Letters

To the Editor: Dabadghao and colleagues have drawn attention to the high prevalence of diabetes mellitus and impaired glucose tolerance (IGT) among Australian women with polycystic ovary syndrome (PCOS).1 Quite rightly, both in this article and in the accompanying editorial by Teede and Stuckey,2 the authors have stressed the need to test women with PCOS for diabetes, and that long-term follow-up and lifestyle modification are important. However, it is important to note that many of these women were attending a reproductive endocrinology clinic for treatment of infertility. Therefore, two other points need to be highlighted. First, the high prevalence of glucose intolerance among this group is of immediate concern, as type 2 diabetes can pose a considerable risk to a pregnancy.3 The dangers include miscarriage, fetal malformation and perinatal mortality. Data from New Zealand indicate that perinatal mortality in pregnancies of women with type 2 diabetes was about triple that in pregnancies of women without diabetes; and, in women with type 2 diabetes which was not detected until after pregnancy was achieved, perinatal mortality was 4.5 times that of women without diabetes.4 Screening for diabetes therefore provides an opportunity to ensure that women with glucose intolerance are adequately prepared for pregnancy, thereby minimising the risks. Important measures include high-dose folate therapy and tight glycaemic control, in accordance with guidelines previously published in the Journal.5 Second, the risk of adverse pregnancy outcomes related to the women’s obesity (mean body mass index, 35.1 kg/m2) is also of concern. Therefore, stringent efforts should be made to take the opportunity presented to normalise the weight of women with PCOS before conception.6 The data presented by Dabadghao and colleagues also provide insights into the most appropriate means of screening for diabetes in this high-risk population. They have shown that screening by fasting glucose level alone will miss a third of cases of diabetes. Furthermore, at least 81% of IGT will also be missed! Glucose tolerance testing is therefore far superior to fasting glucose level for the detection of diabetes and IGT. This is a critical point, given the potential ramifications of undetected diabetes. Given these findings, we urge clinicians to routinely perform a glucose tolerance test for women with PCOS attending for fertility treatment, so that all cases of abnormal glucose tolerance are detected, and appropriately managed, before and after conception. It would be a tragedy for a woman to achieve a pregnancy through in-vitro fertilisation, only to develop complications from undiagnosed diabetes.

N Wah Cheung · Jeremy J N Oats

To the Editor: Drug-eluting coronary stents (DES) were approved for use in Australia in 2002, after they were found to be effective in limiting the incidence of restenosis.1 However, their cost is three to four times that of traditional bare-metal stents, and most Australian states restricted their use in the public health system. In 2006, we reported in the Journal that DES were used in 45% of patients undergoing percutaneous coronary intervention (PCI) in Victorian public hospitals, and that they were largely reserved for patients with risk factors for restenosis, such as diabetes, small vessels, and complex lesions.2 However, in the private health system, DES can be claimed as prostheses from insurance funds, so their use is not limited by financial constraints. In early 2007, multiple reports from around the world noted a small but significant increase in late stent thrombosis occurring 1–4 years after implantation of DES.3,4 This caused concern, as stent thrombosis has a mortality rate approaching 50%. It is now recommended that all patients with DES maintain aspirin and clopidogrel therapy for at least a year, although the appropriate duration of this treatment remains unknown.5 Further, long-term dual antiplatelet therapy is associated with an increased risk of bleeding and is problematic for patients requiring surgery.4,5 We examined the use of DES from February 2006 to June 2007 in 674 patients undergoing PCI by 10 operators in a Victorian private hospital. Monthly use dropped dramatically, from a peak of 91% of patients in July 2006 to 34% in June 2007 (Box). In 118 PCIs performed between March and May 2007, DES were used more often in: diabetic than non-diabetic patients (67% v 47%; P = 0.05); small (≤ 2.5 mm) vessels compared with large vessels (74% v 53%; P = 0.04); and long lesions (> 20 mm stent length) compared with shorter lesions (62% v 52%; P = not significant). This mirrors the pattern previously seen only in patients treated in the public health system.2 Given the issue of late stent thrombosis and the need for prolonged dual antiplatelet therapy, reserving DES for patients who are at high risk of restenosis in both the public and private health systems seems very appropriate. Utilisation is likely to change again with a better understanding of the long-term safety of DES, but a cautious approach should be maintained. Drug-eluting stent (DES) use per month (February 2006 – June 2007) in patients in a Victorian private hospital

