Letters

To the Editor: We read with some dismay the article by Winch and Henderson1 critically reviewing the introduction into health care of process improvement methods pioneered in manufacturing and service industries. We take issue with the article at several points. While the article is titled a “critical review”, it has more of the character of a personal view. For instance, the authors single out “lean thinking” for particular criticism, but the examples cited are in fact a mixture of business process re-engineering, hospital or health system restructuring, and total quality management. These differ substantially from lean thinking, but this is not acknowledged in the text. Then the authors claim that lean thinking has been accepted “somewhat uncritically”, but this is not so. The current peer-reviewed literature contains a number of articles critical of lean health care that have not been referenced by Winch and Henderson (for example, an article by Young and McClean2). The authors’ principal argument is that fragmentation of health care delivery reduces the quality of care provided. We agree. They then argue that process redesign increases the fragmentation and impairs quality of care, but we reject this view. The process redesign programs we have been involved with have been aimed at increasing the time that staff can spend with patients. They explicitly involve staff in designing systems that will deliver this. Rather than trying to “[reduce] the richness of professional health care practice to impoverished snippets of work”,1 we are trying to put broken care processes back together. The authors close by implying that process redesign may “add to the problems of hospital misadventure . . . rather than solve them”, but they provide no evidence for this assertion. In fact, the existing evidence points the opposite way. For example, a recent report from the ThedaCare group in the United States showed a reduction in mortality after coronary artery bypass grafting from 4% to effectively zero as a result of process improvement.3 Here in Australia, the Flinders Medical Centre in Adelaide has seen a striking reduction in serious adverse events after implementing a process redesign program based on lean thinking.4 Interest in process redesign is increasing in health care. All improvement methods benefit from critical discussion, but critiques that are also well supported by evidence are likely to be the most influential.

David I Ben-Tovim · Duncan Stuart · Maarten Kamp · Paul Cullen

To the Editor: As one who works in paediatrics and sees parents bringing their children to hospital for day surgery, and then taking them home again a few hours later, I concur with Winch and Henderson in their critique of “lean thinking” ways of delivering health care.1 Nowhere is this more obvious, and nowhere is it applied with less critical assessment, than in day admissions. This process, which we are told is best for families, may not be. It is best for the hospital, of course, as it means that care can be delivered for a fraction of the cost of keeping people in for several days. But is it best for families? What are we doing to parents when we send them home with a child fresh from surgery? While we might give them some education about what to do if the child has an adverse event, there is not enough time to make sure the parents have understood, are able to read effectively, and have taken any information on board (with their ability to do so potentially hampered by their state of anxiety). How do we know what the infection rates are after surgery? If the child develops an infection, the parents are likely to take the child to a general practitioner rather than return to the hospital, and busy GPs may not report back to the hospital on the child’s visit and the need for treatment. We do not ask parents what financial burden we are placing on them. Have they taken days off work or used their holiday time to look after the child? Does that mean financial hardship for the family? Do we ask them what emotional burden it is placing on them? As a highly educated health professional who knows the ropes, I can only imagine how anxious young parents must be with a child who has just had an operation and for whom there is no health care support at home. Of course, my comments about children are just as salient for adult day surgery admissions. I believe that lean thinking and its penultimate expression in health delivery, the day admission, should be critically re-examined, and there needs to be much more research on the immediate and long-term effects on patients and their families.

Linda E Shields

To the Editor: It is pleasing to see the acknowledgement by contributors of the fundamental premise that the fragmentation of health care may reduce the quality provided, which was a key argument of our article.1 Our aim was to provide space for critical appraisal of “lean thinking” and its application to health care, by questioning the assumed theoretical basis from which this approach is derived and enquiring about the evidence for long-term benefits relating to patient outcomes. We wished to engender discussion and debate rather than provide a systematic review of existing literature. To this end, we think our aim has been achieved. Returning to the central thesis of our article, we argue that the notion of quality is rapidly being subsumed by quantity (understood as patient throughput and the number of measurable errors). This is reflected in the focus of Ben-Tovim and colleagues on process rather than practice.2 We believe that medicine is grounded in the human condition,3 and thus ideas of quality must relate to patient experience, including harms that are not readily measurable. We acknowledge that health care is becoming more and more complex, and increasingly requires the exercise of practical wisdom that informs clinical reasoning.4 Individual differences between patients mean that each situation has to be considered in its own context. Recognition of this difference provides the opportunity for some of the richness and satisfaction inherent in medicine. Finally, medicine and health care are far from immune to adopting and repeating the mistakes of other professions and industries. It has been suggested that the continued rationalisation of health care, such as occurs with “lean” approaches, may contribute to the deprofessionalisation of medicine over time.5 In turn, this may promote the “McDonaldization”6 of health care, whereby efficient turnaround becomes the primary goal. We suspect that, while meeting a need at one level, this would provide little long-term satisfaction for health care providers or patients.

Sarah Winch · Amanda J Henderson

To the Editor: The recent rapid increase in popularity of low-carbohydrate (“low-carb”) beers in Australia, such as Foster’s Pure Blonde and Lion Nathan’s Hahn Super Dry, may represent an insidious health risk. The perception that low-carb beers represent a healthy alternative may result in some consumers: confusing low-carb beers with low-alcohol beers; believing that there will be a significant health benefit associated with consumption of low-carb beers (such as weight loss); drinking more beer in the belief that there are fewer health consequences associated with low-carb beers; or drinking low-carb beer in situations where the consumption of regular beer may be contraindicated because of health conditions such as diabetes or cardiac vulnerability. Particularly vulnerable risk groups include younger people and especially young women, who are often highly body image-conscious, as well as others with weight or health problems. Nutritional information for some of the major beers on the market in Australia is shown in the Box.1-3 The new generation of low-carb beers contain about 0.9 g of carbohydrate per 100 mL. However, there is little, if any, difference in either the amount of alcohol or the total energy content of traditional and low-carb beers, suggesting “low-carb” may not be a nutritionally significant improvement. Given that alcohol is a known cause of short- and long-term problems such as cancer, cirrhosis of the liver, strokes and violent behaviour, we contend that the alcohol content of beer is a far more important health issue than its energy content. Additionally, the alcohol content itself contributes directly to energy intake (1 g of alcohol contributes 29.8 kJ of energy, compared with sugar’s 15.4 kJ).4 Consuming alcohol may also indirectly lead to weight gain because of its association with unhealthy eating behaviour, such as increased snacking, junk food consumption and overeating.5 The Box clearly demonstrates that drinkers are better off consuming low-strength beers in terms of both alcohol content and energy intake. Recognising this fact, the European Parliament adopted the resolution that “Beverages containing more than 1.2% by volume of alcohol shall not bear health claims”.6 We believe that the Australian Government, particularly through its current Review of Food Labelling Law and Policy, should move quickly to enact similar legislation to protect the Australian public from the marketing claims of brewing companies. The message should be made explicit: low-carb beers are not a “healthy choice”. Nutritional information for major beers on the market in Australia1-3 Beer Alcohol by volume Carb (g/100 mL) Energy (kJ/100 mL) Full strength Redback 4.7% 3.6 172 Hahn Premium 5.0% 3.2 172 Cascade Pale Ale 5.0% 3.0 170 Crown Lager 4.9% 3.1 169 Cascade Premium Lager 5.0% 3.0 169 Foster’s Lager 4.9% 3.1 168 Victoria Bitter 4.6% 3.0 165 Carlton Black 4.4% 3.3 161 Tooheys New 4.6% 3.1 161 Tooheys Extra Dry 5.0% 2.5 161 Melbourne Bitter 4.6% 2.9 158 Tooheys Old 4.4% 3.0 156 Carlton Draught 4.6% 2.7 155 Swan Draught 4.5% 2.7 153 XXXX Draught 4.5% 2.1 147 Mid–low strength XXXX Gold 3.5% 1.9 121 Hahn Premium Light 2.6% 3.1 119 Carlton Sterling 2.5% 3.1 114 Cascade Light 2.6% 3.0 114 Hahn Super Dry 3.5 3.5% < 1.0 104 Low-carb Carlton Dry 4.5% 1.9 139 Bondi Blonde 4.5% < 2.0 130 Tooheys Maxim 4.6% 1.6 126 Hahn Super Dry 4.6% 0.9 126 Pure Blonde 4.6% 0.9 125 Carb = carbohydrate.

