Letters

To the Editor: We recently treated two patients with invasive meningococcal disease presenting with cellulitis. This presentation contributed to a delay in diagnosis and appropriate antibiotic treatment. The first patient was a 33-year-old woman, recently diagnosed with nephrotic syndrome, who had been unwell for a week with mild upper respiratory tract symptoms. During this time, her nephrologist began treating her with prednisolone (15 mg daily). The day before presentation, she developed abdominal pain, vomiting, chills, myalgia and headache. A rash developed on the day she presented to hospital. The temperature was 39.2°C, heart rate 148 beats per min, and blood pressure 146/57 mmHg. She had an area, measuring 20 cm × 20 cm, of tender cellulitic rash on the right thigh (Box) and mild neck stiffness. The diagnosis was initially unclear, leading to a delay of several hours before ceftriaxone was administered, and a lumbar puncture performed. Cerebrospinal fluid (CSF) examination revealed a leukocyte count of 4500 × 106/L (98% polymorphs) (reference range [RR], < 5 × 106/L), gram-negative diplococci, and protein concentration of 2073 mg/L (RR, 150–450 mg/L). The patient subsequently required intensive care admission for non-invasive ventilation and inotropic support. Neisseria meningitidis serotype C was detected in the CSF by polymerase chain reaction testing. The patient was discharged well except for mild headache and lethargy after 6 days. At 1-week review, she remained lethargic but was otherwise well. The rash was slowly resolving. The second patient was a 51-year-old woman with fever and a 2-day history of progressive pain, swelling and erythema of the anterolateral area of the neck. The temperature was 38.5°C, heart rate 115 beats per min, and blood pressure 134/86 mmHg. There was no evidence of upper airway involvement. The anterior area of the neck and upper chest wall were swollen, erythematous, tender and warm. No fluid collections or masses were detected on ultrasound examination. The patient was admitted to hospital with a diagnosis of cellulitis, and treatment was begun with intravenous flucloxacillin and metronidazole. After 17 hours, culture of blood taken on admission showed N. meningitidis serotype W135. Antibiotic treament was changed to ceftriaxone. After 5 days, the patient had mild residual inflammation and tenderness of the neck. She completed another week of treatment with oral amoxycillin. Only 14 cases of N. meningitidis cellulitis have been published.1-3 Seven cases involved children with periorbital cellulitis. In adults, three cases involved the face and neck, and four the limbs. N. meningitidis was isolated from blood (eight patients), conjunctival swabs (three), aspirates of the cellulitic areas (two) or CSF (one). There was one death: an elderly woman with bacteraemia and cellulitis of the face and neck.2 As illustrated by our cases, the many guises of meningococcal disease continue to challenge clinicians. Cellulitis in Patient 1 Cellulitic area on the right thigh of a 33-year-old woman with Neisseria meningitidis meningitis.

