Letters

To the Editor: Skov puts the case for an alcohol taxation policy in Australia.1 Few people, if any, in public health would disagree that alcohol is a serious public health issue in Australia, and few would doubt that higher prices will reduce consumption. But why tax the consumers directly? Why not tax the providers? I propose a tax on the advertising budget of alcoholic beverage producers. Further, this tax should be weighted according to the alcoholic content of the products they sell. Yes, this would mean higher prices for drinkers, but set in this way the incentive mechanism is to get sales and consumption down, firstly by reducing advertising, and secondly by lowering the amount of alcohol in what is sold. It has been estimated that more than a quarter of a billion dollars are spent each year on advertising alcoholic beverages in Australia.2 An average 200% tax, graded by alcoholic content of products, would mean a lot of money for the government! It might well make up for the estimated loss from the defeated “alcopops” tax of $1.6 billion over 4 years.3 Indeed, we should hope that it would not bring in half a billion dollars a year, as both advertising budgets and average alcohol content fall. An advertising tax would almost certainly make much greater inroads into reducing alcohol consumption than would the alcopops tax. It would raise the price for consumers, but to a lesser extent for lower alcohol-content beverages. It would severely discourage advertising, especially of high alcohol-content drinks, and would encourage manufacturers to produce beverages that are lower in alcohol. Any increase in cost to the consumer through taxation risks being regressive and might make the poor even poorer if they continue to drink, with a consequent impact on their health. This needs to be watched. But using the revenues raised to devise a targeted counselling program for those who do want to reduce their consumption (and for those who perhaps cannot do so without help) cannot be beyond the wit of Treasury and the health department.

Gavin H Mooney

To the Editor: I write in response to the article by Skov on alcohol taxation policy,1 and in the context of the recent defeat of the “alcopops” tax legislation, which is soon to be reintroduced to the Australian Senate. Our democratic political system has held us in relatively good stead, with a reliable system of checks and balances. However, the rejection of the alcopops legislation arguably represents a failure of democracy and a retrograde step for public health, defeating the first Australian public health-centred alcohol tax policy. For this, Senator Fielding and the Opposition should be held accountable. Yes, the tax is not all encompassing, and expansion to broader initiatives, as proposed by Senator Fielding, is not without merit. However, health experts supported the alcopops tax initiative as an important first step, as outlined in Skov’s evidence-based article.1 Skov highlighted the key issues, including that alcohol-related harm is at unacceptable levels, that action is overdue, and that good evidence from Australia and internationally supports taxation and pricing as being among the most effective measures to reduce alcohol consumption and harm.1,2 Overall, the positives of this initiative clearly outweigh the negatives, and defeating it was arguably naïve and ill informed. Historically, both policy and funding are crucial to public health successes. Following awareness of the problem, change must start somewhere, before broadening over time to deliver health benefits (eg, smoking, seatbelts, speeding — all crucial and effective public health campaigns). The most important aspect of the alcopops tax initiative is likely to be that it is a start and a successful avenue to raise revenue. Extension to a full alcohol content-based tax, education, incentives and regulations will come — but much more belatedly now. The defeat of the alcopops tax legislation has threatened this opportunity to significantly contribute to the fight against alcohol misuse. While opposition is by definition the trademark of Opposition parties, bipartisanship should prevail when community benefits are clear. Perhaps more concerning is that a single politician holding the balance of power can disregard history, expert opinion and popular support, and defeat important public health-centred legislation. The manipulation of our political system with the rejection of the alcopops tax legislation was profoundly disappointing. This initiative should not be defeated again. Our politicians should take heed of history, evidence, expert opinion and public sentiment and vote in the nation’s interest to support the alcopops tax legislation on its return to the Senate.

Helena J Teede

There is nothing a government hates more than to be well informed; for it makes the process of arriving at decisions much more complicated and difficult. — John Maynard Keynes, 1938. To the Editor: I would like to contribute to the debate raised by Skov’s timely article1 on the recently defeated “alcopops” tax legislation — the Excise Tariff Amendment (2009 Measures No. 1) Bill 2009.2 Senator Fielding’s requirement for a ban on alcohol industry advertising during sporting events as a condition for his support of the alcopops tax legislation is rational, visionary and affordable from the additional tax raised. Many of the high-profile individual and public health incidents related to alcohol misuse have been among athletes sponsored by the alcohol industry, and around sporting arenas. As the positive outcome of banning tobacco industry sponsorship of sporting events has demonstrated, such bans have at least as strong an impact as would the increased tax on alcopops on reducing exposure of young people to alcohol.3 It is estimated that the alcohol industry contributes up to 23% ($288 million) of the $1.25 billion in annual sports sponsorship in Australia.4 If the government had agreed to Senator Fielding’s prerequisite amendment, and had also fully taken over sports sponsorship responsibilities, it would have achieved two important public health objectives — a reduction in binge drinking and banning of sports sponsorship by the alcohol industry — and would still have had at least $100 million left to address alcohol-related issues; assuming of course that the real objective of the alcopops tax policy was to prevent alcohol-related harm among youths. Had the government agreed to simultaneously ban alcohol industry advertising in sport and maintain the new alcopops tax structure, it would then be on a moral high ground to implement other important alcohol-related public health measures that require no more than strong political will, such as mandated warnings on alcoholic products at the point of sale. In this respect, the French National Cancer Institute’s recent report that alcohol-related colorectal, breast, oesophageal and liver cancer risks increase from one glass per day, and that the consumption of alcoholic beverages of any type is not advised for anyone,5 is instructive.