Peter G Miller · Stephen P McKenzie · Florentine P de Groot · Sondra L Davoren · Evie R Leslie

To the Editor: Influenza causes around 8% of community-acquired pneumonia (CAP) episodes,1 and during the (H1N1) 2009 influenza pandemic, concurrent bacterial infections were detected in up to 29% of fatal infections.2 Determining microbial aetiology of CAP can guide antibiotic and antiviral therapy. To investigate the usefulness of microbiological diagnostic testing for CAP, we undertook a retrospective review of our pathology department’s electronic database of patients admitted with CAP to a tertiary referral centre (365 beds) and two suburban teaching hospitals (314 and 280 beds) between 1 May 2007 and 30 April 2008. Inclusion criteria were: International Classification of Diseases, 10th revision codes J09–J22 (respiratory tract infections); age ≥ 18 years; and consolidation on a chest radiograph performed within 48 hours of admission. Exclusion criteria were: hospitalisation within the previous 14 days; admission to a unit managing predominantly immunosuppressed patients; HIV infection; active tuberculosis; chest injuries; and previous inclusion in the study. Basic demographic data and microbiological investigation results were collected. We adopted the Australian CAP Study’s criteria for aetiology and classification of good-quality sputum.1 Change in management was indicated for patients with bacteria not covered by empiric regimens recommended in Therapeutic guidelines: antibiotic, version 13, or organisms with public health and infection control implications.3 Continuous variables were analysed using either Student’s t test or the Wilcoxon rank-sum test, and categorical variables with the Fisher exact test. Statistical significance was set at P < 0.05. From 2436 admissions, 341 patients met inclusion criteria. Mean age was 71.1 (SD, 17.1) years, and 72 patients (21.1%) were in residential care. Most patients (251; 73.6%) had investigations to determine aetiology (Box). Ninety-three organisms were identified from 83 patients (33.1%), most commonly Streptococcus pneumoniae (33; 13.1%), Haemophilus influenzae (14; 5.6%), influenza (11; 4.4%) and Legionella spp (9; 3.6%). Good-quality sputum taken within 8 hours of presentation had the highest diagnostic yield (47.1%). Changes to management were indicated for 37 patients (14.7%). Aetiology was identified more often in the suburban hospitals, where S. pneumoniae and Legionella spp were more common than in the tertiary centre (27.7% v 8.1% and 9.2% v 1.6%, respectively; P = 0.001). Patients in the suburban hospitals were younger and less likely to be in residential care than those in the tertiary centre (mean, 67.6 v 72.6 years and 13.7% v 24.3%, respectively; P ≤ 0.03). The Australian antibiotic guidelines recommend appropriate investigations to determine aetiology of CAP.3 Our analysis suggests that usefulness of microbiological investigations varies between different patient populations, and their value may be maximised by using algorithms similar to the recommendations for CAP investigations in United States guidelines.4 Contrary to widespread belief that microbiological diagnostic tests for CAP are low-yield and not helpful, we found that aetiology could be established in up to 55% of patients and a change in management made in 15% by using a combination of diagnostic tests. Our findings should be generalisable to other parts of Australia, as the aetiologies we observed mirror those seen in the Australian CAP Study.1 Diagnostic yield of investigations used to determine microbial aetiology for patients hospitalised with community-acquired pneumonia No. positive/no. tested (% positive) Investigation Suburban hospitals Tertiary centre Total Sputum microscopy, culture and sensitivities 14/40 (35.0%) 23/103 (22.3%) 37/143 (25.9%) Blood culture 5/42 (11.9%) 7/131 (5.3%) 12/173 (6.9%) Urinary antigen test Streptococcus pneumoniae* 14/40 (35.0%) 11/105 (10.5%) 25/145 (17.2%) Legionella pneumophila serogroup 1* 4/39 (10.3%) 1/104 (1.0%) 5/143 (3.5%) Respiratory multiplex PCR† 1/6 (16.7%) 6/17 (35.3%) 7/23 (30.4%) Bronchoscopy‡ 0/2 3/12 (25.0%) 3/14 (21.4%) Serology§ 4/27 (14.8%) 7/66 (10.6%) 11/93 (11.8%) Total patients investigated 36/65 (55.4%) 47/186 (25.3%) 83/251 (33.1%) PCR = polymerase chain reaction. * P = 0.02 for comparison of % positive between hospitals. † Nasopharyngeal swabs tested for influenza A and B, picornavirus, parainfluenza, adenovirus and respiratory syncytial virus. ‡ All bronchoscopy specimens cultured for Legionella spp, bacterial and fungal pathogens, and other investigations as requested by clinicians. § Serological tests for influenza A and B, Legionella spp, Mycoplasma pneumoniae, Chlamydophila spp and Coxiella burnetii.