Karina J Kennedy MB BS · Jhumur Roy MB BS, FRCPA · Paul Lamberth MB BS, FACEM

To the Editor: The CanMEDS 2000 report1 and its 2005 revision2 have emphasised that effectiveness as a medical specialist requires competencies in addition to clinical and medical expertise. These include being a communicator, collaborator, manager, health advocate, scholar and professional. Building the non-clinical skills of doctors has been the focus of a professional development project in Australia that is targeting registrars. Junior doctors usually step up to the role of registrar in the 3rd year of their prevocational training. A national workshop convened by the Postgraduate Medical Council of Victoria in March 2004 agreed on a framework for the professional development of registrars, comprising the following 10 competencies: leadership; communication skills; supervision; mentoring; teamwork; self-awareness and empathy; time management; problem solving; professionalism and ethics; and safety and quality.3 To provide content for these competencies, a job-shadowing exercise involving two registrars at two different Victorian hospitals was undertaken in April 2005 to get a first-hand understanding of the roles of medical registrars as managers. The registrars were voluntary participants, and permission was obtained from all participants. I shadowed the two registrars during their entire 9-hour shifts. No major issues arose in relation to the shadowing process itself, and the consultants overseeing the two registrars were extremely accommodating in this process. The two observed registrars authenticated the veracity of the recorded observations. The observations from the job-shadowing exercise were clustered into competencies using the framework developed for the professional development of registrars discussed above. The Box summarises these observations and highlights the range of registrar interactions that are influenced by non-clinical competencies. While the small number of registrars is an obvious limitation of the study, this job-shadowing exercise did demonstrate that managerial skills, knowledge and behaviour represent a significant component of the work of clinicians, especially as they move up the medical hierarchy. This assertion should not be misconstrued as suggesting that the clinical skills and knowledge become any less important. As noted in the 2005 CanMEDS framework, the medical expert role is the central role for doctors. It is also worth noting here that some pilot professional development programs conducted recently as part of the registrar project show that registrars welcome training that enhances their non-clinical skills, especially when provided professionally in an environment conducive to learning. Observations during job-shadowing of two registrars at two Victorian hospitals Competency Observed interactions Supervision Reviewing patient treatment plans and test results and prescribing a course of action Ensuring that procedures are followed Coaching intern on test procedures, completion of patient records, etc Giving ongoing feedback to intern Delegating tasks to intern Coordinating patient treatment with other units Leadership Dealing with other health professionals, some of whom take directions from the registrar, as well others over whom there is no formal authority Providing advice to intern and role modelling desired behaviour Demonstrating the ability to respond quickly and with confidence Involving subordinates and providing opportunities for them to participate in decision making Using networking skills with other departments Using negotiating skills in dealing with other departments, hospitals, etc Communication skills Using communication skills with patients, intern, medical colleagues, other health care professionals, and service departments Dealing with cross-cultural diversity issues with patients, their families, and staff Using negotiating skills in dealing with other departments, hospitals, patients, and family members Using recording skills to ensure treatment plans properly documented for others Time management Prioritising patient list for ward rounds The constant need to re-assess priorities during ward rounds, in light of time constraints The ability to deal with constant interruptions from other colleagues, to provide necessary clarifications Problem solving Making decisions on patients’ continued treatment or discharge, and stipulating any follow-up action Task contingency management skills to deal with patient treatment plans not proceeding as planned Dealing with information gaps in patient historical records Involving intern and other staff to assist in the decision-making process and raising issues with consultant Professionalism and ethics Dealing with demarcation issues with other doctors and professionals Role modelling professional behaviour to patients, staff, and the public Balancing the interests of patients with hospital needs, without sacrificing patient trust Obtaining patient consent for procedures Teamwork Coordinating treatment plans with other doctors and health professionals Sharing information and agreeing on treatment plans with allied health staff Joint meeting with other colleagues to advise a patient and family members on surgical procedures and associated risks Ability to work in both collaborative and individual modes during the day Mentoring Providing advice to intern to be more assertive and confident when dealing with consultant Self-awareness and empathy Patience and empathy in giving bad news to family Dealing with patients who are aged or mentally or physically challenged Safety and quality Knowledge and application of safe practices in relation to patient management Ensuring that procedures are followed, such as obtaining consent, ordering of tests, etc Reviewing records before dispensing treatment Recording treatment plans and medications

Jagdishwar Singh PhD

To the Editor: We were pleased to read Turnbull and Parisi’s short piece on the effectiveness of shade structures, highlighting the challenges of ensuring adequate and effective shade protection, particularly in children’s settings.1 Cancer councils in various states have long recognised these challenges and provided assistance to those who design or manage facilities for children, in the form of training workshops, resources and guidelines. Epidemiological evidence indicates that childhood exposure to ultraviolet (UV) radiation is a strong determinant of risk of melanoma but there is also evidence of its contribution to the development of non-melanocytic skin cancer.2,3 It is estimated that living in Australia for the first 15 years of life contributes about two-thirds of the lifetime risk of melanoma of a lifelong resident.4 Sun exposure in childhood, especially that leading to sunburn, is the main environmental determinant of the number of melanocytic naevi. An individual’s number of naevi is the strongest measurable predictor (after age and ethnicity) of risk of melanoma.5 Our publication, Under Cover, referred to by Turnbull and Parisi, is one such resource, developed as a comprehensive reference tool for anyone involved in shade planning and design in New South Wales and has been adapted for use in other states by state cancer councils.6 Turnbull and Parisi comment that Under Cover provides inappropriate advice regarding the use of deciduous trees, as solar UV radiation levels can be hazardous during winter in subtropical Queensland. As might be expected, the NSW edition of Under Cover does not address winter solar protection issues in northern Queensland. We note that the “requirements for effective shade” cited by Turnbull and Parisi are identical to those prescribed in Under Cover. For those interested in determining when UV protection is required throughout the year in different locations, an interactive shade planning software program will be available shortly at <www.webshade.com.au>. In it, ShadeCalendar recommends what type of shade would be most appropriate for comfort and solar protection in different months of the year. The Bureau of Meteorology now issues the SunSmart UV Alert when the UV Index is forecast to reach 3 or above, highlighting when sun protection is required (www.bom.gov.au/products/uvindex_national.shtml). The SunSmart UV Alert is reported in most newspaper, television and radio weather forecasts across Australia. Shade is only one of a range of sun protection strategies recommended by the Cancer Council. With Australia having the highest skin cancer rates in the world, general practitioners play a pivotal role in providing sun protection counselling advice to parents of children aged 1–13 years.7 The Cancer Council NSW recommends a range of sun protection measures including UV avoidance during the peak UV times (10:00–14:00 or 11:00–15:00 during daylight saving time), shade, clothing, hats, sunglasses and use of sun protection factor 30+ broad spectrum, water resistant sunscreen.

