular risk factors than other Australians,1 with some risk factor differences between males and females. Further, recent evidence suggests differences in standards of stroke care in regional (Queensland) hospitals.3 We found disparity in hospital care of Indigenous patients, and this requires further detailed investigation. A prospective, community-based study is urgently needed. 1 Baseline characteristics for 110 patients admitted to Royal Darwin Hospital with subarachnoid, intracerebral, and other non-traumatic intracranial haemorrhages and cerebral infarction in 2001–02 Baseline characteristics Indigenous Other P Number of patients 45 65 Female sex 22 (49%) 19 (29%) 0.018 Mean age (years) 54 61 0.005 Rural dwelling 41 (91%) 22 (34%) < 0.001 Ischaemic stroke 36 (80%) 42 (65%) 0.081 2 Risk factors and medication use for the 78 patients who had ischaemic stroke Risk factors and medications Indigenous Other P All patients 36 42 Smoking 23 (64%) 11 (26%) 0.001 Diabetes mellitus 16 (44%) 10 (24%) 0.030 Rheumatic heart disease 8 (22%) 1 (2%) < 0.001 Males 19 (53%) 30 (71%) 0.089 Smoking 14 (74%) 12 (40%) 0.017 Diabetes mellitus 10 (53%) 7 (23%) 0.030 Females 17 (47%) 12 (29%) 0.089 Smoking 9 (53%) 0 0.002 Rheumatic heart disease 6 (35%) 0 0.026 Antiplatelet therapy Before admission 11 (31%) 19 (45%) 0.078 Admission 20 (56%) 38 (91%) < 0.001 Discharge 18/32 (56%) 29/35 (83%) 0.013 Anticoagulant therapy Before admission 4 (11%) 1 (2%) < 0.001 Discharge 4/32 (13%) 6/35 (17%) 0.235 3 Risk factor differences between Indigenous males and females who had ischaemic stroke Males Females P Number of patients 19 17 Hypertension 16 (84%) 6 (35%) 0.003 Non cerebral vascular disease 6 (32%) 1 (6%) < 0.001 Excessive alcohol intake 7 (37%) 1 (6%) < 0.001

Elizabeth May Pepper · Dominique A Cadilhac · Dora C Pearce · James Burrow · Tarun S Weeramanthri

Annabelle D Donaldson,* Raymond C Chan,† Iain B Gosbell‡ * Infectious Diseases Registrar, Department of Microbiology and Infectious Diseases, Liverpool Health Service, Sydney, NSW; † Infectious Diseases Physician, ‡ Director, Department of Microbiology and Infectious Diseases, South Western Area Pathology Service, Locked Bag 7090, Liverpool BC 1871, and Conjoint Associate Professor, School of Medical Sciences, University of New South Wales, Sydney, NSW. i.gosbellATunsw.edu.au To the Editor: Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is usually susceptible to a wider range of antibiotics than nosocomial or multiresistant MRSA, but evidence is lacking to guide antibiotic choices. Rifampicin plus fusidic acid is commonly used in multiresistant MRSA infection, and familiarity makes this combination attractive for CA-MRSA. We report two cases of CA-MRSA infection in which rifampicin resistance developed during treatment. Non-compliance may have been a significant factor, but high bacterial load and persistent foci of infection were also likely contributors. We caution against using regimens containing rifampicin in such cases. Patient 1: A previously well 16-year-old girl presented with a 4-day history of left knee pain. She had fever and a moderate joint effusion. Plain x-rays were unremarkable, and blood cultures showed no growth. An aspirate of the knee joint had a white blood cell count of 1100 × 106 cells/L, but showed no growth on culture. Non-multiresistant MRSA (sensitive to all non-β-lactams) was subsequently grown from a synovial biopsy specimen. She was treated with 7 weeks of intravenous vancomycin, followed by 6 months of oral rifampicin (450 mg daily) plus fusidic acid (500 mg twice daily). Her compliance was uncertain, and she did not return for follow-up appointments. The patient presented again 12 months later with increasing pain in the left knee and thigh. X-ray and magnetic resonance imaging revealed extensive osteomyelitis of the distal femur. Culture of purulent material removed at sequestrectomy grew MRSA with the same sensitivity profile as previously, but now resistant to rifampicin. She was treated with clindamycin, but required further sequestrectomy. She continues to take clindamycin long term. Patient 2: A 74-year-old man developed severe cellulitis and an abscess of his left hand after a golfing injury. He had bacteraemia with non-multiresistant MRSA (sensitive to all non-β-lactams). He also had significant pain in his left prosthetic hip. After 7 weeks of intravenous vancomycin and oral moxifloxacin, levels of inflammatory markers remained high. He was treated with oral rifampicin (600 mg daily) plus fusidic acid (500 mg twice daily) for several weeks until lost to follow-up. Four months later, the patient still had pain in the hip, and rifampicin plus fusidic acid treatment was begun again. After 3 months with no improvement, he underwent surgical exploration, and the loose femoral prosthesis was replaced. Culture of debrided material showed MRSA with the same sensitivity pattern as previously, but now resistant to rifampicin. He was treated with intravenous vancomycin for 6 weeks, followed by trimethoprim–sulfamethoxazole, which was later changed to clindamycin because of intolerance. He remains taking indefinite clindamycin suppression therapy. Traditional oral therapy for MRSA infection is rifampicin plus fusidic acid, but alternative oral agents for non-multiresistant CA-MRSA include clindamycin,1 tetracyclines2 and trimethoprim–sulfamethoxazole.3 There is wider experience with clindamycin, which penetrates well into skin and soft tissues, has good oral bioavailability, and has been used successfully.1 However, a concern is erythromycin-inducible clindamycin resistance, which may lead to clindamycin failure, particularly in severe infections.4 Its prevalence varies. Studies in vitro have shown that rifampicin resistance develops as readily in CA-MRSA as in nosocomial MRSA,5 through a single-step mutation. Resistance did not develop in vitro to clindamycin,5 suggesting it may be a more reliable alternative in situations where compliance is uncertain, the bacterial load is high, or the source (eg, an infected prosthesis) cannot be removed. Further in-vitro and in-vivo investigations are urgently required to determine the optimal drug therapy for CA-MRSA infections.