Adrian R Tramontana · Vincent Sinickas

To the Editor: We present this case to highlight the differential diagnosis of afebrile seizures in patients from many asset-poor nations. A 3-year-old Congolese girl presented with sustained loss of consciousness after a prolonged generalised seizure. She had migrated, with her family, 12 months previously after a long period in a Zambian refugee camp. She was intubated briefly and given intravenous benzodiazepines. She made an uneventful recovery; she was discharged from hospital after 2 days. This was her first seizure and there was no history of fever, trauma or poisoning. The parents declined long-term anticonvulsants. Apart from mild malaria, she had been previously well and showed normal development. HIV serology and results of blood films for malarial parasites were negative; other blood tests, including an eosinophil count, were normal. Cerebral magnetic resonance imaging (MRI), performed because the diagnosis was unclear and the patient had had a prolonged seizure, revealed a single 8 mm cyst, with an enhancing wall and surrounding oedema, in the left frontal lobe. The cyst contained a scolex, pathognomonic of neurocysticercosis (Box). There were multiple foci throughout the brain, indicating active and resolving cysts. Serology results for Taenia solium were negative at presentation and 3 months later. The child was treated with 8 days of albendazole and 3 days of dexamethasone. Repeat MRI 2 months after presentation showed significant improvement, with a residual 3 mm calcified focus. The child has remained seizure-free for 18 months. Neurocysticercosis is caused by larvae of the pork tapeworm T. solium, which may encyst in the brain, eye or spinal cord, after ingestion of ova-contaminated food or water.1 In contrast, ingestion of encysted larvae (cysticerci) in undercooked meat results in intestinal infection with the adult tapeworm.1 Neurocysticercosis is common in many asset-poor countries, including those in Asia and sub-Saharan Africa from where many people in humanitarian refugee programs originate.2 In areas where it is endemic, T. solium is a leading cause of epilepsy in children and adults.3 The diagnosis of neurocysticercosis is difficult and the diagnostic differential is broad. Cerebral imaging showing typical lesions containing a scolex is diagnostic. T. solium serology is insensitive, especially in children with few cysts. Anticercal antibodies or cysticercal antigens in the cerebral spinal fluid are helpful, but these investigations are not widely available (they are available from the Centers for Disease Control and Prevention, Atlanta, United States). Treatment with anthelmintics is controversial; parasites may die spontaneously and treatment may cause local inflammation (reduced by steroids), which potentially exacerbates seizures or causes local tissue damage.4 Ocular cysticercosis should be excluded before anthelmintic treatment as the resultant inflammation may compromise sight; surgical excision should be considered if ocular cysticercosis is present.4 Empirical anthelmintics, often given before departure or following resettlement to people at risk, may potentially precipitate seizures.5 We treated this child with albendazole as there were multiple lesions likely to contain live parasites, and because anticonvulsants were declined. This case highlights that neurocysticercosis is a possible treatable cause of afebrile seizures in patients migrating from, or with a history of visiting, endemic areas, including resettled refugees. Clinicians in affluent countries are often unfamiliar with the disease, yet are managing increasing numbers of people at risk. Misdiagnosis is of particular concern because brain imaging is not routinely performed in children presenting with their first afebrile seizure. Magnetic resonance image of brain of 3-year-old girl showing cysticercus Encysted scolex of Taenia solium, surrounded by enhancing wall and significant oedema, in left frontal cerebral lobe.

Juliette M Lucey · James McCarthy · David P Burgner

To the Editor: Two recent publications have described programs of carrier testing for cystic fibrosis (CF) gene mutations.1,2 The authors conclude that CF carrier testing of women in early pregnancy and their partners, as well as couples contemplating pregnancy, can successfully identify those who are at risk of having a child with CF and provide them with reproductive choices. The authors use these proof-of-concept studies, in the absence of Australian economic data, to call for all couples to be offered CF carrier testing that is supported by government funding. Although reproductive choice is clearly an individual’s right, what obligation does the community have regarding government funding of specific services to generate information that might assist such couples? Genetic screening policies have often been determined on the basis of technological capability, rather than through a rigorous evidence-based review process.3 Decision making should also take into account evidence of clinically effective screening programs, ethical principles, and opportunity costs, given the limited resources available in the health sector. A simple economic analysis of these publications highlights some issues that need to be addressed. Massie and colleagues identified nine carrier couples by screening 3200 individuals (3000 females) before conception or during early pregnancy (CF carrier frequency, one in 30). Two of the nine carrier couples had affected pregnancies, which equates to a cost of $300 000 per CF case. In Christie and colleagues’ dataset of 1000 individuals, 73% had no family history of CF; 27 of these individuals carried CF mutations, and two carrier couples but no affected pregnancies were identified. Based on population gene frequency statistics (CF carrier frequency, one in 25; 75% of CF gene mutations being p. F508del),1 Massie et al’s screening model2 would, on average, require 3585 women to be screened to detect one affected pregnancy, costing about $740 000. Christie et al’s expanded one-step model1 would require about 3763 couples to be screened to detect one affected pregnancy, at a cost of more than $430 000. Among the 270 individuals with a family history of CF who were screened in the latter model, 126 were carriers of CF mutations (carrier frequency, one in two). It is clear that cascade screening of those with a family history would be a more effective strategy. There is an ethical argument that projected economic benefits from the termination of affected fetuses should not play a role in decisions to offer testing.4 Nevertheless, technological capability needs to be considered together with evidence of cost-effectiveness and community acceptance before public funding of community CF carrier screening can be justified.

Peter C O’Leary · Susannah J Maxwell · Leanne M Youngs · Kate J Brameld · Ian R Walpole

In reply: Our aims in publishing the outcomes of offering cystic fibrosis (CF) carrier testing to couples were to demonstrate the high acceptability rate and report the reproductive choices made by high-risk couples. Not all decisions resulted in termination. O’Leary and colleagues rightly raise the question of screening costs. Laboratory costs will reduce with economies of scale and centralisation of testing. The recent release of a position paper on population screening for CF by the Human Genetics Society of Australasia1 will influence the demand for testing. It recommends that all couples intending to have children, and women in early pregnancy and their partners, be made aware of the availability of CF carrier testing, and that couples should be offered testing for 10 CF transmembrane conductance regulator gene mutations using an expanded one-step or two-step model. O’Leary and colleagues suggest that cascade testing of those with a family history of CF would be a more effective strategy. However, only 10% of children born with CF have a family history.2 Studies have demonstrated that costs of CF screening are less than the averted medical care costs associated with fewer births of infants with CF.3-5 Although economic considerations are important, these should not form the primary goal of any screening program.

Louise M Christie · Angela J Ingrey · Gillian M Turner · Anne L Proos · Gloria E Watts

To the Editor: Hellard and Wang1 are correct in emphasising the importance of the general practitioner in the management of hepatitis C virus (HCV) infection. As the authors note, HCV infection is a considerable source of morbidity and mortality in the community, and the infection may cause a substantial burden of illness in the future if it is not appropriately managed. The GP plays a pivotal role in managing HCV infection, being the first and most likely point of contact for patients. However, Hellard and Wang fail to note that the GP’s most useful role is to inform patients that “alcohol abstinence is strongly recommended before and during antiviral therapy”.2 The well recognised role of alcohol in disease progression is emphasised in the position papers of both the American Gastroenterological Association and the United States National Institutes of Health.2,3 From a public health perspective, it is difficult to think of a more cost-effective approach to the management of such a public health issue.