Kay R Coppa MPH · John S Greenwood

To the Editor: Investigators in the recent Canberra Heart Study1 highlighted the importance of improving the detection of heart failure in the community, given the high proportion of people with preclinical disease. The accompanying editorial2 expressed concern about the lack of major Australian initiatives that focus on the prevention and treatment of this disease. We fully endorse the authors’ view that under-recognition and under-treatment of heart failure is an important national issue. While we support their call for sustained and adequately funded programs, we feel it is important to note that there are initiatives under way to attempt to improve the situation. The National Prescribing Service, the National Heart Foundation of Australia and the National Institute of Clinical Studies joined forces in 2004 to improve the diagnosis and management of heart failure in primary care. A national program, undertaken in partnership with 45 divisions of general practice, began in October 2004 and will conclude in early 2006. Nationally, the program provided newsletter materials to all general practitioners, pharmacists and physicians.4 In participating divisions, educational outreach visits and interactive small group meetings involved over 1600 GPs and local specialists in discussions of the role of echocardiography in diagnosis, and pharmacological and lifestyle management issues. Patient education materials were also widely disseminated.5 Outcomes of this large-scale quality improvement program are currently being evaluated, and results are expected to be available in early 2007. Other groups have also recognised heart failure as an important issue — for example, it is one of the featured conditions in the Department of Veterans’ Affairs Medicines Advice and Therapeutics Education Services program.6

Heather H Buchan MBChB, MSc, FAFPHM · Susan M Phillips DPhil · Lynn M Weekes BPharm, MSc, PhD · Judith M Mackson BPharm, MMedSci(ClinEpi) · Andrew N Boyden MB BS(Hons), MPH, FRACGP · Andrew M Tonkin MB BS, MD, FRACP

To the Editor: Q fever is a serious disease caused by Coxiella burnetii, and usually occurs in people exposed to livestock. In Australia, acute Q fever generally manifests as nonspecific febrile illness. We report a case of spontaneous splenic rupture as a complication of acute Q fever acquired in Australia. A 29-year-old, previously well man presented in March 2005, with 5 days of fever, rigors and severe headache. On examination he had a temperature of 40°C, was tachycardic at 100 beats per minute, but normotensive. There were no focal examination findings. Investigations revealed thrombocytopenia at 123 × 109/L, a normal white cell count, and clear chest x-ray. The patient worked at a factory that processed animal placentas and fetal products. A provisional diagnosis of Q fever was made based on the illness and this exposure. The man was admitted and treated with empiric doxycycline, penicillin, and ceftriaxone. On Day 1 of the admission, he developed sudden, severe, left upper quadrant abdominal pain with shoulder tip radiation, diaphoresis and hypotension. An urgent computed tomography scan of the abdomen revealed splenomegaly with a diameter of 14 cm, and a crescentic, subcapsular splenic haematoma with rupture into the peritoneal space (Box). There was no history of trauma. He was admitted to the high dependency unit for monitoring. His haemoglobin level dropped from 151 g/L to 102 g/L, but he was managed conservatively and discharged from the high dependency unit 24 hours later. Acute Q fever was confirmed by polymerase chain reaction on Day 2, and antibiotic therapy was simplified to doxycycline 100 mg twice daily for 14 days. He was discharged from hospital on Day 5, and recovered fully. Seroconversion to Q fever was subsequently confirmed. His workplace now practices Q fever prevention policies, including pre-employment vaccination. Common presentations of Q fever include nonspecific febrile illness, pneumonia and hepatitis. There are five reported cases of Q fever associated with spontaneous splenic rupture, but this is the first Australian case.1-5 The other patients presented with flu-like symptoms and abdominal pain of 2–14 days’ duration, and required splenectomy between Day 1 and 4 of admission. Clinicians should be aware of splenic rupture as a potential complication of Q fever in Australia. Abdominal computed tomography scan A crescentic, subcapsular splenic haematoma is visible (arrow).