Suzanne M McLean · David J Clark

To the Editor: After the recent New South Wales parliamentary inquiry into Royal North Shore Hospital, one might ask whether the deliberations will deliver real change to the hospital system. An article in the Lancet draws attention to some adverse outcomes in London hospitals.1 One such case is reported from the evidence and conclusions of the Islington Coroners’ Court into the death of a man as a result of his outpatient management. The report states: The jurors have . . . taken into consideration the large number of patients attending Guy’s Hospital as casual patients, [and] are of the opinion that the skilled supervision is insufficient, and should be increased; but they . . . believe the deceased received all the care and attention which the present arrangement of the hospital affords. The report goes on to discuss the effect of the excessive numbers of patients each house surgeon is expected to manage daily. The writer is of the mind that “the reported cases are now so frequent that something will have to be done”. As for immediate solutions, the report suggests: The officers of hospitals will have to be a little more careful. The committees and governors of hospitals must not impose impracticable quantities of work on one man’s shoulders; they must take steps either to diminish the amount of casual out-patient work, or they must increase the number of competent and qualified persons. The article concludes that “there is another party in these questions who is not entirely free of blame — viz., the public”. The writer supports the public’s right to “express indignation at defective diagnosis and accommodation in hospitals” but implores the public to be more liberal with hospital funding. The conclusions are straight to the point: The committees of hospitals cannot multiply beds and qualified house-surgeons without funds, any more than one can make bricks without straw. And if the maimed and the diseased are not to be denied skilled advice and accommodation at hospitals, or are not to be passed from one hospital to another, the public must be far more liberal in its support of hospitals than it has been. This report was published in the Lancet on 20 August 1881. Has nothing changed?! The public has now relinquished its responsibility for running public hospitals to the state. I hope more permanent solutions to the problem will follow the recent inquiry! As the writer suggested in 1881, “something will have to be done”.