Anne E Duggan · John M Duggan

In reply: Duggan and Duggan are correct to highlight the well recognised role of alcohol consumption in progression of hepatitis C virus (HCV) infection. Alcohol consumption has been found to increase viral load and accelerate hepatic fibrosis in HCV infection.1,2 While studies have reported that a history of alcohol consumption adversely affects treatment outcomes (with some reporting a dose–response relationship),3,4 treatment success has also been reported among patients who continue to consume moderate amounts of alcohol during treatment.5 Although there are biologically plausible mechanisms through which alcohol consumption might negatively affect treatment, low rates of treatment success among drinkers may also be related to lack of adherence to treatment regimen in this population.1 To date, no study has specifically measured the effect of alcohol consumption during treatment while adequately controlling for the effects of compliance, disease progression and baseline viral load. Until studies are undertaken that measure the direct effect of alcohol consumption on treatment success, while adjusting for compliance, it seems reasonable to advise patients to decrease their level of alcohol consumption before and during HCV treatment. However, given that some patients have successfully completed treatment without abstaining from alcohol consumption, this should not be an automatic exclusion criterion.

Margaret E Hellard · Yung-Hsuan J Wang · Rachel Sacks-Davis

To the Editor: The recent letter by Cox, about transfer of pregnant women from remote communities to Cairns for birthing,1 mirrored my experiences while working in general practice and psychiatric community outreach in rural Australia for many years. The removal of people from their familiar surroundings (especially for extended periods) in itself exacerbates health problems, even more so when they are already hindered by impaired socioeconomic status or ethnic disadvantage. Almost always, the security of their attachment and capacity to maintain resilience are strained. Furthermore, this displacement often occurs in emotionally charged or threatening health situations, where it is likely to be most damaging: childbirth, treatment of life-threatening disease caused by malignant neoplasm or cardiovascular disease, and management of mental disorders or substance misuse. The increasing concentration of “expert” treatment centres in fewer and fewer (usually metropolitan) centres, together with the degradation and de-skilling of rural and remote services that I have observed for the nearly 30 years I have worked in Australia, are sad. However, even worse is the failure of government to do anything to reverse the trend, despite repeated hand-wringing and talking about the rural health “problem”.

Robert D Craig

To the Editor: The Australian Medical Council recognises the importance of clinical experience in general practice for all medical students.1 In their recent article in the Journal, Vickery and colleagues identify three significant barriers to clinical teaching by Australian general practitioners: time, space and opportunity costs.2 They suggest that General Practice Super Clinics will be well placed to address the issue of space and, with additional funding, could also overcome the barriers of opportunity cost and lack of time. The latter claim may be true, but we need to invest in all teaching practices, not just in Super Clinics. The Australian Government is currently committed to establishing 35 Super Clinics. Even if more are set up in the future, it is difficult to see how they will ever make a major contribution to providing general practice placements for the 3000-plus students entering medical training each year. There are many high-quality general practices across Australia that have been committed to teaching for years. For this, they receive a $200 Practice Incentives Program payment per student per day. This amount has not increased since 2004, and is widely seen as insufficient to meet practice teaching costs. There is an urgent need to increase the sessional payment for teaching to an amount that realistically reflects the time and opportunity costs to practices. In addition, a national fund for capital investment in teaching practices would help address the third barrier that Vickery et al identify: many excellent practices are unable to provide student placements due to lack of space.

Timothy P Usherwood

To the Editor: A 69-year-old Indigenous Australian man, with no known Caucasian ancestry, presented in 2008 with a 7-week history of depigmentation of the face and neck, which was initially intensely pruritic and erythematous. He had neither a personal history nor family history of vitiligo, but a 2 mm thick, Clark level III, superficially spreading melanoma had been widely excised from his right lateral calf in 2001; results of a right inguinal sentinel node biopsy had been negative. In 2005, multiple small local recurrences on the right lower leg had been surgically removed. Two years later, further histologically confirmed local cutaneous and subcutaneous recurrences were excised, but new lesions continued to develop. His medical history included type 2 diabetes mellitus, hypertension, atrial fibrillation and coronary artery bypass grafting. He had no family history of melanoma. The onset of facial inflammation and depigmentation over a few days in 2008 was associated with complete regression of some leg lesions and partial regression of others. The facial inflammation settled spontaneously within a week. Computed tomography of the abdomen and pelvis at this time did not show any distant disease. The patient was unconcerned by the depigmentation and declined treatment. Over the following 5 months, the extent of his head and neck depigmentation increased (Box, A) and he developed more melanomas on his right lower leg, including one with a depigmented rim (Box, B). Positron emission tomography identified several areas of focally increased metabolism corresponding to the right lower leg lesions, but no evidence of disease elsewhere. The leg lesions have demonstrated only slow progression, and the patient continues to have 6-monthly follow-up at our department, as well as ongoing local review. Cutaneous melanoma is rare in Indigenous Australians, with only two reported cases of acral lesions.1,2 In melanoma, immunogenic factors may play a key role in disease course. Antibodies that cross-react with antigens on melanocytes and melanoma cells, such as tyrosinase, tyrosinase-related-protein-1 and tyrosinase-related-protein-2, can lead to both vitiligo-like autoimmune depigmentation and tumour regression.3 T-cell-mediated responses to melanoma antigens, such as MART-1 (melanoma antigen recognised by T-cells-1), are also enhanced in melanoma patients with depigmentation,3 which has been reported in approximately 3% of patients with stages III and IV melanoma.4 Vitiligo is a positive prognostic factor and has been reported in association with tumour regression distant from the depigmentation.4 In conclusion, this case of vitiligo-like depigmentation, affecting both the head and neck and a cutaneous metastasis, highlights the immune responsive potential of metastatic melanoma. Vitiligo-like depigmentation associated with melanoma in a 69-year-old Indigenous Australian man A: Extensive depigmentation of the face and neck 5 months after the onset of vitiligo. B: Depigmentation around the largest subcutaneous metastasis on the right lower leg.