Niyi Awofeso

To the Editor: A 70-year-old woman presented to the emergency department with intense pain, erythema, oedema and haemorrhagic bullae of the right lower leg. Twenty-four hours earlier, she had fallen into warm seawater on the south coast of New South Wales, sustaining a penetrating wound by an unknown object. She reported developing excruciating pain and the noted leg changes within hours of the injury. She had a history of systemic lupus erythematosus (SLE), managed long-term with 7.5 mg oral prednisone daily. Soon after presentation, she rapidly developed septic shock, becoming hypotensive, tachycardic, hypoxic and confused. She was experiencing rigors and required inotropic support. On examination, there was marked cellulitis of the right lower leg with purpura and bullae. No crepitus was detectable in the tissues. There was no clinical or laboratory evidence of disseminated intravascular coagulation. Broad-spectrum empirical antibiotic treatment with intravenous gentamicin, cephazolin and metronidazole was commenced, and urgent, extensive surgical debridement of the lower limb was performed (Box). Wound culture swabs and tissue samples were sent for microbiological and histopathological examination. On Day 2, blood cultures taken at initial presentation were positive for Vibrio vulnificus, as were tissue swabs. Based on susceptibility testing, antibiotic therapy was reduced to a single agent, intravenous ciprofloxacin 400 mg twice daily. The patient’s postoperative clinical recovery was slow, but her SLE did not flare up, and on Day 23 she was transferred to a tertiary referral centre for lower-limb skin grafting. Cellulitis is a common presentation to emergency departments, and common organisms are usually implicated. However, in some cases, the presence of more unusual pathogens, such as V. vulnificus, should be considered. V. vulnificus is a virulent halophilic (salt-loving) gram-negative bacterium associated with seawater temperatures (usual range, 18°–24°C). It has two distinct clinical presentations.1,2 The first, well recognised, is septicaemia after ingestion of raw or undercooked seafood, such as oysters, causing acute gastrointestinal disease. The second, not always considered, is necrotising wound infections, as in this case. Open wounds can be directly inoculated with V. vulnificus from seawater containing the organism. “Vulnificus” is a Latin term meaning “inflicting wounds”. Hippocrates described perhaps the first recorded case of a fisherman with pain in the foot, fever, delirium and blistering skin.3 Patients with primary wound infections caused by V. vulnificus develop painful, rapidly progressing cellulitis. More unusually, our patient developed fulminant sepsis from an open wound infection. Patients who are immunocompromised, especially those with alcoholic liver disease, hepatitis B or hepatitis C, have a higher risk of infection with V. vulnificus, as well as patients, like ours, who take long-term steroid therapy.2 Management requires timely recognition, antibiotic therapy and prompt surgical review. Cellulitis of right lower leg caused by infection with Vibrio vulnificus

Tamara C Preda · Veronica A Preda · Allan P Mekisic

To the Editor: A 27-year-old man who had recently emigrated from Sudan was admitted to our department with a 7-hour history of constant peri-umbilical pain. Physical examination revealed inconstant voluntary guarding of the lower abdomen. Full blood and electrolyte examinations were unremarkable. Urinalysis showed protein and traces of blood. A condition requiring surgery was considered unlikely and further investigations were undertaken. Significant bladder calcification was noted from an abdominal x-ray. A computed tomography scan confirmed this finding (Box), and also revealed circumferential distal ureteric calcification, appendiceal thickening with appendicolith, and adjacent fat stranding. Repeat abdominal examination demonstrated right iliac fossa tenderness with a positive Rovsing sign. Acute appendicitis was diagnosed and an inflamed, thickened, retrocaecal appendix was removed laparoscopically. The patient was discharged 2 days later, but did not attend his post-operative review. Histological examination of the appendix demonstrated transmural neutrophil infiltration, without eosinophils. Within the lumen there were numerous oval-shaped helminth ova, some with terminal spines, consistent with acute appendicitis caused by schistosomiasis. The patient did not have a general practitioner, therefore a referral to an infectious diseases clinic was made. He was thereafter lost to follow-up. Infection by schistosomes leads to chronic granulomatous inflammation in many body systems, including the gastrointestinal tract. Adult worms are not usually harmful to the host — eggs provoke a Th2-mediated immune response.1 Three major species of Schistosoma cause schistosomiasis in humans, of which two are endemic in sub-Saharan Africa — Schistosoma mansoni and Schistosoma haematobium. S. haematobium migrates against portal venous flow to the vesical venous plexus, causing urinary tract calcification through chronic inflammation and fibrosis. This species has also been described as a cause of appendicitis.2 Examinations of appendices removed from patients with acute appendicitis in endemic areas have demonstrated schistosomiasis in 2.3%–4.2% of samples, with 2.7% having histological evidence of acute schistosomal appendicitis in one study.3,4 Schistosomiasis can be diagnosed by histological analysis, or urine and stool microscopy. Serological testing cannot be used to differentiate past and present infection, however positive serological results are the basis for treatment of patients in endemic areas. After diagnosis, praziquantel should be prescribed. It is assumed that our patient did not receive praziquantel. He thus risks significant morbidity and mortality from possible gastrointestinal, hepatic, urinary, pulmonary and neurological complications related to chronic schistosomal infection. Surgeons and pathologists should be aware of the atypical pathology of acute schistosomal appendicitis. The number of immigrants arriving in Australia from endemic areas has increased markedly in recent years and further presentations may occur. Non-contrast computed tomography scan of a 27-year-old man with schistosomal appendicitis Calcification of the bladder (black arrow) and distal ureters (white arrows) is evident.

Jordan K Webb · Graeme Thompson

To the Editor: A 4-year-old girl presented with a flyblown scalp to a district aid post outside Madang, Papua New Guinea (PNG). Coincidentally, we were present at the aid post in our capacity as students and lecturers in the tropical paediatrics module of the James Cook University Masters in Public Health and Tropical Medicine course. The child was otherwise healthy, and her scalp had been normal until about 2 days previously, when her mother noticed two developing “sores”. These had deteriorated into circular, foul-smelling ulcers about 1.5 cm in diameter and 2 cm apart on the crown of her head (Box, A), in which live maggots could be seen squirming. The child’s mother had extracted some maggots with a pair of toothpicks (Box, B), and about 10 more were removed at the aid post with tweezers. When no further movement was apparent in the wounds, they were covered with petroleum jelly to suffocate any “stragglers”. No dead larvae were seen the following morning, and the wounds healed rapidly. We believe the most likely culprit was Chrysomya bezziana, or Old World screw-worm fly, although we were unable to preserve a larva for formal identification (by “curing” in very hot water and transporting in 70% ethanol). Old World screw-worm fly is an obligate myiasis-producing fly endemic in PNG. Its larvae are found only in living vertebrate tissues. The child’s mother had not noticed a prior lesion, and we assumed entry was through a graze on the scalp. Although screw-worm fly is endemic throughout tropical and subtropical regions of Asia and Africa, it is not found in Australia. If it became established here, it could devastate the livestock industry, particularly by striking the umbilical region of newborn calves and infesting their abdominal contents.1 The fly is known to be able to travel 100 km,2 further than the distance between the islands of Torres Strait, but has not yet migrated from PNG to Australia. It could also be introduced in livestock vessels returning from Asia or the Middle East; the Australian Quarantine and Inspection Service has strict regulations to prevent this, with all returning vessels thoroughly cleaned before reaching Australian waters. This is justified as it has been documented that sheep shipped from Australia arrived in Bahrain with fly infestation. Presumably, flies were attracted to the ship as it passed the coast of Oman or the United Arab Emirates.3 Infestation is self-promoting, as ovipositing females are particularly attracted to the odour of an existing myiasis, resulting in expansion of the lesion. In our patient, the application of petroleum jelly to the lesions fortuitously covered the odour, reducing the likelihood of reinfestation. Ivermectin is useful in treating affected animals,4 as well as humans5 when the larvae cannot be physically extracted. Scalp of a child with fly infestation A: Circular ulcers on the child’s scalp. B: Removal of larvae with toothpicks.