Catherine E Storey

To the Editor: We report elevated mercury levels in three infants, each the only child of Chinese parents living in Sydney. All three children had eaten fish congee (a rice and fish porridge) as a weaning food and ate fish regularly as toddlers. Their parents had sought medical advice for either developmental delay or neurological symptoms in the children. A 2-year-old boy had demonstrated increasingly aggressive behaviour for the past 6 months. A general practitioner had diagnosed mercury poisoning in the boy’s father 2 months earlier, following investigation for complaints of allergies, rashes, abdominal pain and diarrhoea. The family ate fish (usually salmon, barramundi or snapper) at least five times a week, and had used unspecified herbal medicines in the past. The child had eaten fish regularly since weaning. The boy’s blood mercury level was 158 nmol/L (normal range [NR], < 50 nmol/L), a random urine mercury/creatinine (Hg/Cr) ratio was 9 nmol/mmol (NR, < 6 nmol/mmol*), and his hair mercury level was 1.42 mg% (NR, < 0.18 mg%). The boy’s father and mother (who was pregnant) also had elevated hair mercury levels, of 4.3 mg% and 6.0 mg%, respectively. The father and child were treated with chelation therapy elsewhere. * The two laboratories reported different normal ranges for the urine Hg/Cr ratio. A boy aged 2 years and 10 months presented with delayed speech and some autistic features. Since weaning, he had eaten fish (barramundi, sea perch, salmon and rock cod) up to eight times a week. He had no history of herbal medicine use, and his thyroid function, blood lead level, and a DNA screen for fragile X syndrome were normal. The child’s blood mercury level was 350 nmol/L and urine Hg/Cr ratio was 14 nmol/mmol (NR, < 10 nmol/mmol*). The boy’s father did not eat fish, and his blood mercury level was 19 nmol/L. The child’s mother did eat fish, and had a blood mercury level of 27 nmol/L. Two weeks after removing fish from the diet, the child’s blood mercury level had fallen to 99 nmol/L and his urine Hg/Cr ratio to 7 nmol/mmol. However, his behaviour did not improve, and he was subsequently diagnosed with classical autism. A 15-month-old boy presented with delayed development since birth. Fish had been introduced to his diet at 8 months of age, and he had since continued to consume fish four to five times a week. He had recently eaten either ling or salmon. The boy’s mother had consumed ling three to four times a week after the fifth month of her pregnancy. The child’s thyroid function, DNA screen for fragile X syndrome, chromosome karyotype, and urinary metabolic screen were normal. His blood mercury level was 143 nmol/L, but fell to 19 nmol/L over a period of 1 year after ceasing fish intake. His longer-term developmental status is unknown. Fish congee, made with either freshwater species or locally caught fish, is a common weaning food in coastal regions of southern China and South-East Asia.1 Adding fish to the weaning diet has health benefits,1,2 such as reducing anaemia, and is actively promoted. However, fish, particularly the large pelagic (open ocean) species more likely to be bought in Australia, may also contain mercury. Excessive consumption of mercury has been associated with neurological impairment.3-5 The Box shows that the consumption by infants of fish congee made from portions of large fish species may exceed the provisional tolerable weekly intake (PTWI)7 for methylmercury of 1.6 μg/kg bodyweight/week (the limit considered sufficient to protect a developing fetus). Food Standards Australia New Zealand’s most recent risk assessment concluded that median-level consumers of fish are unlikely to exceed the PTWI for methylmercury,6 but frequent consumers might if all their consumption is of predatory or long-lived fish species, which tend to acccumulate higher concentrations of mercury. It has been previously noted in the Journal that public health policy regarding fish consumption needs to balance the health benefits for cardiovascular disease and anaemia with the possible ill effects of mercury on neurological development in infants.8 We recommend that multilingual information about fish and mercury be made available to pregnant women and mothers, especially targeting groups who are likely to be frequent consumers of fish and who use fish in weaning and infant foods. Regulatory and health promotion activities could also be informed by surveillance of blood or hair mercury levels in infants from ethnic groups at high risk of mercury intoxication, and of the frequency of fish consumption in this age group (by type of fish). Estimated weekly mercury intake in infants consuming fish congee Mean mercury concentrations in fish tissue* (μg/kg fish) Child’s estimated weekly mercury intake† (μg/kg bodyweight/week) Fish fillets‡ Maximum 50 1.25 Median 16 0.40 Minimum 5 0.13 Barramundi Maximum 310 7.75 Minimum 40 1.00 Snapper Maximum 520 13.00 Minimum 52 1.05 * For species consumed in Australia.6 † For a 12-month-old child weighing 10 kg; weekly fish consumption is estimated to be 0.25 kg, assuming 50 g servings five times per week. Provisional tolerable weekly intake for methylmercury = 1.6 μg/kg bodyweight/week.7 ‡ Average concentrations of all fillets purchased.