Amanda J Wade MB BS · Tim Walker MB BS · Eugene Athan MB BS, FRACP · Andrew J Hughes MB BS, FRACP

To the Editor: Current Australian guidelines for urgent warfarin reversal recommend withholding warfarin, and giving vitamin K as well as factor replacement (Prothrombinex HT; PTX) with or without fresh frozen plasma (FFP).1 PTX administration without FFP is recommended only when FFP is unavailable, as PTX factor VII levels are low and unquantified.2 Transfusion of 25–50 IU/kg PTX and 150–300 mL of FFP is advised. We examined the effectiveness of warfarin reversal using PTX alone or combined with FFP. One hundred and fifty-five patients given PTX were identified from the transfusion medicine unit’s computer records. Fifty patients were excluded — no warfarin (19), non-hospital patients (11), no record of PTX administration (14), no monitoring (5), normal international normalised ratio (INR) (1). One hundred and five patients who had received warfarin were reviewed. The reasons for anticoagulation were atrial fibrillation (45 patients), venous thromboembolism (22 patients), cardiac valve replacement (21 patients), myocardial infarction (9 patients), and other (8 patients). PTX was administered for bleeding in 51 patients (32 had major bleeds), suspected bleeding in eight patients, high INR in 11 patients, and before a procedure in 35 patients. Bleeding severity was graded using published criteria.3 Post-treatment INR and patient details were used to determine clinically significant INR lowering and haemostasis. The patients were divided into two groups — patients administered PTX without FFP (n = 74) and patients administered PTX and FFP (n = 31) (Box 1). Seventy-four patients (71% receiving PTX; 67.7% PTX + FFP) were given vitamin K (71 intravenously) to ensure ongoing correction of coagulopathy. This was administered within 2 hours of PTX (77%), with doses 1–2.5 mg (44 patients), 3–6 mg (13 patients), and 10 mg (17 patients). The mean PTX dose used was 862 IU or 12.9 IU/kg. Slightly higher PTX doses were administered to patients in the PTX group (913 IU or 13.1 IU/kg) than to patients receiving PTX and FFP (742 IU or 12.3 IU/kg) (Box 1). Seven of 89 patients (7.9%) received the published recommended PTX dose.1 The remaining patients received < 25 IU/kg. Neither the degree of warfarin coagulopathy nor FFP transfusion appeared to influence PTX doses administered. One patient in the PTX group with end-stage renal impairment failed to show any reduction in INR, but did achieve haemostasis. All patients with bleeding achieved haemostasis after PTX. The degree of INR correction after PTX varied considerably, with the percentage reduction in INR after PTX ranging from 0 to > 90% per vial of PTX transfused (Box 2). Achievement of haemostasis did not require normalisation of INR (Box 2). The INR is designed for monitoring therapeutic warfarin levels and its accuracy declines with excessively prolonged clotting times. As PTX is more likely to produce correction of coagulopathy through increased thrombin rather than through factor VII replacement, INR may not be the best test for monitoring haemostatic changes after PTX. Our data suggest that FFP may be unnecessary when PTX is used to reverse warfarin coagulopathy. We have also shown that doses of PTX under 25 IU/kg are effective. Administration of low-dose PTX will produce cost savings and may reduce PTX-associated adverse events (including infusional reactions, thrombocytopenia [secondary to heparin], and thrombosis). The risks associated with FFP transfusion (including allergic reaction, transfusion-related acute lung injury, fluid overload, and infection transmission) would be eliminated. A prospective study is necessary to confirm our findings and assess the efficacy of lower PTX doses, so that, if our results are confirmed, warfarin reversal guidelines can be reviewed. 1 International normalised ratio (INR) before transfusion of Prothrombinex HT (PTX) and dose of PTX in patients in the two groups (PTX and PTX + fresh frozen plasma [FFP]) at increasing levels of anticoagulation INR before PTX PTX group (n = 74) PTX + FFP group (n = 31) No. of patients PTX dose IU (range) PTX IU/kg* (range) No. of patients PTX dose IU (range) PTX IU/kg† (range) FFP units (range) < 2.0 8 556 7.69 1 500 9.09 2 (500–1000) (5.32–11.1) — — — 2.0–3.9 22 929 12.81 16 562 8.48 2.2 (500–2000) (4.85–31.25) (500–1000) (5.1–17.54) (1–10) 4.0–5.9 12 1083 16.2 7 1000 15.51 4 (500–3000) (6.67–34.8) (500–2000) (7.14–44.4) (2–6) 6.0 + 32 1187 14.17 7 929 12.65 4.7 (500–2000) (4.17–27.03) (500–1000) (7.69–19.23) (2–10) * PTX doses calculated for the 89% of patients in the PTX group whose weight was recorded in notes. † Doses calculated for the 77% of patients in the PTX + FFP group whose weight was recorded in notes. 2 Absolute and percentage reduction in international normalised ratio (INR) per vial of Prothrombinex HT (PTX) transfused for the 74 patients in the PTX group (treated with PTX without fresh frozen plasma) INR after PTX INR before PTX < 1.5 1.5–1.9 2.0–2.9 3.0–3.9 4.0–5.9 6.0 + < 2.0 No. of patients (no. with bleeding) 5 (0) 3 (1) — — — — Mean percentage reduction in INR (range) 18.6% (7.1%–31.3%) 9.3% (0–16.7%) — — — — 2.0–3.9 No. of patients (no. with bleeding) 7 (4) 9 (2) 6 (1) — — — Mean percentage reduction in INR (range) 35.9% (21.4%–53.6%) 23.5% (9.1%–44.4%) 30.5% (9.6%–40.0%) — — — 4.0–5.9 No. of patients (no. with bleeding) 1 (1) 7 (5) 3 (3) 1 (1) — — Mean percentage reduction in INR (range) 33.8% 34.4% (9.9%–65.5%) 31.7% (25.5%–39.5%) 21.8% — — 6.0 + No. of patients (no. with bleeding) 8 (4) 4 (1) 8 (5) 8 (2) 2 (1) 2 (0) Mean percentage reduction in INR (range) 52.8% (19.4%–86.4%) 66.9% (44.5%–90.1%) 55.7% (33.6%–82.5%) 37.8% (19.9%–40.2%) 39.6% (35.7%–43.5%) 26.7% (19.0%–34.4%)