Elizabeth M Christou · Diona L Damian · John F Thompson

To the Editor: I read with interest the article by Grange and colleagues suggesting that vaccination with BCG vaccine or past severe infections may help protect against the development of melanoma.1 They do not mention the work of Coley. Coley was a surgeon at the Hospital for the Ruptured and Crippled in New York, who, after observing the regression of tumours in patients who developed erysipelas involving the tumour site, reported in 1891 in the Annals of Surgery,2 and again in 1893 in the American Journal of the Medical Sciences,3 that injecting Streptococcus pyogenes from erysipelas isolates into the patient’s tumour induced regression. Thus the relationship between neoplasia and bacterial infection has been recognised for 118 years. Coley is considered the father of cancer vaccines.

Michael G E O’Rourke

To the Editor: We report a case of desmoplastic small round cell tumour (DSRCT) in the liver of a 23-year-old woman who presented with a recurrent non-pruritic rash. The woman had a generalised macular rash, predominantly on the back and upper thighs. She reported recurrent similar skin rashes over the previous 4 months that had been treated with intermittent courses of oral antibiotics. She had felt mild fatigue during the 3 weeks prior to presentation. She was otherwise well, but had non-tender hepatomegaly (17 cm) on examination. There was no peripheral lymphadenopathy. Levels of cholestatic liver enzymes were mildly raised (γ-glutamyl transpeptidase, 198 IU/L; alkaline phosphatase, 246 IU/L), but bilirubin and immunoglobulin levels were normal. The serum level of cancer antigen 125 (CA125) was 141 U/mL (reference range, < 35 U/mL). A computed tomography scan of the chest and abdomen showed multiple hepatic lesions (Box 1). A radiologically guided biopsy was taken, and histological examination revealed the typical morphology and immunophenotype of DSRCT (Box 2). Our patient was counselled regarding diagnosis and likely poor prognosis. We did not attempt to preserve fertility, because we felt treatment should not be delayed and that life expectancy was limited. Chemotherapy with alternating VAC (vincristine, doxorubicin and cyclophosphamide) and IE (ifosfamide and etoposide) cycles was started promptly. Molecular testing for EWS1/WT1 (see below) was not performed, as there was insufficient biopsy tissue available. The patient’s rashes disappeared after one treatment cycle, and we postulate that the rashes were paraneoplastic and immune-mediated. Restaging scans after four cycles of chemotherapy demonstrated a partial response. Stem cells were pre-emptively mobilised to store for possible subsequent autologous transplantation. The patient will be reassessed after eight cycles. If there is a significant response, the options of high-dose chemotherapy with autologous stem cell transplantation and/or debulking surgery will be explored. To our knowledge, this is the first Australian report of DSRCT in a woman presenting with recurrent rash. DSRCT is a rare, aggressive tumour that predominantly affects males in early adulthood.1 There is a single Australian report of a 15-year-old boy who died of DSRCT 20 months after diagnosis.2 The histogenesis of DSRCT is unknown, but it exhibits divergent differentiation, expressing epithelial, muscular and neural proteins. It is characterised by the chromosomal translocation t(11;22)(pl3;ql2), formed by fusion of the Ewing sarcoma gene (EWS1) to the Wilms tumour suppressor gene (WT1).3 Patients typically present with non-specific symptoms, and the tumours are usually intra-abdominal. The level of CA125 is often raised, but this does not assist with diagnosis or monitoring.1 Diagnosis is by histology and immunohistochemistry, complemented by cytogenetic identification of an EWS1/WT1 translocation. Patients with DSRCT have a poor prognosis, with a median survival of 15 months. Given the rarity of the tumour, there are no data from randomised phase III trials to guide management. Aggressive multimodality treatment offers the highest chance of disease control and prolonged overall survival.1,4 Palliative debulking can be of benefit if curative resection is not feasible. Radiotherapy is best employed as consolidation treatment after chemotherapy and surgery.1,5 Combination chemotherapy is the backbone of therapy and offers improved progression-free survival. The P6 protocol,6 which uses alternating cycles of VAC and IE with 21 days between cycles, is most widely employed. Subsequent high-dose myeloablative chemotherapy with autologous stem cell support may be beneficial.4 1 Pre-treatment computed tomography scan of the patient’s abdomen, showing multiple hypodense lesions in the enlarged liver 2 Histological sections from a core biopsy of a desmoplastic small round cell tumour (DSRCT) in the liver A: Irregular nests of small round hyperchromatic tumour cells were embedded in a prominent fibrotic stroma (haematoxylin–eosin stain, original magnification ×250). A diagnosis of DSRCT was confirmed by immunohistochemical stains (B–D). B: The muscle marker desmin. C: An epithelial marker AE1/3. D: The Wilms tumour marker WT1. (Original magnification of images B–D ×100.)

Meena Okera · David Moffat · Sudarshan Selva-Nayagam

To the Editor: Over-the-counter herbal supplements to promote weight loss have become increasingly popular. Several of these products contain potentially hepatotoxic substances. We present the first reported Australian case of acute hepatotoxicity associated with the weight-loss product Hydroxycut Hardcore (Iovate Health Sciences, Blasdell, NY, USA). Hydroxycut contains various ingredients, including extracts of the herbs Garcinia cambogia and Camelia sinesis (green tea root), and the chromium salt, chromium polynicotinate. A recent review cites these three ingredients as possible causes of Hydroxycut hepatotoxicity.1 A 23-year-old, previously well, construction worker presented to his doctor with a 2-month history of lethargy and jaundice. Test results confirmed serum liver enzyme derangement, and the patient was advised to stop taking the weight-loss supplement. Results of repeat testing a week later showed worsening liver enzyme levels and he was referred to our hospital. On arrival, the patient denied any symptoms except moderate lethargy and icteric sclera. He was usually well with no relevant medical or surgical history. He weighed 83 kg. He denied drinking alcohol, using prescription or non-prescription drugs, or receiving a blood transfusion. He had had unprotected sexual intercourse 2–3 months earlier. A previously obtained tattoo was being extended by a reputable tattoo parlour. He had been using Hydroxycut Hardcore daily for 10 weeks (obtained from his local outlet of a global nutritional products retailer) in an attempt to lose weight and tone muscle. He claimed to have taken the dosage recommended by the manufacturer (six capsules daily); he was taking no other supplements. Physical examination revealed mild jaundice without other features of chronic liver disease or portal hypertension. However, in addition to abnormal blood levels of liver enzymes, bilirubin and iron, results of the patient’s liver biopsy showed severe acute hepatitis (Box). The abnormal test results were consistent with acute drug toxicity. The patient improved without specific treatment and was discharged 8 days after presentation, with near-normal serum liver enzyme levels. He was well on follow-up at 4 weeks. Two reports from the United States link Hydroxycut Hardcore to acute liver injury in otherwise well young males.2,3 The American Food and Drug Administration in May 2009 advised consumers to stop using the product, based on 23 reports linking it to serious injury, including one case of liver failure leading to death.4 In May 2009, Australia’s Therapeutic Goods Administration (TGA) issued a warning to consumers about the product, although noting that no adverse events had so far been reported in Australia.5 In view of this first reported Australian case of Hydroxycut hepatotoxicity, we advise medical practitioners and consumers in this country to be wary of the product, and call on the TGA to re-examine its continued availability. Investigation results for a 23-year-old man with liver dysfunction after using Hydroxycut Hardcore Investigation Result (reference range) Blood tests Aspartate aminotransferase (U/L) 1182 (12–36) Alanine aminotransferase (U/L) 2950 (5–40) Alkaline phosphatase (U/L) 121 (50–140) Bilirubin (µmol/L) 113 (3–18) Prothrombin time (seconds) 13 (11–15) Iron (µmol/L) 68 (11–30) Ferritin (µg/L) 1897 (30–400) Iron saturation (%) 99 (16–50) Paracetamol Not detected Hepatitis A, B, C Negative HIV Negative Autoantibodies Not detected Epstein–Barr virus, cytomegalovirus, toxoplasma, leptospira, coxiella Negative Haemochromatosis genetic testing No abnormality Other tests Abdominal ultrasound No abnormality Percutaneous liver biopsy Severe acute lobular hepatitis with areas of bridging necrosis; no bridging fibrosis or cirrhosis were seen Hepatic iron index 1.1 (< 2.0)