Stephen J Corbett · Christopher C S Poon

To the Editor: Prostate cancer screening remains controversial. There is currently a lack of evidence that treating prostate cancers identified by screening leads to prolonged survival,1 and the main screening test (serum prostate-specific antigen [PSA] concentration) has poor sensitivity and specificity. Patients with an elevated PSA level usually undergo a transrectal ultrasound-guided (TRUS) prostate biopsy for definitive diagnosis. TRUS biopsy is associated with risks that include bleeding, urinary tract infections, prostatitis and bacteraemia. Infective complications can occur even when prophylactic antibiotics are administered.2 Gram-negative bacteraemia is usually associated with a mortality rate of at least 5%.3 We reviewed prostate biopsy-associated bacteraemia in Australian Capital Territory residents using data collected over the 5-year period from 2002 to 2006. All patients in ACT public hospitals who have positive blood culture results are followed as part of a bloodstream infection surveillance program. Although all prostate biopsies are performed in the private sector, nearly all patients who develop major complications are cared for in public hospitals. The number of biopsies performed on ACT residents during the study period was obtained from Medicare Benefits Schedule statistics (item numbers 37215, 37218 and 37219).4 Over the 5-year period, we identified 19 episodes of bacteraemia following 1843 prostate biopsies, representing a 1.0% risk of bacteraemia (95% CI, 0.6%–1.6%) (Box). No patients died, but five required admission to the intensive care unit. A 1% bacteraemia rate associated with prostate biopsies would be an underestimate of the true rate, for a number of reasons: some patients were also admitted with severe sepsis syndromes but with negative blood cultures; some patients may have been treated in another state; and some patients may have presented to private hospitals, specialists or general practitioners and been treated empirically without blood cultures being collected. Three additional cases of bacteraemia following TRUS biopsies were excluded from our rate calculations because they involved New South Wales residents. It has been estimated that, if a million men over 50 years of age were screened, about 110 000 would have raised PSA levels.5 Of these, about 90 000 would undergo a biopsy and 20 000 would be diagnosed with prostate cancer. Our data show that TRUS biopsies carry a risk of serious infective complications and, notably, about 75% of these complications would occur in men without prostate cancer. We believe that data on the likely complication rates resulting from PSA testing and TRUS biopsies must be factored into considerations of the benefits versus risks and the cost-effectiveness of any prostate cancer screening program. Prostate biopsies and associated bacteraemia episodes, Australian Capital Territory, 2002–2006* 2002 2003 2004 2005 2006 Total Prostate biopsies performed 322 324 465 377 355 1843 Bacteraemia episodes 6 3 2 4 4 19 Proportion of biopsies resulting in bacteraemia 1.9% 0.9% 0.4% 1.1% 1.1% 1.0% * Three New South Wales residents who were diagnosed and treated for bacteraemia in the ACT were excluded (two had biopsies in Sydney and one in the ACT). Two patients had two episodes of bacteraemia (each more than 1 month apart). Fifteen episodes of bacteraemia were caused by Escherichia coli and one each by Klebsiella pneumoniae, Group C Streptococcus, Citrobacter freundii and Proteus mirabilis.

Francis J Bowden · Jan Roberts · Peter J Collignon

To the Editor: The report by Risson and colleagues of a fatal case of necrotising pneumonia caused by community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA)1 appropriately highlights the emerging issue of CA-MRSA infections in Australia,2 and the possibility that severe S. aureus sepsis may follow recurrent furunculosis. We wish to draw attention to the association between severe staphylococcal pneumonia and a preceding influenza-like illness. In September 2006, a 56-year-old woman of European background with a history of chronic back pain and depression presented to the Royal Darwin Hospital after a 4-day influenza-like illness characterised by cough, fever and sore throat. She then developed dyspnoea and pleuritic chest pain, followed by an abrupt respiratory deterioration. She was intubated and admitted to the intensive care unit with severe sepsis. A chest x-ray showed widespread bilateral pneumonia. We began broad-spectrum antibiotic therapy with piperacillin–tazobactam and azithromycin as per the hospital’s dry-season protocol for severe community-acquired pneumonia. Further history from her husband revealed an episode of boils 1 month previously, which responded to antibiotic therapy. We added vancomycin to the therapy and, when sputum and blood cultures showed MRSA 48 hours after admission, we also added rifampicin and gentamicin. On Day 5 of admission, her clinical condition deteriorated further and we replaced rifampicin and gentamicin with linezolid. Complement fixation testing of serum taken on admission showed an influenza A antibody titre of 128, consistent with recent acute infection. Despite ongoing intensive supportive care, the patient died from refractory respiratory failure 10 days after admission. Typing of the S. aureus isolates from blood and sputum showed that their single nucleotide polymorphism and variable gene profile was consistent with the Queensland clone (ST93-MRSA-IV) of CA-MRSA, and that the Panton–Valentine leukocidin gene was present. S. aureus has long been a recognised cause of influenza-associated pneumonia. Of concern, two recent reports from the United States identified 25 patients with CA-MRSA associated with severe pneumonia following influenza-like illnesses.3,4 Most of these patients were young (median age of 21 years3 and 17.8 years,4 respectively) and otherwise healthy. Combined mortality in these two studies was 40%. With an increasing prevalence of CA-MRSA in areas of Australia,2 CA-MRSA pneumonia should be suspected in patients presenting with worsening respiratory status and sepsis following an influenza-like illness. We stress the importance of annual influenza vaccination for those at increased risk of influenza-related complications.5