Julie H Crawford MB BS · Bradley M Augustson FRACP, FRCPA

To the Editor: Obesity-related glomerulopathy (ORG) is a condition that is partially reversible by weight loss. A 48-year-old morbidly obese man presented with massive proteinuria (8.4 g/day; reference range[RR], < 0.03 g/day). His medical history included hypertension of 4 years, morbid obesity, gout and impaired fasting glycaemia. His hypertension had been relatively well controlled, with no known end-organ complication until the current review. His urinary protein excretion rate measured 6 months earlier had been 0.13 g/day. Longstanding medications included aspirin, lisinopril and allopurinol. The patient weighed 125 kg and was 1.77 m in height (body mass index, 40 kg/m2 [class III obesity]). His blood pressure was 130/70 mmHg, with no postural hypotension. The fundi were normal, with no evidence of hypertensive retinopathy. There was no peripheral pitting oedema and there were no tendon xanthomata. A repeat urinary protein measurement showed an excretion rate of 7.9 g/day, confirming the earlier result. Renal and liver function tests were normal. Other laboratory tests produced the following results: fasting cholesterol, 5.5 mmol/L (RR, < 4.0 mmol/L); triglycerides, 2.4 mmol/L (RR, < 1.8 mmol/L); serum creatinine, 92 μmol/L (RR, 60–110 μmol/L); albumin, 38 g/L (RR, 35–45 g/L); fasting glucose, 6.8 mmol/L (RR, < 5.5 mmol/L); serum insulin, 66 mU/L (RR, 5–25 mU/L); and C-peptide, 6.8 nmol/L (RR, 0.2–0.6 nmol/L). All relevant tests for glomerulonephritis, including serum antinuclear antibodies, antinuclear cytoplasmic antibodies, C3 and C4 levels, protein electrophoretic studies, and hepatitis B and C serology were negative, making a diagnosis of glomerulonephritis unlikely. While awaiting the renal biopsy, the patient decided to attempt rapid weight loss. He began consuming mostly one meal a day of about 5000 kJ (which included about 2000 kJ of protein). Six weeks later, his weight had fallen to 118 kg and his blood pressure was 130/80, with no oedema. His urinary protein excretion rate was 7.6 g/day. After 18 weeks, the patient weighed 110 kg and his urinary protein excretion rate had fallen to 2.1 g/day. At 6 months, his weight loss had plateaued at 102 kg and urinary protein excretion was 0.85 g/day. The renal biopsy showed features consistent with ORG1 (Box). No other abnormality was detected. A concomitant minimal change lesion with spontaneous remission would be a possible explanation, but such a lesion is exceedingly rare and difficult to exclude in the absence of electron microscopy. It is also unlikely given the patient’s age and abnormal light microscopy finding. It is apparent that class III obesity, through unknown mechanisms,2 is a major contributing factor in causing ORG and massive proteinuria — conditions that can be readily improved by weight loss. It remains to be seen in this case whether further weight reduction will further reduce the proteinuria, which, on the other hand, may also be confounded by the hypertension. Impaired fasting glycaemia is not a cause of proteinuria.3 This clinical vignette reinforces the need to check vigilantly for proteinuria and rigorously advise obese patients to attempt weight reduction, especially now that obesity has been confirmed to be an independent risk factor for end-stage renal disease.4 Histopathology of a representative glomerulus There is prominent vascular pole/perihilar sclerosis (broken circular line) and mild fibrosis of the Bowman capsule (arrow) (haematoxylin–eosin stain; original magnification, 3 40). No evidence of hypertensive diabetic nephropathy or tubular disease was detected. Other histological findings (not shown here) included glomerulomegaly, peripheral hyalinosis and mild basement membrane thickening.1 Morphologically, obesity-related glomerulopathy can be difficult to separate from idiopathic focal and segmental glomerulosclerosis.1