Annabelle D Donaldson · Raymond C Chan · Iain B Gosbell

Tania Shelby-James,* Amy P Abernethy,† David C Currow‡ * Research Fellow, Southern Adelaide Palliative Services, Repatriation General Hospital, 700 Goodwood Road, Daw Park, SA 5041; † Assistant Professor of Medicine, Duke University Medical Center, Durham, North Carolina, USA; ‡ Professor, Department of Palliative and Supportive Services, Flinders University, Adelaide, SA. tania.shelby-jamesATrgh.sa.gov.au To the Editor: Aoun and Kristjanson’s article highlighted some of the difficulties facing researchers in palliative care1 and questioned the role of randomised controlled trials (RCTs). These difficulties do not exempt palliative care from seeking to improve care through thoughtful research but, rather, highlight areas that need to be specifically designed to cope with these difficulties. In our recently completed large RCT of palliative care in southern Adelaide, for which we recruited 461 patients,2 we were able to overcome many of the obstacles cited by these authors. As they rightly stated, many trials in palliative care are pragmatic. This should not be seen as a bad thing, as pragmatic studies are designed to test clinically relevant interventions3 within diverse populations across different settings and to report on a broad range of health outcomes. Such studies are more in keeping with the realities of palliative care. We would argue that traditional RCTs that examine a specific intervention within a specific patient type are less applicable to a palliative care population. In such a population, unlike many other areas of health, the diagnosis and prognosis do not dictate care needs. Among the methodological issues, recruitment and retention are perhaps the biggest hurdles to be overcome. We found that developing systematic, evidence-based protocols, which were pilot tested before initiating the trial, significantly enhanced recruitment.4 To minimise burden, we ensured that all data collection was kept to a minimum and, where possible, data were recorded by study staff or collected from other sources as part of routine clinical encounters. Sample size calculations need to allow for attrition caused by increasing severity of disease. This will, however, inflate the numbers required for a study. Use of multiple sites for recruitment is a strategy that we have used successfully to reach sample size goals. The article states that “RCTs are seldom acceptable to patients and their families”.1 This has not been our experience. Patients are willing to participate in research and find it a meaningful way to give back to the community.5 The challenge is to ensure that this willingness to participate in research is not exploited by palliative care researchers. The other ethical concern raised by Aoun and Kristjanson is the use of a control arm in which patients “deliberately have support services withheld”. We would agree that, if that were to happen, it would be a serious ethical breach. For RCTs in palliative care, the control arm should consist of the standard care provided — the rationale for doing a trial is that there is equipoise regarding the benefit of the intervention. We feel that RCTs are feasible and appropriate for palliative care research.