Steven Y C Tong · Nicholas M Anstey · Gary D Lum · Rachael A Lilliebridge · Dianne P Stephens · Bart J Currie

To the Editor: The recent editorial by Collignon and colleagues emphasised the importance of infection control mechanisms in reducing patient harm from antibiotic-resistant organisms.1 It focused on disinfection of the hands of health care workers in hospitals. However, a vigorous education and surveillance program in a hospital in Victoria failed to achieve compliance among health care workers of even 50%.2 Top of the list of self-reported factors leading to poor compliance is “skin irritation and dryness associated with the use of hand hygiene agents”.3 There have been no properly controlled trials, with clinically important endpoints, of currently recommended hand-hygiene practices. With the likely poor compliance rates, such trials would likely fail. A different approach might be more effective. Reducing skin contact between health care workers, patients and their immediate environment seems logical. Data show that skin contact produces two-step transfer of material in 82% of cases.4 The Victorian study did include gloving as an alternative to disinfection in measuring hand-hygiene compliance.2 However, in what might be a backward step, a recent study concluded that physicians should be encouraged to shake hands with patients!5 Perhaps an educational campaign to avoid skin contact with environmental surfaces and other health care workers, with use of disposable gloves for patient contact, could be the basis of a successful trial to address more effectively the transmission of antibiotic-resistant organisms in hospitals.