John S Whitehall · Richard Speare · Heidi E Best · Philippa J Price · Deborah J Mills

To the Editor: A recent review of medical textbooks found that the topic of intravenous fluid therapy is poorly covered.1 Hence, the recent article by Hilton and colleagues provides interesting hypothetical examples of the risk of hypovolaemia and hypervolaemia, as well as imbalances in fluid tonicity, in patients receiving intravenous fluid therapy.2 In particular, the authors recommend the use of intravenous 0.9% saline, as it is reportedly isotonic and hence avoids potential imbalances in serum sodium concentration. However, Hilton and colleagues discuss only tonicity as the determining factor when selecting the type of fluid to give patients. They do not mention that 0.9% saline, also known as “normal” saline, distorts fluid, electrolyte and acid–base balance, despite being isotonic. In healthy subjects, 25% more volume is retained 6 hours after infusion of 2 L of 0.9% saline compared with 2 L of Hartmann’s solution.3 Infusion of 0.9% saline also results in hyperchloraemia, which decreases glomerular filtration rate, and is not seen with infusion of Hartmann’s solution.3 Certainly, the most important side effect of 0.9% saline infusion is metabolic acidosis, caused (according to the Stewart approach) by a reduction in the strong ion difference.4 Using the Stewart approach once again, Hartmann’s solution is “balanced”, ensuring the eradication of infusion-related metabolic acidosis.4 Although tonicity is important in considering the appropriate intravenous fluid therapy, it should not take precedence in the choice of therapy. Such an approach ignores the volume, electrolyte and acid–base disturbances induced by 0.9% saline infusions.

Alexander D Franke

In reply: Franke presents some well known problems associated with intravenous administration of large volumes of 0.9% NaCl, particularly its relatively slow elimination (as compared with Hartmann’s solution), and hyperchloraemic acidosis.1 In isolation, we do not dispute these facts. However, 0.9% NaCl is not unique in having problems — no intravenous fluid therapy is without risk, especially when given in excessive volume, or when the composition is inappropriate for the patient’s needs. It is also important to distinguish maintenance therapy from resuscitation. For postoperative maintenance therapy, we advocate a conservative approach with initial use of minimal volumes of isotonic fluids, to decrease the risk of common complications such as postoperative fluid retention, impaired respiratory function, and prolonged bowel dysmotility. We encourage close monitoring of volume and electrolyte status, and do not exclude the later use of hypotonic fluids.2 Disorders of volume and tonicity (hypo- or hypernatraemia) are the most common serious problems associated with intravenous fluid therapy. The approach we recommend follows the priorities of the kidney: restoration of volume, restoration of tonicity, and restoration of acid–base balance, in that order. If the patient’s requirements for fluid volume and tonicity are met, and tissue perfusion and gas exchange restored, then significant morbidity or death is unlikely to be a direct consequence of isolated 0.9% NaCl-induced hyperchloraemic acidosis.

Carlos D Scheinkestel · Andrew K Hilton · Vincent A Pellegrino

To the Editor: We agree with Smith and Gray that the uptake of telemedicine is slow despite the availability of hardware in many facilities.1 Not every field in medicine is amenable to videoconferencing consultations. Specialties in which the physical examination needs to be performed by the specialist, such as cardiology, are not suitable. However, decisions in medical oncology are based on history, pathology and imaging studies, making the specialty well suited to telemedicine. If physical examination is needed, it can be performed by a proxy examiner. Towns with high patient loads are probably not suited, but towns with fewer patients would be ideal for this method. For the past 2 years, Townsville Hospital’s Department of Medical Oncology has managed cancer patients in Mount Isa (800 km — a 2-hour flight or 10-hour drive — from Townsville, one way) using weekly videolinked clinics. The team comprises a medical oncologist in Townsville, and a senior medical officer (SMO), a chemotherapy nurse, patients and families in Mount Isa. Except for the initial period of familiarisation, running the clinics has been smooth. Forty patients have been managed in Mount Isa in over 200 consultations. Consultations have included new cases, ward consultations and reviews. Four patients were considered for palliation only and were managed in Mount Isa without being transferred to Townsville, which was particularly helpful for those at terminal stages. In 2008, we conducted a survey to assess the level of patient satisfaction and assessed the safety of chemotherapy delivery. We found that all 25 patients who participated in the survey were satisfied with the service, with scores of more than 80% on a five-point Likert scale (ie, “agree” or “strongly agree”).2 Ninety-two per cent of patients would rather “see” the specialist via videoconference than travel to Townsville. All three SMOs and both nurses felt they were able to communicate more effectively with and receive support from the specialists. Thirty-two patients received active chemotherapy between 2006 and 2008. Rate of occurrence of severe side effects among patients in Mount Isa was similar to that of patients treated in Townsville (< 5%). Four patients were admitted for complications, but there were no treatment-related deaths. We believe that this technology is safe and appreciated by patients. The technology can be adopted by medical oncologists to manage patients in rural areas, where travel by specialists and patients is not cost- or time-effective. The major advantages are that the patients have the opportunity to be treated closer to home, and doctors receive specialist support on a weekly basis.