N Nudrat Rashid · Jason Grant

To the Editor: The editorial by Buchbinder et al suggesting that the effectiveness of vertebroplasty has been determined by the two studies she and her co-authors published1 is misleading. Both studies2,3 contain major flaws. In both, 70% of eligible patients declined to participate. No details of these patients are published, but they may have been the patients with more severe pain. The median duration of pain in the Australian study2 was 9 weeks (compared with 16 weeks in the US study3); only 30% of patients had pain for less than 6 weeks. No information on the need for hospitalisation because of severe pain was given in either study. The average length of hospital stay was not published. In the Australian study, the inclusion criteria were the presence of back pain of less than 12 months’ duration and the presence of one or two recent fractures.2 In this group of patients, whose average age was 74 years, there will be many possible causes of back pain. The fracture may be the main cause of pain, a part-player, or may not be significant. In patients with milder pain and longer duration of pain, non-fracture causes are more likely. In the US study,3 patients were selected on the basis of x-ray unless the fracture “was of uncertain age”. I have performed an audit of my practice and found that in patients with an unequivocal x-ray diagnosis of fracture level, magnetic resonance imaging (MRI) identified another fracture not seen on x-ray in 23 of 63 patients (36%), and in 10 of the 63 patients (16%), a fracture that was presumed acute showed no oedema on MRI. In the Australian study,2 the experience of the radiologists performing the vertebroplasty is not made clear; no details are given about the number of patients they had previously treated. The incidence of osteomyelitis (3.8% at best, 30% at worst, depending on which centre was involved), despite prophylactic antibiotic therapy, is unacceptable. In the US study, injury to the thecal sac in one of 78 patients suggests incompetence. The protocol stated that cement injection was ceased if “cement reached the posterior quarter of the vertebral body or leaked into intraosseous structures”. This sometimes happens after 1 mL of cement has been injected. Experienced operators will perform various manoeuvres to ensure an adequate spread of cement occurs throughout the vertebral body. It would appear this was not done. The volumes of cement injected are not published, except an estimate of “about 3 mL”. The sham procedure was not a true placebo. Injection of local anaesthetic onto the pedicle would likely block the dorsal ramus nerve and provide partial analgesia of the fracture if the fracture extended into the pedicle. Those who perform vertebroplasty regularly see patients who are bedridden, in severe pain, intolerant of analgesics, and who have undergone various procedures including epidural injections or facet joint injections without benefit, and who then respond to vertebroplasty within 24 hours. Efforts should be aimed at refining technique and patient selection, rather than throwing out the baby with the bathwater on the basis of inappropriate studies.

Paul J Graziotti

To the Editor: Clinical trials study a restricted patient group, so their results may not be generalisable to a different population subgroup or the population as a whole. The editorial by Buchbinder, Osborne and Kallmes1 about their recent vertebroplasty studies2,3 concludes that vertebroplasty offers no benefit over placebo. They suggest that, in light of their trials, the decision to list vertebroplasty on the Medical Benefits Schedule will be reviewed later this year. I understood the review to have been part of the original listing on the benefits schedule and not as a result of their studies, and I suggest that their editorial generalises results to a subpopulation of early acute vertebral fractures that they did not study. The duration of symptoms in osteoporotic vertebral fracture is critical, as most fractures heal quickly with a good outcome by 3 months, and only a very small group of patients continue to experience pain.4 A fracture that is still painful months after the event is not a “normal fracture”, and I suggest is less likely to respond to the same management concepts as an acute fracture. In the study by Buchbinder and colleagues, patients had persistent pain and were recruited up to 1 year after their vertebral fracture.2 Nearly three-quarters had significant ongoing pain for at least a month after their fracture, and most for at least 2 months. The study by Kallmes and colleagues also included symptomatic fractures up to 1 year old, with the interquartile range (8–38 weeks) suggesting that they had an even longer period between fracture and inclusion in the trial.3 While vertebroplasty appears to be unhelpful for patients who continue to have chronic pain months after an acute osteoporotic fracture, the authors have not robustly excluded vertebroplasty as improving quality of life and pain management in those who undergo vertebroplasty within days to a month of the fracture. Such an outcome is suggested by Rousing et al, who showed that vertebroplasty within 2 weeks of fracture led to a rapid reduction in pain within 12–24 hours, similar to the result of conservative management at 3 months.4 Any review of the role for vertebroplasty should consider the populations studied and, hence, should define the characteristics of patients in whom to intervene or not intervene.