Keith V Woollard

To the Editor: The magnitude and distribution of the problem of health care-associated methicillin-resistant Staphylococcus aureus (MRSA) in Australia can be gauged from the report of a forum on MRSA control conducted at the Australasian Society for Infectious Diseases (ASID) in March 2007.1 This report contrasted approaches to control of health care-associated MRSA and quantified the population incidence rate of health care-associated MRSA bacteraemia across Australia from data derived from direct surveillance systems (Box). Reporting of MRSA infections is thought to be complete from all jurisdictions except Victoria and New South Wales. Figures for Victoria were extrapolated from accurate surveillance data representing 50%–60% of events. The degree of incompleteness of reporting in NSW could not be determined, and a range based on reports to NSW Health over 3 years was used. Overall morbidity of health care-associated MRSA in Australia is much higher, as only a minority of MRSA infections lead to bacteraemia. The ASID report estimated that between 699 and 924 cases of bacteraemia would be prevented if other states and territories reduced their incidence of MRSA bacteraemia to that of Western Australia through implementation of more stringent infection control measures. The mortality of MRSA bacteraemia is 8%–50% (average, 29%).2 A recent study showed that more than half (59%) of such deaths were directly attributable to MRSA3 rather than other non-infective causes. These outcome proportions provide a minimum estimate of between 120 and 158 preventable deaths per annum in Australia directly caused by health care-associated MRSA — comparable to the annual South Australian road toll. As identified recently in the Journal by Collignon and colleagues, there are significant structural barriers to achieving infection control — especially inadequate isolation resources and pressure on bed stock.4 Other dimensions of the MRSA problem include the high incidence of MRSA in many aged care facilities, the epidemic emergence of community strains of MRSA (best described in the recent report from WA on MRSA notification data up until 20025), the possibility of significant zoonotic reservoirs,6 and the role played by imprudent antibiotic use. MRSA colonisation or infection needs to be made a nationally notifiable disease, with a system in place to enable typing of isolates. As in WA, such a system would enable more effective identification of MRSA carriers before hospital admission, the detection of emerging epidemic strains, and timely investigation of MRSA outbreaks occurring in community groups, such as in aged care facilities. Most importantly, all states and territories need to adopt, and provide resources for, consistent, stringent approaches to surveillance, prevention and control of health care-associated MRSA that are in keeping with internationally recommended approaches. Given the scale of preventable injury occurring in many states, MRSA control must be made one of the highest priorities for patient safety. Relative burden of health care-associated MRSA morbidity across Australia1 Area Health care-associated MRSA bacteraemia events Year(s) of data Rate per 100 000 population Darwin 16 2006 13.3 New South Wales/ACT*† 437–602 2003–2005 6.2–8.5 Queensland* 133 2005 3.4 South Australia* 37 2006 2.4 Tasmania* 3 2006 0.6 Victoria*† 270–330 2000–2006 5.4–6.6 Western Australia* 22 2006 1.1 Total 918–1143 4.5–5.7 MRSA = methicillin-resistant Staphylococcus aureus. ACT = Australian Capital Territory. * Figures from these jurisdictions include private hospital event estimates. † Figures from NSW and Victoria are minimum estimates, because of incompleteness of current reporting in these states.

John K Ferguson · Helen Van Gessel

To the Editor: The recent editorial by Collignon and colleagues challenged Australian physicians and health care leaders to confront the rising burden of methicillin-resistant Staphylococcus aureus (MRSA).1 Compared with Australia, the United States has a bigger problem with MRSA; more than 60% of all hospital-acquired S. aureus infections are now caused by MRSA.2 Appropriately, the medical community has made an urgent call for action. For example, the Institute for Healthcare Improvement (a not-for-profit organisation based in the US that aims to improve health care throughout the world) incorporated specific MRSA prevention measures into its recent 5 Million Lives Campaign (see http://www.ihi.org/ihi). One of these prevention measures, a recommendation for active surveillance, has generated controversy. Specifically, the cost-effectiveness of this strategy is still vigorously debated in the infection control literature.3 At present, it is unclear what surveillance testing method should be used in the laboratory, and whether testing should be done for all patients or just those identified as high risk. The cry for help from community activists in the US and the United Kingdom has reached the ears of their legislative representatives. In two northern US states, lawmakers are considering bills that require universal active surveillance in their hospitals. Mandating resource-stretched health systems to implement obligatory active screening is not a prudent use of resources. The Society for Healthcare Epidemiology of America and the US Association for Professionals in Infection Control and Epidemiology recently published a joint position paper opposing this legislative activity, noting that data in support of active surveillance have been restricted to high-risk populations.4 We support this position and remind readers that active surveillance does not obviate the need for adherence to basic and consistent hand-hygiene practices. Complacency and lack of clinical leadership remain the greatest challenges in the efforts to reduce the transmission of MRSA. Why do we accept this epidemic as a fact of life as our health care workers complacently contribute to the nosocomial transmission of MRSA? By implementing simple prevention policies, feedback of data on nosocomial transmission of MRSA, and increased infection-control education, we have achieved a 22% reduction in MRSA infections in our network of community hospitals.5 Still, we acknowledge the absence of a zero-tolerance approach to failures in hand-hygiene practices. More needs to be done. We challenge our clinical leaders to demand higher standards for hand hygiene. Most cases of nosocomial MRSA transmission represent failures of basic hygiene practices. The problem is surmountable. Infection control is not a skill of a few, but the responsibility of every team member. The onus is on all of us.