Sabe S Sabesan · Pieter Nel · Suresh C Varma

To the Editor: Climate change has an adverse impact on health.1 Procurement, waste production, transport, and energy and water consumption (ie, the ecological “footprint”) all contribute to climate change. If the principle underpinning the work of all health professionals is “do no harm”, addressing the harmful effects of the health care industry on the natural environment must become a priority. We argue that one way to rapidly achieve this would be to mandate more sustainable practices as part of hospital accreditation. The United Kingdom has specifically targeted its health system to reduce its large ecological footprint,2 but in Australia, progress towards environmental sustainability within health care is uncertain and unmonitored. The contribution by health care to Australia’s national carbon emissions is unclear, but we do know that, for example, Victoria’s public hospitals consume 60% of the total energy used by the state’s government departments,3 so we have the opportunity to make a major impact. There are excellent examples of hospital energy- and water-saving projects with financial recovery within 10 years.2,4 The Environment Protection Authorities of several Australian states are now mandating that heavy users of energy and water (including larger hospitals) have Environment and Resource Efficiency Plans to reduce their footprints,5 but action from hospitals has been unclear. Progress has typically been made on an ad-hoc basis by hospitals acting in isolation, although the Institute of Hospital Engineering, Australia is facilitating a more systematic approach.4 The Australian Council on Healthcare Standards (ACHS), through its Evaluation and Quality Improvement Program (EQuIP)6 accredits Australian hospitals against mandatory and preferred criteria. However, EQuIP does not currently include mandatory criteria that address issues such as energy, water and waste auditing, energy efficiency and the presence of a hospital environmental committee. The accreditation process offers an opportunity to encourage hospitals to prioritise these issues. The ACHS has awarded hospitals in the past for “environmental excellence”, but without a solid framework from the ACHS, the goal of all of our hospitals pursuing sustainability seems unlikely. In 2009, it is out of step with Australia’s shift to a low-carbon future that there are no requirements that hospitals achieve more sustainable use of energy, water and transport, and improve procurement and waste reduction. The introduction of broad environmental standards as part of the accreditation process could be a vehicle for achieving rapid improvements in sustainability across the hospital sector and shift our health system to one that “does no harm”.

Forbes McGain · Grant A Blashki · Kevin P Moon · Fiona M Armstrong

To the Editor: A 71-year-old man presented with a firm erythematous painful swelling over the sternoclavicular region. He had undergone coronary artery bypass grafting (CABG) 18 months earlier. A chest x-ray showed the presence of sternal wires and mediastinal clips from the surgery, and pleural thickening in the right costophrenic angle. There were no focal abnormalities seen on the x-ray when compared with pre-CABG radiographs. A computed tomography scan of the chest showed a destructive lesion of the manubrium, with an associated soft tissue mass extending into the pectoralis muscle and anterior mediastinum. A sternal suture was noted within the lesion, and a separate surgical clip was identified in the suprasternal notch region (Box, A). Surgical exploration of the sternotomy wound revealed tumour in the muscle around the proximal sternum, with bone destruction. Histopathological examination of the tumour confirmed the presence of an osteosarcoma (Box, B). (A section of normal trabecular bone [Box, C] is shown for comparison.) There have been few reported cases of primary sternal tumours. To our knowledge, primary osteosarcoma arising contiguous to a surgical suture has never been reported. It is unknown why the osteosarcoma originated in the part of the sternum that contained the sternal suture rather than originating de novo in another part of the bony skeleton. Chronic localised sternal inflammation or mechanical irritation of the proximal sternum by the suture may have been contributory factors in triggering carcinogenesis in this uncharacteristic site.1 However, the effect of trauma and mechanical stimulation on development of primary cancers and their metastases has never been proven. Patients who present with bony tumours frequently have a history of previous trauma to the area where the tumour develops. While there have been numerous reports suggesting some relationship between trauma/chronic inflammation and oncogenesis,1-5 there is no evidence that a single incident of trauma can cause cancer. The combination of trauma, in-situ metal and malignancy after CABG is rare, and there are currently no grounds for suspecting a direct relationship between them. A: Computed tomography scan of the chest showing a destructive lesion in the cortex of the manubrium. A sternal suture, surgical clip and soft tissue mass are visible within the tumour (A = anterior, R = right). B: Histopathological section of osteosarcoma of the sternum. Pleomorphic and hyperchromatic cells are present in a disorganised immature bone matrix (osteoid) (haematoxylin and eosin stain; original magnification, × 20). C: Histopathological section showing normal trabecular bone of the sternum (haematoxylin and eosin stain; original magnification, × 2.5).

Laurence Weinberg · Joseph Mathew

To the Editor: We report a case of reactive arthritis with an unusual cause in a previously well 47-year-old male landscape gardener. The patient presented with acute onset of left ankle arthritis. He had a 10-day history of a productive cough associated with mild fever, back pain and arthralgias. His temperature was 37.7°C and occasional crackles were audible at the lung bases. His left ankle was tender, with decreased range of movement. The provisional diagnosis was atypical pneumonia with reactive arthritis. A chest x-ray was normal. Laboratory tests showed an elevated white cell count of 11.93 × 109/L (reference range [RR], 4–11 × 109/L), with a C-reactive protein level of 326 mg/L (RR, < 3 mg/L). Arthrocentesis showed increased white cells but was negative for crystals and bacteria. Serological tests were positive for Chlamydia psittaci (IgM, IgA and IgG were all elevated and increased during illness), and the patient was also positive for human leukocyte antigen (HLA)-B27. He was initially treated with meloxicam for the arthritis. Oral prednisone was added when his joint symptoms became more disabling. Weaning of prednisone was attempted, but symptoms recurred. Sulfasalazine was subsequently added. Symptoms took about 8 weeks to resolve. Sufferers of psittacosis are infected by inhaling the obligatory intracellular bacterium, Chlamydia psittaci, from the faeces of infected birds in soil or grass. As a landscape gardener, our patient was at risk. Clinical presentations of psittacosis vary considerably, but patients usually present with flu-like and respiratory symptoms.1 Reactive arthritis is unusual, being more commonly associated with pathogens such as Salmonella, Shigella, Campylobacter and Yersinia spp.2 Although reactive arthritis usually involves asymmetrical large joint oligoarthropathies, patients with Chlamydia psittaci infection usually have a polyarticular pattern.3 HLA-B27 has a high association with spondyloarthropathies, including reactive arthritis. Contact with infected birds is often not obvious, making the diagnosis challenging. Microimmunofluorescence (showing a fourfold increase in antibodies or IgG titre greater than 16) has become available for diagnosis. Differential diagnosis of reactive arthritis includes other causes of arthritis such as sepsis and crystal deposition. Management of Chlamydia psittaci reactive arthritis includes early use of the antibiotics doxycycline or erythromycin, or possibly ceftriaxone.4 Anti-inflammatory drugs are the mainstay for symptomatic treatment of all reactive arthropathies. Intra-articular steroid injections may be helpful. There is conflicting evidence regarding the benefit of systemic corticosteroids. Sulfasalazine may be a helpful adjunct.5 For gardeners, preventive measures include the use of masks, gloves and lawnmower catchers.