Huy A Tran FRACP, FRCPA

To the Editor: Motor neurone disease (MND) is a relentlessly progressive neurodegenerative disease with a median survival of 1–3 years. It results in the death of nearly 400 Australians per year.1 The management of MND remains problematic, tending to be offered in a heterogeneous and ad-hoc fashion across Australia. This heterogeneity arises in part from a lack of understanding of the aetiology of the disease and its progression in different patients,2 the absence of established guidelines for standard care,3 and a lack of concentrated experience among medical practitioners, nursing and allied health care workers in treating patients with MND. With new diagnostic techniques, treatments and interventions for MND undergoing trials, there is a clear need for more baseline information on MND management and outcomes and a method for monitoring any changes on a population basis.4 To facilitate this, the Australian Motor Neurone Disease Registry (AMNDR) has been developed. The Registry is governed by a steering committee comprising specialist physicians from each state and territory around Australia, neuroscientists, an epidemiologist and patient representatives. AMNDR was launched in Sydney in June 2004 to coincide with Motor Neurone Disease Global Awareness Day and, to November 2005, had enrolled 351 patients from 67 study locations, with 88% of registrations coming from 10 major sites. As of September 2005, 90 patients had undergone at least one further follow-up assessment. A copy of the registration, assessment and completion case report forms can be viewed on the AMNDR website (http://ww.amndr.org.au). From the patient information collected in the registration data, three distinct clinical phenotypes have emerged (Box). Patients with the “global” MND phenotype (combined upper and lower motor neurone signs in at least two regions) tended to have the shortest survival time. AMNDR was designed to obtain information that will increase the understanding of MND and its progression in different patients. Through the process of registry establishment, those involved in care, management and scientific research related to MND have been galvanised into a more effective and cooperative working unit. Ownership of the database has been retained by all who have contributed to data collection, and the information has been increasingly used to promote research into the causes and treatment of MND, locally and internationally.5 Through participation, it is expected that treating doctors will be able to evaluate their current management and associated patient outcomes relative to other centres around Australia. Demographic data for 351 patients with motor neurone disease enrolled in the Australian Motor Neurone Disease Registry to November 2005, by phenotype Phenotype, site of symptom onset Percentage of all registrations* Mean age at onset in years (SD) Sex ratio (F : M) Mean survival time in months (SD; range)† Deaths (%) Global† Bulbar 27% 64 (13) 1.5 : 1 27 (10; 20–48) 24% Cervical 25% 55 (19) 0.4 : 1 20 (10; 7–33) 13% Lumbar 19% 61 (10) 1.1 : 1 36 (16; 14–63) 24% Flail limb§ Arm 10% 63 (13) 0.07 : 1 95 (85; 30–238) 27% Leg 10% 58 (10) 2 : 1 59 (28; 33–100) 7% Primary lateral sclerosis¶ All regions 11% 54 (9) 0.9 : 1 103 (55; 24–259) 0 * Sum > 100% because of rounding. † Censored at November 2005. ‡ Global phenotype = combined upper and lower motor neurone signs in at least two spinal regions. § Flail limb variants = predominantly lower motor involvement of arms or legs, with prolonged disease duration. ¶ Primary lateral sclerosis = characterised by pure upper motor neurone involvement.