Kevin D Pile

In reply: The letters by Graziotti and Pile raise spurious issues that in no way threaten the key message of our trials. Participation rates in both trials were better than other controlled trials of vertebroplasty or kyphoplasty.1,2 Eligible patients who declined enrolment in the Investigational Vertebroplasty Efficacy and Safety Trial (INVEST) had similar levels of pain and disability to those who participated.3 Both trials adhered to stringent eligibility criteria, ensuring that only patients with pain due to acute or subacute fractures were included. All operators were trained and experienced, and the low incidence of serious adverse effects in both trials is consistent with the literature. There is no evidence that the outcome of vertebroplasty is influenced by cement distribution or volume.4 Local anaesthetic infiltration of the periosteum of the pedicles, as occurred in one trial,3 is unlikely to have a sustained effect. As Pile points out, most osteoporotic vertebral fractures heal quickly; this implies that most people would be unlikely to benefit from early invasive intervention. Consistent with this, public funding for vertebroplasty in Australia only has interim approval for patients whose pain is not controlled by conservative medical therapy. While duration of medical therapy is not specified, historically, this has ranged from at least 4 to 6 weeks. Thus, both trials included patients similar to those who would qualify for government-subsidised funding of the procedure in Australia. While Pile acknowledges that vertebroplasty appears to be of no value in patients with persisting symptoms (the group most likely to derive benefit), he seems to suggest that it may have a role in early treatment (within days to a month). As well as being at odds with his earlier statement, this is not supported by the available data. Many participants in both trials had short symptom duration (Australian trial, 32% < 6 weeks; INVEST, 20% < 6 weeks and 41% ≤ 13 weeks), and neither trial found evidence that symptom duration was a treatment effect modifier. The trial by Rousing et al reported comparable outcomes from vertebroplasty and conservative treatment in patients with acute symptoms (40 patients, < 2 weeks; 10 patients, 2–8 weeks).5 While no data were presented, the immediate (12–24 hours) benefit from vertebroplasty reported in this open study, like clinical experience, could be attributable to many factors including local anaesthesia, regression to the mean, and expectation bias. The onus remains on proponents of vertebroplasty to prove that any benefits of vertebroplasty outweigh the potential risks.

Rachelle Buchbinder · Richard H Osborne · David Kallmes

To the Editor: In their letter of 5 October 2009, Wong and colleagues highlight the importance of providing training for surgical specialties in the private sector.1 With 64% of surgical activity in Australia now occurring in the private sector,2 and public hospital activity constrained due to ongoing budget imperatives, the Royal Australasian College of Surgeons (RACS) has been actively exploring this idea for some years. The new Surgical Education and Training (SET) program selects trainees into one of nine specialty programs.3 Currently, there are 1254 trainees in the SET program across Australian, New Zealand and overseas positions. Once selected into a specialty program, trainees who succeed in achieving the educational goals will be able to progress through its entirety. Consequently, to enable completion of training in the program, each SET Level 1 post needs to be matched in the public or private sector with more senior training positions to ensure appropriate progression. The RACS has worked with a number of private hospitals and the federal government to identify and fund 50 training positions suitable for surgical education across Australia. The funding has predominantly been provided through the Australian Government’s Expanded Specialist Training Program. This program was established following the release of the Medical Specialist Training Steering Committee report4 to encourage training in settings other than public teaching hospitals. The RACS is keen to have this program substantially enhanced and is attempting to identify models with the federal government that can achieve this. This is where the work by Wong and colleagues1 is so important. The public and private sectors are different. Both can be highly useful for the education of a skilled surgeon. However, all educational environments need enthusiastic supervisors and trainers. The community and our patients also need to be understanding, supportive and enthusiastic for education of surgical trainees to occur. The RACS applauds Wong et al for progressing this discussion and highlighting the benefits that can result from expanding surgical training into the private sector.

Ian R Gough · Ian D Civil · Spencer W Beasley · Bruce H Barraclough · David J Hillis

To the Editor: I note, with a breath of fresh air, your recent column about managing hospital staff rosters1 and, in the same issue, the article by Dietz, calling for a simpler, more resilient health bureaucracy.2 We are stuck in an environment where process seems to be disassociated from outcome and, if the outcome is not what is wanted, then more process is added, thus compounding the problem. Surely it is time to step back a bit and look strategically at bureaucratic processes, and how they work and don’t work? No one would deny that we need good administration — it is one of the very bastions of our way of life. We seem to study most things in an evidence-based manner, or at least try to. Why can’t we have chairs of bureaucratic studies in our universities to rigorously research our bureaucratic processes? Armed with sound evidence, we could develop template systems and other tools to break the nexus in which we find ourselves. Dare I say the spin-off would be greater than just health care. Food for thought.

Robert N Atkinson

To the Editor: We write to encourage policy debate over newborn screening for congenital adrenal hyperplasia (CAH). Classical CAH is a severe, life-threatening disease affecting about one in 15 000 liveborn infants in Australia.1 An inexpensive screening test for newborns is available, but this test is not included in the current newborn screening program in Australia. Three-quarters of children with CAH have the severe salt-wasting type that typically presents with failure to thrive, and progresses to severe hyponatraemic, hyperkalaemic dehydration and shock due to an adrenal crisis within weeks of birth. CAH is the most common cause of ambiguous genitalia in neonates (due to virilisation from adrenal androgens in utero); girls with CAH may be incorrectly assigned as boys unless the diagnosis is made without delay. CAH can be easily detected in neonates before the onset of illness by an established heel-prick newborn screening test that has good specificity and sensitivity, especially when used together with second-tier testing. Screening for CAH has been available for 30 years internationally, and is used in all American states, New Zealand and many countries in Europe, Asia and Latin America. Newborn screening reduces mortality and incorrect sex assignment.2 Case reports from Australia3 and overseas4 have shown that undiagnosed CAH is a cause of apparent sudden infant death syndrome. These deaths could have been prevented if newborn screening was in place. A pilot study in New South Wales showed that newborn screening for CAH prevented salt-wasting crises and their potential long-term consequences.1 The cost-effectiveness of newborn screening is difficult to measure, and there is little published evidence on this subject. Although a recent study suggested that CAH screening is not cost-effective,5 the only outcome assessed was mortality; other benefits of early diagnosis and intervention — including reduced morbidity and psychological impact — were not assessed. Newborn screening for CAH is not expensive; the cost per test within the laboratory is about $2, and the incremental cost per infant is in line with other newborn screening tests. In a recent survey, the Australasian Paediatric Endocrine Group found that 91% of paediatric endocrinologists considered provision of newborn screening for CAH in Australia to be very important. The Newborn Screening Joint Subcommittee of the Human Genetics Society of Australasia unanimously supports the inclusion of newborn screening for CAH in all Australian states. Two Australian parent and patient advocacy organisations — the CAH Support Group Australia, and Caring and Living as Neighbours — also strongly support the proposal for adding newborn screening for CAH to the current screening program. Despite clear predicted benefits and agreement among key stakeholders and expert advisers, no state in Australia currently screens for CAH. It is the state governments — guided by the Australian Health Ministers’ Advisory Council — who decide on funding for newborn screening tests, and who should be accountable for acting against the weight of expert opinion and systematic evidence.