Peter N Gonski · Bobby Chan

To the Editor: The management of pregnant women with pre-existing diabetes is often challenging for clinicians. A 38-year-old woman presented with an unplanned pregnancy at 8 weeks’ gestation. She had a 4-year history of type 2 diabetes treated with metformin, which she stopped taking on confirmation of her pregnancy. Her glycated haemoglobin (HbA1c) level was 9.0% at her first antenatal visit, and therapy with pre-meal insulin aspart and twice daily isophane was commenced. Her insulin requirement rapidly escalated, rising to 400 units per day by the end of the first trimester. Metformin therapy was reintroduced in the second trimester. Despite strategies including splitting her insulin doses and trialling different insulin regimens, control of her diabetes remained poor. At 30 weeks’ gestation, U-500 insulin became available, and that allowed rapid titration of insulin doses (Box). Her HbA1c level improved to 6.4% in the third trimester. At 35 weeks, her daily insulin requirement had reached 1455 units and her membranes ruptured prematurely. During labour, an intravenous insulin infusion rate of 90 units per hour was needed to achieve normoglycaemia. At birth, the neonate weighed 2005 g (11th percentile) with no evidence of congenital abnormalities, but she suffered transient hypoglycaemia on Day 1. Postpartum, the mother’s daily insulin requirement decreased to 28 units per day. In pregnant women with pre-existing type 2 diabetes, the insulin requirement increases substantially in the second half of pregnancy.1 In the past 12 months, among 25 pregnant women with type 2 diabetes who attended our antenatal clinic, the median insulin dose at the end of their pregnancies was 123 units per day, with 6 women requiring doses exceeding 200 units per day. At daily doses above 200 units, the therapeutic response to further increments in the insulin dose is attenuated.2 Current insulin preparations in Australia (100 units/mL) can be problematic for these patients as it is difficult to administer large volumes of insulin subcutaneously. U-500 is a preparation of regular insulin at a concentration of 500 units/mL. It is invaluable for patients with extreme insulin resistance, as a smaller volume is needed for injections. Its application during pregnancy has been previously reported.3-5 U-500 insulin is not readily available in Australia, and the preparation has to be administered by syringe. Hence, the volume of insulin must be drawn up accurately, as insulin syringes in Australia are designed for conventional lower-concentration insulin preparations (100 units/mL). This case highlights one of the many difficulties in managing pregnant women with pre-existing diabetes. The use of U-500 may be considered for women on extremely large doses of insulin and whose diabetes is still suboptimally controlled. The safety aspects of U-500 during pregnancy will need further examination. Insulin requirements during pregnancy of a 38-year-old woman with diabetes

Vincent W Wong · Alexia V Pape

To the Editor: In November 2008, a residential balcony collapse in Brisbane, Queensland, resulted in one person killed and 25 injured.1 Moments after the accident, tertiary hospitals across the city were placed on alert. Valuable hospital resources, including intensive care beds and staff, were allocated to the care of potential casualties; surgical theatres were kept on standby; and elective operating lists were cancelled. In 2008, injuries in more than 40 people across Australia and New Zealand were caused by residential balcony collapses.1-3 About 8000 Australian timber balconies are considered at risk of collapsing and potentially causing human fatality.4 Timber balconies constructed between 1970 and 1990 are at most risk of collapse.4 Many were constructed with inappropriate timber, without building approvals, and by unqualified tradespeople. When properly constructed, a well maintained timber balcony generally lasts for about 20 years.4 Collapse is not limited to timber balconies. In February 2002, a concrete cantilever balcony on a Sydney apartment fell under its own weight, shearing off the balcony under it.5 According to the Australian Concrete Repair Association (ACRA), many concrete balconies appear “safe” but have never been loaded to their maximum capacity, giving residents a false sense of security.5 As balcony parties and outdoor living become more popular, the ACRA believes that it is only a matter of time before more balconies collapse.5 A well maintained concrete balcony can be expected to last for about 40 years.4 In April 1995, the Cave Creek disaster in Pararoa National Park, NZ, resulted in the deaths of 14 people when an unstable wooden viewing platform, unable to support the weight of the 18 park visitors who had crammed onto it, collapsed into a gully.6 Following the accident, the NZ Department of Conservation made it mandatory that warning signs, indicating the maximum number of people permitted, be installed at every public viewing platform in the country.6 Why do suspended structures and public transport vehicles (such as viewing platforms, elevators and buses) have clearly displayed maximum capacity warning signs, but not balconies? Warning signs showing maximum capacity and recommended inspection dates would remind people to maintain and use their balconies safely. A prospective buyer of a home with a balcony should find out when the balcony was built and check local government records for building approvals. If no record exists, a balcony should be professionally inspected. We believe regular safety inspections and clearly displayed maximum capacity warning signs should be mandatory for all balconies. We also believe a review of building codes and standards is needed to protect residents of older homes and apartments — perhaps with an initial amnesty on unapproved balcony constructions — to encourage owners to seek professional inspections and have structural deficits corrected so that future tragedies need not occur.

Shinichiro Sakata · Craig A McBride · James W Nixon · Roy M Kimble

To the Editor: Population health and clinical researchers have long endured time-consuming submission of applications for a single study to multiple human research ethics committees (HRECs), which each have their own application forms and processes. Each HREC form collects similar information, with slight variation but much repetition. They invariably differ in emphasis and space provided, precluding a simple cut-and-paste among forms. The resource burden of completing this step in the research process has been highlighted previously.1,2 Rarely does completion of multiple applications add value. Responding to researchers’ protestations, the Australian Health Ethics Committee developed a National Ethics Application Form (NEAF). An improved version (NEAF2) was released in August 2008, with recommendations it be adopted by ethics committees Australia-wide.3 While some state health departments have embraced the new form and reform processes,4 rationalisation has not occurred in all jurisdictions. As investigators on a 3-year (2008–2010) study of cardiovascular disease that is funded by the National Health and Medical Research Council (NHMRC) and requires access to hospital records throughout Western Australia, our first ethics application was submitted in November 2007. Sequential preparation and submission to other HRECs led to the requisite approval from all 12 HRECs taking a further 12 months to achieve after the first approval. Few of these committees accepted an application using NEAF at the time. Adopting the current version of NEAF5 — adding supplementary questions pertinent to each institution (if necessary) — and rationalisation of processes to access public hospital medical records would be enormously more efficient for researchers. Centralised processes could also reduce the impost on HRECs. Our experience with contrasting requirements of the various HRECs has included different reporting timelines (6–12 months), different reminders to report, different periods of study approval (1–4 years), use of institutional letterhead, requirements for at least one chief investigator to be a staff member of the institution auspicing the HREC, requirements that investigators personally attend the HREC meeting, and differences in whether faxed and digital signatures are accepted. Such differences in requirements and processes are documented,2,6 and inevitably delay substantive research. This ongoing waste of resources and energy — in processes that distract from quality research but do not enhance ethical integrity — increases the burden on both researchers and members of HRECs. Rationalising and streamlining ethics processes could free resources, allowing greater attention to research monitoring by HRECs and research translation by researchers. We urge expedited implementation of NEAF2 and further reform. State health departments and affiliated organisations should collaborate to rationalise processes and expedite centralised or reciprocal approvals where appropriate. The bold proposal for a national system to streamline the ethics review process within and across Australian jurisdictions7 will invigorate discussion of overdue reform.