Matthew C Kiernan PhD, FRACP · Paul Talman FRACP · Robert D Henderson FRACP · Rodney Harris BA, GradDipBusStud, MAICD · on behalf of the Australian Motor Neurone Disease Registry Steering Committee

Noel McK Bennett Infectious Diseases Physician, Victorian Department of Human Services, 14A Marquis Street, Ashburton, VIC 3147. bennettnATbigpond.net.au To the Editor: In a recent issue of the Journal, Chew et al described a woman from Vietnam with skin nodules that, on histological examination, showed lobular panniculitis with granulomatous inflammation.1 No mycobacteria were visible and a polymerase chain reaction test for Mycobacterium tuberculosis was negative. Two months after starting quadruple antituberculous therapy (including rifampicin), her lesions had resolved. Erythema induratum (ostensibly due to hypersensitivity to M. tuberculosis) was diagnosed, despite the absence of evidence of tuberculosis. Other possible diagnoses were considered, but leprosy was not mentioned. In regions of Australia where leprosy is not endemic, the disease is frequently overlooked.2 Birrell3 described a man from Malta with recurring skin lumps. Biopsy showed panniculitis with giant cells, and the man was initially misdiagnosed as having “Weber–Christian syndrome” or “relapsing febrile non-suppurative nodular panniculitis”. Soon after, another Maltese patient presented similarly. This time, leprosy was suggested, and a biopsy revealed the presence of Mycobacterium leprae.4 Re-examination of slides from the first case showed similar organisms, confirming leprosy.5 The patients described by Chew et al and Birrell had migrated from countries in which leprosy was endemic, and biopsies revealed granulomatous panniculitis. Weber–Christian syndrome and erythema induratum are rare, ill-defined conditions with confused aetiologies, and both lack a specific diagnostic test. Therefore, cases of leprosy can be easily misdiagnosed as one of these conditions. That the biopsy in this patient did not show visible M. leprae is against a diagnosis of leprosy. But in my experience, even in lepromatous (multibacillary) disease, occasionally a skin smear of a lesion or (more rarely) a biopsy specimen may fail to reveal bacilli. Of course, this would be likely if the patient had received specific treatment for leprosy previously. Respectfully, I suggest that Chew et al should attempt to exclude lepromatous leprosy in their patient by looking for possible missed stigmata of leprosy, enquiring whether she has ever been treated for leprosy, asking whether any close acquaintances have had the infection or a chronic skin condition, and following up the patient in the long term.

Noel McK Bennett

James B Muir Dermatologist, Southeast Dermatology, 1202 Creek Road, Carina Heights, QLD 4152. arnoldmuirAToptusnet.com.au To the Editor: One of the Journal’s recent Lessons from Practice illustrates common errors in the approach to dermatological conditions.1 As in all areas of medicine, an accurate diagnosis is crucial to the management of any skin disease. This is especially so if a medical practitioner institutes treatments, such as oral steroids, that have considerable potential for causing morbidity. The lessons I would draw from the case of erythema induratum described are as follows. If you suspect an unusual presentation of a common condition, perform investigations to confirm your suspicions. Although erythema nodosum classically occurs on the anterior lower leg, lesions above the knee may occasionally be seen. To make a diagnosis, investigations need to be appropriate. The battery of blood tests ordered in the case described would not have shed light on the pathological process occurring in the skin. There is a reluctance among the general medical community to perform skin biopsies. These procedures cause little morbidity, have a high diagnostic yield, and should be within the skill set of any medical graduate. Concern over causing a scar is often cited as a reason for not doing a biopsy. But, in my experience, patients are rarely worried about such a prospect. Missing the diagnosis is surely of much greater concern. Taking a simple biopsy, including fat, at the initial presentation would have saved the patient in question a lot of trouble and risk. If there is no response to your treatment, it may well be that the initial diagnosis was incorrect. For example, it is common to see “steroid-resistant eczema” that is actually intraepidermal carcinoma. Erythema nodosum will usually show at least some response to non-steroidal anti-inflammatory treatment. Lack of response to a treatment that usually works should lead to a re-evaluation of the diagnosis. Systemic steroids should not be used for a dermatological condition without a firm diagnosis. Firstly, they can suppress many of the clinical and histological changes that allow a diagnosis to be made. Appropriate investigations need to be done before starting steroids. Secondly, a drug like prednisolone may well make matters worse, especially if, as here, there is an infectious aetiology. Patients from areas in which tuberculosis is endemic should have this condition excluded before being given systemic steroids. A lack of obvious exposure to or symptoms of tuberculosis is not unusual in patients from such areas who are subsequently shown to harbour this infection. The authors state that, as erythema induratum can resolve with corticosteroid treatment, this can lead to an erroneous diagnosis of erythema nodosum. Using response to treatment as a quasi-diagnostic test is dangerous indeed. Steroids will cause many conditions associated with significant inflammation to improve or even appear to resolve. But this does not mean that there is no infectious or malignant aetiology.