Garry L Warne · Katrina L Armstrong · Thomas A Faunce · Bridget M Wilcken · Avihu Boneh · Elizabeth Geelhoed · Maria E Craig

To the Editor: Our positive experience with insulin pump therapy (IPT) in children without private health insurance contrasts with that of Thong and colleagues,1 who found that IPT did not significantly reduce glycated haemoglobin (HbA1c) levels in uninsured adults. IPT improves metabolic control, reduces the risk of microvascular complications and improves quality of life in children with type 1 diabetes mellitus.2,3 Private health insurance fully rebates the cost of an insulin pump, but many uninsured Australian children with type 1 diabetes are denied access to IPT because their family cannot afford the $8000 purchase price of an insulin pump. The other major impediment to using IPT is the paucity of access to skilled local IPT teams. In November 2008, to improve access to IPT, the federal government introduced a means-tested subsidy (to a maximum of $2500 per child) to be administered through the $5.5 million Type 1 Diabetes Insulin Pump Program.4 By 30 June 2009, the program had subsidised only 31 children for insulin pump purchase (unpublished correspondence from the Hon Mark Butler MP, Parliamentary Secretary for Health, to Mr Darren Chester MP, Member for Gippsland, July 2009). The largest user of this scheme, Gippsland Paediatrics (a private practice in rural Victoria), commenced IPT in 11 of the 31 children. Through local service clubs and other charitable institutions, we raised the funds required to pay the $5500 balance for all 11 children.5 Six other financially disadvantaged Gippsland Paediatrics patients had obtained insulin pumps through grants or community fundraising before the government subsidy program was introduced. Thus we have experience of 17 children, aged between 4 and 18 years (mean, 10.8 years) who were recipients of “donor” pumps. This sample represents about a quarter of the local children with type 1 diabetes and almost two-fifths of the 46 patients we have commenced on IPT. To evaluate the metabolic outcome of IPT for these 17 children, we conducted a retrospective analysis of glycaemic control by comparing the average level of HBA1c during the 12 months before commencing IPT with the most recent HbA1c level. The pre-IPT mean HbA1c level of children using the donor pumps was 9.2% (SD, 1.45%), which fell to 7.6% (SD, 0.83%) (P < 0.001) after a mean IPT duration of 10.2 months (SD, 6.1 months). In children aged 12 years or under (10 patients), the mean HbA1c level fell from 9.0% (SD, 0.94%) to 7.6% (SD, 0.43%) (P < 0.001) after a mean IPT duration of 11.9 months (SD, 7.6 months). In the remaining seven patients, aged 13–18 years, the mean HbA1c level fell from 9.4% (SD, 2.0%) to 7.8% (SD, 1.43%) (P = 0.03) after a mean IPT duration of 7.6 months (SD, 1.4 months). Gippsland Paediatrics uses the RADICAL (Rural Australian Diabetes — Inspiring Control Activity & Lifestyle) model of care.6 The model consists of a collocated multidisciplinary team, including a general paediatrician, diabetes educator and counsellor, with the patient and family receiving proactive emotional support, consistency of personnel, and point-of-contact HbA1c testing. We individualise our approach through regular case conferences and try to match therapy with desired lifestyle. Our study demonstrated that, using this model, IPT improves glycaemic control in uninsured children targeted by government policy — at least in the short term. To improve short-term health and reduce long-term diabetic complications in families who cannot afford insulin pumps, government programs need to make IPT more accessible to those families and support local multidisciplinary IPT teams.2

Peter W Goss

To the Editor: Norovirus, previously known as the Norwalk agent, is a recognised cause of acute diarrhoeal illness in all age groups, but its significance in hospitalised children is poorly described. Noroviruses cause infection worldwide and year-round, with a distinct increase in disease occurrence in colder months.1 Rotavirus has long been recognised as the most important viral cause of gastroenteritis in young children, causing significant morbidity, as well as cost to the community of hospital admission and lost parental productivity.2 In July 2007, two new rotavirus vaccines were licensed for use in Australian infants; their use has reduced severe rotavirus disease requiring hospital admission.3 One difficulty in accurately documenting the role of norovirus in childhood acute diarrhoeal illness has been the limited availability of routine diagnostic testing. Enzyme-linked immunosorbent assay (ELISA) for noroviruses is now available commercially; it has limited sensitivity of 55%–93% but good specificity of 73%–97%. We retrospectively reviewed the frequency of detection of norovirus in the faecal samples taken from inpatients and outpatients with acute gastroenteritis at a tertiary paediatric hospital. We tested stool samples of 3962 children with episodes of acute diarrhoeal illness in a 12-month period (2007) and detected norovirus in 122 (3.1%). Ninety-one of the children infected with norovirus were admitted to hospital; 63 patients had a stay of less than 7 days with a median of 1 day, while 28 patients where in hospital for more than 7 days. The norovirus infection in 30 of the inpatients (33%) was hospital-acquired. Most hospital-acquired infections occurred in patients hospitalised for more than 7 days (19 of 28; 68%), and most of these patients had predisposing medical conditions, predominantly immunosuppression due to treatment for malignancy or other causes. Norovirus is a significant cause of viral gastroenteritis in infants and children. Our findings are comparable with those of other studies, which indicate that norovirus infection causes 20%–88% of viral gastroenteritis in children and is responsible for a significant proportion of hospital admissions of children with gastroenteritis.4,5 With the introduction of universal rotavirus vaccination for Australian infants, the importance of norovirus as a cause of gastroenteritis in infants and children is likely to increase. We recommend that hospitals which admit children consider using norovirus testing to establish the incidence and prevalence of disease, and to inform public health authorities responsible for infection control policy and practices.

Alison M Kesson · Nicola Benwell · Elizabeth J Elliott

To the Editor: Rudkin and colleagues1 remind readers of the importance of detecting congenital glaucoma early to reduce the risks of permanent eye damage, including blindness. The first clinical signs of congenital glaucoma are reported to be blepharospasm, photophobia and excessive tears, all difficult to discriminate in an infant. If the condition is untreated, the cornea progressively loses clarity, and diagnosis becomes more obvious. In giving this account of my personal experience, I remind general practitioners, paediatricians and ophthalmologists that early oedema of the cornea may be detectable before other signs. Our daughter was born uneventfully and without medical problems. Four weeks after the birth, my wife, while gazing into her newborn’s eyes, commented, “Do you think her right eye is . . . more “shiny” than the left?” Looking at all angles, the anxious medical parents were convinced it was. Various medical friends were consulted. “Maybe, possibly”, they indulged us. A call to the senior paediatric ophthalmology registrar at our local children’s hospital was made along the lines of, “Is there such a thing as loss or increase in shine to the eye of a newborn?” In the absence of any other signs, such as inflammation, misery or excessive tears, we were told not to worry. Not reassured, we prevailed upon another ophthalmology registrar who, in a fit-in appointment, confirmed subtle corneal oedema caused by bilateral glaucoma, worse in the left eye. In retrospect, the diagnosis was obvious. “Couldn’t have been anything else”, except the presenting sign was not a cloudy cornea, blepharospasm or misery — it was simply light reflecting off one eye less brilliantly than the other. “It ain’t fine, if it don’t shine.”

Peter J Lewindon