Sandra C Thompson · Frank M Sanfilippo · Tom G Briffa · Michael S T Hobbs

To the Editor: We read with interest Talley’s excellent and informative editorial about the risks associated with proton-pump inhibitors (PPIs).1 Other possible serious side effects of PPIs that need to be taken into account are potential drug interactions with aspirin and clopidogrel. Aspirin is a weak acid that crosses the mucosa in its lipid state. The suppression of acid production reduces the lipophilic nature of this drug and, theoretically, might reduce its absorption and bioavailability.2 On the other hand, clopidogrel is a prodrug that is converted in the liver to an active metabolite. This bioactivation is mediated by hepatic cytochrome P450 isoenzymes,3 with cytochrome P450 2C19 (CYP2C19) playing a particularly important role. There is evidence suggesting that some PPIs (omeprazole, lansoprazole and rabeprazole) can inhibit CYP2C19, which would alter the effectiveness of clopidogrel and potentially lead to an increased risk of adverse cardiovascular outcomes. In a recent Canadian case–control study among patients prescribed clopidogrel after acute myocardial infarction, current use of PPIs was associated with an increased risk of reinfarction (adjusted odds ratio, 1.27; 95% CI, 1.03–1.57).4 The risk was limited to patients currently taking a PPI (the authors did not find any association with more distant exposure to PPIs), and did not extend to pantoprazole, a drug that does not interfere with the conversion of clopidogrel to its active form.

Francisco J Fernández-Fernández · Gonzalo Pía · Pascual Sesma

To the Editor: In his recent editorial, Talley discusses a range of risks of proton-pump inhibitors (PPIs).1 Another rare but serious side effect of PPIs of which every doctor should be aware is hyponatraemia. Eleven cases of hyponatraemia caused by PPIs have been published.2,3 Consistent features were the rapid onset of hyponatraemia within days of commencement of the PPI therapy, the severity of hyponatraemia often being associated with confusion or delirium, and rapid recovery after cessation of the PPI medication. Test results in each case were consistent with inappropriate release of antidiuretic hormone. One case occurred 5 days after a patient changed from lansoprazole to esomeprazole.4 Hyoponatraemia needs to be considered whenever there is clinical deterioration, even after brief exposure to a PPI.

Adam P Morton

In reply: Proton-pump inhibitors (PPIs) are often coprescribed for patients taking aspirin and clopidogrel to reduce gastrointestinal bleeding. There are emerging data that omeprazole diminishes the therapeutic effect of clopidogrel because the active enzyme in the liver, cytochrome P450 2C19 (CYP2C19), metabolises omeprazole and activates clopidogrel.1,2 In a large cohort study of 8205 patients with acute coronary syndrome and taking clopidogrel, 64% were also taking a PPI (60% omeprazole); 21% of those who were taking clopidogrel but no PPI died or were rehospitalised for acute coronary syndrome, versus 30% of those taking clopidogrel as well as a PPI.3 Notably, not all the PPIs have the same metabolic pathway. For example, omeprazole and esomeprazole are principally metabolised by CYP2C19 in contrast to lansoprazole, which is metabolised by cytochrome P450 3A4 (CYP3A4), and pantoprazole, which is metabolised by CYP2C19 O-demethylation then rapid sulfate conjugation. Thus, the negative interaction with clopidogrel may not apply to all PPIs (and pantoprazole may be the drug of choice if a PPI is required, as cytochrome P450 interactions are least likely).1 However, until more data are accumulated, all PPIs should probably be avoided where possible in patients who have been prescribed clopidogrel, unless there is no alternative. It is correct that hyponatraemia has, rarely, been reported in patients taking PPIs. However, this knowledge is based solely on case report data, and therefore the level of evidence for cause and effect is relatively weak.

Nicholas J Talley · Aneta Dimoska · Kevin Gan

To the Editor: I read with interest the article by Medi and colleagues,1 but note that the authors do not mention the effect of supraventricular tachycardia on atrial natriuretic peptide — a hormone that causes vasodilation and renal excretion of sodium and water. Plasma levels of atrial natriuretic peptide increase markedly during supraventricular tachycardia.2 Pacing studies reveal that release of atrial natriuretic peptide occurs when the heart rate is greater than 120 beats/min.3 The resultant diuresis would lead to an urge to urinate and, in a prolonged episode of tachycardia, to polyuria.4,5

Weekitt Kittisupamongkol

To the Editor: We read with interest the article by Alexander and colleagues on child protection issues in severe childhood obesity.1 With one quarter of Australian youth either overweight or obese, individual families (or the health care system) will not benefit from widespread involvement of child protection services in obesity. The authors are clear on this, and describe their case as “sufficiently extreme”. The difficulty lies in defining what is “extreme” and, as health professionals, we have a duty to the community to emphasise that these kinds of cases rarely occur. The illustrative case in the article by Alexander and colleagues required an amalgamation of details from several patients (for confidentiality purposes), and we believe it would be very unusual for a 40 kg 4-year-old girl to exhibit the degree of obesity-related comorbidity described.2,3 Such a degree of “medical urgency” is usually absent when managing young obese children and, in our experience, is thankfully very extreme and markedly different from the more usual scenario of discussions around potential long-term health problems. Also, there are currently no fail-safe mechanisms in place to be 100% certain that there is not an underlying genetic, hormonal or metabolic reason for continuing weight gain in a young child. With the childhood obesity pandemic, it is impossible to routinely investigate all obese youth and, even if it were, research teams are continually finding new causes for why some children continue to gain weight irrespective of lifestyle change. Indeed, the more severe the obesity, the more likely for there to be an organic cause.4 It is not in anyone’s interests for child protection services to be automatically involved because of standard recommendations when, at a later date, an underlying medical cause is discovered. Alexander and colleagues should be congratulated on re-igniting a public discussion on this highly emotive and difficult area of health care. We agree that parenting styles may influence weight regulation in young children5 but, for the above reasons, we would urge extreme caution when considering that parents may be “neglectful”. Within our obesogenic environment, perhaps (deliberate or intentional) non-compliance is an indication that society is neglecting parents, rather than that parents are medically neglecting their children? We are concerned that the development of child protection guidelines will alienate parents and families, leading to a decline in the uptake of programs aimed at preventing and/or treating overweight and obesity. We would recommend that each case be taken on its individual merit and that primum non nocere is as important as Aristotle’s phrase of “practical wisdom”.