James B Muir

Gary Y Chew,* Christopher Henderson,† John W Quin‡ * Registrar, ‡ Director of Clinical Immunology, Department of Immunology, Liverpool Hospital, Bigge Park Centre, PO Box 103, Liverpool, NSW 2170; † Anatomical Pathologist, South Western Sydney Area Health Service, Liverpool, NSW. john.quinATswsahs.nsw.gov.au In reply: We thank Bennett and Muir for their pertinent comments. Our patient did not have any history or clinical evidence of lepromatous leprosy. The skin biopsy did not reveal any dermal granulomatous involvement, and there were definitely no organisms seen on an auramine stain of the biopsy specimen. Subcutaneous involvement in leprosy is uncommon except in erythema nodosum leprosum or as a neurotropic phenomenon. When present, it tends to be a neutrophil-rich hypersensitivity necrotising vasculitis — no features of which were seen in this case. Neither the woman’s partner nor child had a chronic skin condition or clinical history of leprosy or tuberculosis. Furthermore, the patient has been followed up for 12 months, with no recurrence of the rash. We agree with Muir that an accurate diagnosis is crucial to managing any skin disease and that there were many lessons to be gathered from this case apart from the five points we listed. It is our usual practice not to begin definitive treatment until we have examined a skin biopsy of any suspicious lesion and made a diagnosis. As this patient was very concerned about getting a scar, we did not perform a skin biopsy initially, but informed her that we may need to do so if the condition did not respond to treatment. We agree that patients from areas where tuberculosis is endemic should have tuberculosis excluded before instituting systemic steroid treatment. In this case, the patient was given a chest x-ray by the appropriate authorities before her migration to Australia. She has not returned to Vietnam since then. Furthermore, the patient had failed a trial of a non-steroidal anti-inflammatory drug and found the lesions cosmetically distressing. Consequently corticosteroids were instituted.

Gary Y Chew · Christopher Henderson · John W Quin

Mu Li,* Kay V Waite,† Gary Ma,‡ Creswell J Eastman§ * Senior Lecturer, School of Public Health, University of Sydney, Sydney, NSW 2006; † Technical Officer, ‡ Principal Scientist, § Director, Australian Centre for Control of Iodine Deficiency Disorders, ICPMR, Westmead Hospital, Sydney. muliAThealth.usyd.edu.au To the Editor: Iodine is essential for production of thyroid hormone. The recommended daily intake is 100 μg for children, 150 μg for adults and 250 μg for pregnant and lactating women.1 Sporadic surveys of population iodine intake in Sydney, New South Wales, between 1985 and 1992 showed median levels of urinary iodine excretion (UIE) > 200 μg/L, indicating iodine sufficiency.2 However, a recent national study demonstrated mild iodine deficiency (median UIE < 100 μg/L) in New South Wales and Victoria, borderline levels in South Australia and adequate intake in Queensland and Western Australia.3 The major sources of dietary iodine are dairy milk and dairy products, seafood and iodised salt. In Australia, few people purchase iodised salt, and, except in Tasmania, the food industry does not use iodised salt in the production and preparation of food.4 For decades, milk contaminated with iodine residues from sanitising solutions (iodophors) used in the dairy industry has probably been the largest source of iodine in the Australian diet. We undertook a survey of the iodine content of milk samples from supermarkets around metropolitan Sydney in 2001 and 2004. In each year, iodine levels were measured in 13 samples, comprising a range of milk types (including whole, full cream, lite and skim) and brands (including Dairy Farmers, Devondale, Farmdale, Farmland, Perfection, Pura and Woolworths). Iodine concentrations were highly variable. Median concentrations were 140 μg/L in 2001 (range, 60–220 μg/L) and 195 μg/L in 2004 (range, 66–412 μg/L). Iodine concentrations varied between samples of the same brand and type by up to 100 μg/L. Many samples contained less than 200 μg/L (10/13 in 2001 and 7/13 in 2004). A 1975 survey of iodine concentration in milk conducted by the Australian Consumers’ Association found mean concentrations of 593.5 μg/L and 583 μg/L in NSW and Victoria, respectively.5 Because of concerns about iodine toxicity, Food Standards Australia and New Zealand specified an iodine limit of 500 μg/L in the Food Standards Code 1982. The replacement of iodophors by other sanitisers in the dairy industry appears to be the reason for the decrease in iodine content of Sydney milk. The perception that milk is a rich source of iodine is no longer true. A cup (250 mL) of milk a day would provide at most 50–60 μg iodine, approximating a third of the daily requirement for an adult. We suggest that the reduced amount of iodine in milk is likely to be one of the explanations for the re-emergence of iodine deficiency in Sydney and perhaps elsewhere in Australia. Despite these changes, dairy milk remains an important source of dietary iodine. The iodine content in milk should be monitored.

Mu Li · Kay V Waite · Gary Ma · Creswell J Eastman

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