Tania Shelby-James · Amy P Abernethy · David C Currow

Jennifer Tieman,* David C Currow† * Project Manager, † Head, Department of Palliative and Supportive Services, Flinders University, c/- Repatriation General Hospital, 700 Goodwood Road, Daw Park, SA 5041. Jennifer. TiemanATflinders.edu.au To the Editor: Aoun and Kristjanson’s viewpoint on palliative care research reminds us of the possible limitations of an evidence schema that is built on efficacy of intervention studies.1 For emerging fields and for care areas that cross disciplines, the possible sources of useful knowledge to guide practice — particularly in advance of the establishment of a significant evidence base — need to be recognised and valued. To further complicate the gathering of evidence for such fields are the difficulties of accessing useful knowledge. Preliminary research on search strategies suggests that even good quality searches may recover fewer than half the articles relevant to palliative care in the general biomedical literature.2 More disturbing is the possibility that much of the research and thought in this field is not published, and therefore cannot be easily and actively searched. In a systematic review of publication rates associated with conference presentation, the usual publication rate was seen to be around 45%.3 A recent investigation into publication rates associated with conference presentation in palliative care in Australia suggests a “conversion” rate of less than 20%.4 Publication represents an important step in the spectrum of knowledge dissemination. Such a low rate of publication of conference abstracts therefore represents a significant loss of information, opinion and evidence for the discipline of palliative care. Evidence issues for complex and emerging areas are complicated not only by the restrictions of an evidence hierarchy that is intervention based, but also by the difficulties in searching and retrieving existing knowledge and evidence in such fields.

Jennifer Tieman · David C Currow

C Scott Masters,* Michael J Yelland† * Vice-President, Australian Association of Musculoskeletal Medicine, Caloundra Sports Medicine Centre, 39 Minchinton Street, Caloundra, QLD 4551. † Associate Professor of Primary Health Care, Griffith University, QLD. scotty1ATozemail.com.au To the Editor: Paoloni and Orchard provided a concise summary of the evidence for injections for soft-tissue injuries,1 but omitted some important references on the mechanism of action of corticosteroids and on prolotherapy. An important action of corticosteroids is blocking of transmission in nociceptive C-fibres.2 Given the lack of evidence of inflammation in chronically painful tendinopathies,3 this is a more probable mechanism of action than the suppression of inflammation. Paoloni and Orchard correctly report that steroids have only a temporary effect in suppressing soft tissue pain. However, in low back pain, if their use is preceded by manual therapy and exercises they have the potential to give more prolonged relief of pain and disability.4 A recent Swedish randomised controlled trial (RCT) of polidocanol prolotherapy injections for chronic Achilles tendinopathy showed reduced pain and normalisation of ultrasound abnormalities.5 Similarly, a New Zealand case series of glucose prolotherapy injections showed very positive results for the same condition.6 An Australian RCT into prolotherapy for chronic low back pain (average duration, 14 years) showed sustained reductions in pain and disability with glucose prolotherapy injections, although similar results were obtained with saline injections.7 A pilot study of glucose prolotherapy in 24 elite male kicking-sport athletes with chronic groin pain (mean duration, 15.5 months) who had failed physical therapy reported a pain-free state and return to sports in 82% at an average follow-up of 17.2 months.8 This evidence would suggest there is a role for this glucose prolotherapy in managing soft-tissue pain, especially as musculoskeletal pain is one of the major presentations to primary practice in Australia. Training primary care physicians in prolotherapy injection techniques should be a priority in medical education.

C Scott Masters · Michael J Yelland

Justin A Paoloni,* John W Orchard† * Conjoint Senior Lecturer, Orthopaedic Research Institute, St George Hospital Campus, University of New South Wales, Sydney, NSW. † Sports Physician, Sports Medicine at Sydney University, Sydney, NSW. pao_26AThotmail.com In reply: We thank Masters and Yelland for their interest in this topic and their notification of additional references, some of which were published after our article was written. We stated in our article that “the mechanism of any effect of corticosteroid injections in reducing symptoms in purely degenerative tendinopathies is unknown”, and that only where bursitis or tenosynovitis is present would the implication of an anti-inflammatory effect be appropriate.1 While blocking nociceptive C-fibres in normal tendon is demonstrated in the study quoted by Masters and Yelland,2 we still believe that corticosteroids should be used with caution for any tendinopathy where tendon weakening would be potentially harmful. We agree that corticosteroids have a much greater potential role in low back pain, which is a broad entity involving both soft-tissue and joint disorder. At the time of writing our article there was a pilot study on polidocanol in painful tendons displaying neovascularisation;3 we thank the authors for advising that a randomised controlled trial has since been published.4 While undoubtedly an exciting new therapy, proponents of polidocanol do not consider its mechanism to be simply a “prolotherapy” effect; they also consider sclerosing the neovessels to be critical, and therefore, that hypertonic glucose (the most commonly recommended prolotherapy agent) may not work as well. We still maintain that prolotherapy currently lacks evidence of efficacy for the treatment of soft-tissue injury in general, although it is relatively cheap and generally free of side effects. Both chronic low back pain, and chronic groin pain, are multifactorial conditions involving joint/bone abnormality which we considered slightly beyond the scope of an article on soft-tissue injuries. We await further publications on the efficacy of prolotherapy with interest.

Justin A Paoloni · John W Orchard