Matthew A Sabin · Zoe McCallum · Kay Gibbons · George A Werther · Joseph Proietto

In reply: Primum non nocere means both “first, do no harm” and “above all, do no harm”. We acknowledge there may be both potential harms (the most significant being removal of the child from the family) as well as hoped-for benefits in involving child protection services in cases of severe childhood obesity. Though we strenuously oppose notification of child protection authorities as a general policy, we raised the idea that, in exceptional circumstances, health care professionals may nonetheless have a professional and legal obligation at least to consider notifying such authorities. We did so cautiously because we fear an exception becoming a rule, particularly in services such as ours where we frequently care for children very like the “child” we describe. We agree that the development of obesity usually has multifactorial causes which will include a genetic element. We also agree on the need for public health approaches to the prevention of childhood (and adult) obesity. But whatever the underlying cause of severe obesity in a particular case, and especially in circumstances where parents seem unable to attend to the physical needs of their child, health professionals have an obligation to consider all reasonable means to limiting excess weight gain.

Shirley M Alexander · Louise A Baur · Roger Magnusson · Bernadette Tobin

To the Editor: We report a case of proximal myopathy attributed to varenicline therapy to assist with smoking cessation. A previously fit and well 27-year-old man presented to the emergency department with a 1-week history of lethargy, myalgia and limb weakness. The pain and progressive weakness incapacitated the patient to the extent of him requiring assistance to move from bed to chair. The patient’s only medication on admission was varenicline (Champix [Pfizer]), which he had started taking about 6 weeks previously to assist with smoking cessation. He denied drinking excessive alcohol or using illicit drugs. There were no symptoms of recent infection. On examination, a proximal myopathy with weakness of grade 2/5 for both upper and lower limbs was noted. The patient’s muscles were mildly tender, reflexes were preserved, and both cranial nerves and sensory examinations were normal. Respiratory function was not impaired and there was no evidence of fatigability. The clinical impression was of proximal myopathy of uncertain cause. An adverse drug reaction to varenicline was considered and the medication ceased. Appropriate blood investigations and clinical neurophysiological studies were requested. A full blood count, thyroid function tests and autoimmune screen were all normal, as were levels of electrolytes, calcium, phosphate and magnesium. The erythrocyte sedimentation rate was 15 mm/h (reference range [RR], 1–15 mm/h), the C-reactive protein level was 20 mg/L (RR, < 5 mg/L), and the creatine kinase level was 1100 U/L (RR, 30–190 U/L). Cushing disease was excluded. Two days after cessation of varenicline, the muscle weakness had improved and the creatine kinase level had normalised. The patient declined neurophysiological studies and was discharged home. On review 1 week later, he had made a full recovery. Varenicline is a recently marketed smoking cessation drug treatment that has been shown to be more effective than placebo and bupropion treatment.1 Varenicline acts as a partial agonist at nicotinic acetylcholine receptors in the brain.2 The agonist activity at these receptor sites reduces the symptoms of nicotine withdrawal and craving, while the antagonist activity blocks the reinforcing and rewarding properties of nicotine binding. Recognised adverse effects include nausea, headache, insomnia and abnormal dreams. Musculoskeletal effects are uncommon and limited to joint stiffness and muscle spasms.2 Potential mechanisms for myopathy include muscle cell degeneration induced by excess acetylcholine activity at the neuromuscular junction3 or possibly by varenicline’s affinity for the serotonin receptor.4 Enquiries to the Australian Adverse Drug Reactions Advisory Committee (ADRAC) and searches of the Canadian adverse drug reaction database and PubMed database failed to identify any reports of myopathy associated with varenicline. Thus we believe this to be the first reported case of proximal myopathy due to varenicline, and have reported the case to ADRAC accordingly.

Shelley E Wood · P Gerry Fegan

To the Editor: We are pleased that Simpson and colleagues brought the important matter of drug-dose calculation skills among Australian hospital doctors to the attention of the wider medical community.1 Data similar to theirs, suggesting inadequate calculation skills, have been reported from the United Kingdom and Germany.2-4 As teachers in the MB BS course of the University of Adelaide, we have been concerned with deficiencies in the clinical numeracy skills of our students for some time. Such deficiencies among medical students have been reported from North Carolina,5 but to our knowledge no information has been available about Australian medical students. In 2008, we included three questions on drug-dose calculations in the 90-item multiple choice question (MCQ) section of the final examination for Years 1, 2 and 3 of our course. For each question (Box), students were required to select one correct answer from five options. Although Question 1 required the knowledge that one standard drink contains 10 g of ethanol, as well as calculation skills, Questions 2 and 3 solely examined numeracy skills. The exam was completed by 177 students in Year 1, 155 in Year 2, and 119 in Year 3. The distribution of their responses is shown in the Box (with correct responses in bold). The percentage of correct responses to these questions was significantly lower than the overall score for the MCQ paper, with the exception of Question 3, which may have been too easy (as it did not discriminate between students). We believe these data support our hitherto anecdotal concerns that many students in the MB BS program have inadequate calculation skills. Although tertiary students’ numeracy problems have been attributed, at least in part, to the level of mathematics teaching in secondary schools,6 we consider they must be addressed at university level. We plan to make available an online calculation learning tool that begins with real-life non-medical examples. We are currently developing this tool with the University of Adelaide’s Mathematics Learning Centre and plan to publish our experience, including evaluation, with a view to making the tool widely available. Distribution of medical student responses to examination questions requiring numeracy skills* Question 1 (Year 1 and Year 3) A 21-year-old woman recalls drinking 5 glasses of champagne at her birthday party. Her glass holds 200 mL and the champagne has an alcohol content of 12.5%. How many standard drinks did she consume during her party? % of respondents Options Year 1 (n = 177) Year 3 (n = 119) A. 12.5 standard drinks* 50% 49% B. 5 standard drinks 6% 7% C. 18 standard drinks 1% 2% D. 6.25 standard drinks 20% 15% E. 10 standard drinks 23% 27% Question 2 (Year 2 and Year 3) You are treating a 60 kg patient for a laceration, which you will need to suture under local anaesthetic. Given that the maximum safe dose of lignocaine is 3 mg/kg, what is the maximum volume of a lignocaine 1% weight per volume (w/v) solution that can be administered safely? Options % of respondents Year 2 (n = 155) A. 1.8 mL 46% B. 6 mL 2% C. 18 mL* 35% D. 20 mL 14% E. 60 mL 1% Year 3 (n = 119) A. 60 mL 1% B. 6 mL 0 C. 180 mL 41% D. 18 mL* 38% E. 180 μL 19% Question 3 (Year 3) A 10 kg infant has viral meningitis and a high temperature. You want to treat her fever symptomatically with oral paracetamol. The preparation is paracetamol 50 mg/mL and the recommended dose is 15 mg/kg. How many mL of paracetamol syrup is the equivalent of one dose? Options % of respondents (n = 119) A. 1.5 mL 0 B. 3 mL* 96% C. 6 mL 1% D. 12 mL 2% E. 15 mL 1% * The correct options are shown in bold.

Kingsley J Whittenbury · Hubertus P Jersmann · Anne L Tonkin

To the Editor: The Australian Medical Council (AMC) now includes Indigenous health in its accreditation standards for medical schools,1 with guidelines stating that medical curricula must contain the “. . . appropriate use of educational expertise, including the educational expertise of Indigenous people, in the development and management of the medical course [emphasis added]”.1 These AMC requirements arose from the Indigenous Health Curriculum Framework, which was endorsed by the Committee of Deans of Australian Medical Schools.2 The second encounter of the Indigenous Simulated Patient Program at the University of Melbourne In the second encounter, the “patient” is concerned both about the conflicting information they have been given concerning diabetes and the need to attend multiple clinics. The “patient” attempts to explain that family and work obligations mean they cannot wait in outpatient clinics all day. The students in this session are encouraged to work with the “patient” to problem solve the issues that arise. The “patient” has been instructed to provide realistic reasons why these solutions will not work for them, highlighting possible differences in family responsibilities and living arrangements for some Indigenous community members, and demonstrating the conflicting priorities and expectations between the “patient” and the medical system. The University of Melbourne School of Medicine developed the Indigenous Simulated Patient Program in 2002 as one element of an integrated Indigenous health curriculum. The Program meets some of the goals of the framework by acknowledging and incorporating the educational expertise of Indigenous people, exposing students to Indigenous peoples’ lived experiences and world views, and by linking the simulated patient experience with other teaching content regarding the many ways in which history has affected Indigenous health. Indigenous simulated patients are used both early and late in the medical course. The early patient scenario is used within an uncomplicated communication skills tutorial, in which students practise their developing patient-interviewing skills and discover that the “patient” is Indigenous. The later scenario is more complicated (Box) and builds upon the first experience. In both scenarios, students are encouraged to ask the Indigenous patient, both in and out of character, questions about their personal experiences. The aim is to use the Indigenous Simulated Patient Program to help students understand that they will encounter Indigenous patients in their clinical studies and as junior doctors, and that these patients will have both the same and different issues from non-Indigenous patients. Solutions need to be tailored to meet the individual needs of the patient, and should include lessons from previous teaching within the curriculum — for example, the role of Aboriginal health workers in hospitals. The impact on Indigenous community members who participate in the program has been strongly affirming, with one actor commenting, “Today I felt like I really contributed to the training of medical students in issues that were important to me and my community”. Students also rate the experience very highly.3

Shaun C Ewen · Margo E Collins · Jennifer A Schwarz · Eleanor M Flynn

To the Editor: The Hon. Kevin Rudd, Prime Minister of Australia, addressed federal Parliament on 26 February 2009 regarding the Closing the gap on Indigenous disadvantage: the challenge for Australia report.1 In his speech, he asserted that government strategy to close the gap will focus on the treatment of Indigenous Australians’ illnesses “largely through the mainstream health system, because that is where 70% of Indigenous people are treated”.2 Unfortunately, the 70% figure is an urban myth based on one poorly worded question in the Australian Bureau of Statistics (ABS) National Aboriginal and Torres Strait Islander Health Survey 2004–05.3 At the National Aboriginal Community Controlled Health Organisation (NACCHO), we are concerned about the use of distorted evidence regarding the health of Aboriginal peoples, in particular the use of questionable data to formulate policies that undermine investment in Aboriginal community controlled health services (ACCHSs). In the ABS survey, a small sample of the Indigenous population were asked “Where do you usually go when you have a problem with your health?” The respondent was permitted one answer from choices that included: an Aboriginal medical service (AMS); a hospital; a doctor or general practitioner (outside hospital or AMS); traditional healer; other; or nothing. Such a question is bound to elicit misleading answers when, for example, a patient who sees his or her regular GP at an AMS selects “GP” rather than “AMS”. The technical distinction between these options is not clear, and the degree of reproducibility and reliability with which surveyors clarify the options is untested. Other Australian studies of primary care contradict the ABS findings. A recent study using 2007–08 data of the Bettering the Evaluation and Care of Health (BEACH) program found 0.9% of GP encounters are with Aboriginal and Torres Strait Islander patients.4 Over a 10-year period, this proportion has ranged from 0.7% to 1.6%.5 More than 70% of general practices do not see a single Indigenous Australian, and for the vast majority of those that do, less than 5% of their total encounters are with Indigenous Australian patients.6 In contrast, ACCHSs delivered 1 680 000 episodes of patient care to about 257 000 Aboriginal and Torres Strait Islander clients for the year 2005–06.7 Against an estimated national Indigenous population of 517 000, this indicates about 50% of Indigenous Australians use ACCHSs. ACCHSs also have more clients with complex disease than do private general practices,8,9 which supports our belief that ACCHSs target those who are “hard to reach”. Closing the gap in Aboriginal disadvantage depends on supporting Aboriginal communities towards their greater participation in primary health care. The right of Aboriginal peoples to participate in decision making that affects their health and wellbeing is the principle at stake here. The ultimate expression of this principle is community control and governance. This makes ACCHSs different to general practices, and it’s that difference that can close the gap.

Sophie Couzos · Dea Delaney Thiele