Luke F Chen · Deverick J Anderson · Keith S Kaye · Daniel J Sexton

In reply: We thank Woollard for his comments on hand hygiene. While important, hand hygiene is just one component of what is needed to decrease the spread of methicillin-resistant Staphylococcus aureus (MRSA) in hospitals. Decontamination of the environment, contact precautions for colonised patients, active surveillance and screening, effective programs to prevent common infections such as intravascular catheter sepsis, good antibiotic stewardship and better hospital design are also indispensable.1 We do not accept that “There have been no properly controlled trials, with clinically important endpoints, of currently recommended hand-hygiene practices”. For instance, the recent study quoted by Woollard showed that hand hygiene reduced infections hospital-wide, using the clinically important endpoint of serious bloodstream infections (MRSA and antibiotic-resistant gram-negative bacteria).2 Thus, at least two large peer-reviewed studies show that alcohol-based hand-hygiene programs reduce hospital-acquired MRSA infections2,3 (Level III evidence4). There is nothing wrong with using disposable gloves, as suggested by Woollard, provided they are changed every time a health care worker moves between patients. Otherwise, gloves spread MRSA just as efficiently as unclean hands. Applying good-quality hand-hygiene products is less cumbersome than changing gloves and also allows direct human contact, which Woollard reminds us is important to patients. How MRSA is spread in hospitals is now well known — our problem is getting health care workers to remember to practise good hand hygiene all the time, every day, before and after every patient contact. The data shown by Ferguson and Van Gessel reaffirm how common and serious a problem we have with MRSA bacteraemia. They estimate there are about five episodes per 100 000 people annually across Australia. However, we believe that the true rate is double this. The rate of S. aureus bacteraemia (ie, MRSA and methicillin-sensitive S. aureus combined) in Australia is around 35 per 100 000 per year,5 with 27% caused by MRSA.5 This crudely translates to an MRSA rate of 9.5 per 100 000. The rates are probably much higher in the states with more health care-acquired MRSA (New South Wales and Victoria). More recent data suggest that 36% of hospital-acquired invasive S. aureus infections were caused by MRSA, with the highest percentages in NSW (41%) and Victoria (39%).6 It is also worth noting that, when MRSA bacteraemia became notifiable in England in 2001, there was a 50% increase in reported S. aureus bacteraemia episodes.1 This suggests that under-reporting is common in any voluntary reporting scheme, and is also likely for Australian data. Worryingly, Chen and colleagues point out that MRSA is an even bigger problem in the United States than in Australia. However, we are not far behind.6 Although we share their concerns about legislative impositions, some external controls and measurements can be an advantage. Western Australia, the only Australian state where MRSA is notifiable, has the lowest rates of health care-associated MRSA. While we do not want imposed “one size fits all” legislated controls, we do need change: the practice of the past 40 years has not worked. Every institution needs to have an effective MRSA control program, with components chosen according to the local situation. Institutions should measure MRSA and report centrally, especially if their rates are high and not falling continually (eg, over a year). Shop-floor quality improvement programs with empowered workers are much better than top-down management-imposed regulation (eg, from government). We need to shake our complacency and that of our health care colleagues, accept clinical leadership and take control. Otherwise, legislative controls will be imposed on us.

Peter J Collignon · M Lindsay Grayson · Paul D R Johnson

To the Editor: Xue and colleagues reported an interesting randomised, single-blind trial of acupuncture for persistent allergic rhinitis (PAR) and concluded that acupuncture is an effective treatment for this condition.1 I am not entirely sure that this is true. The authors state that “once needling sensation (known as de-qi) was obtained, the needles were manipulated . . .”. In the sham group they inserted needles at non-acupuncture points where, according to acupuncture theory, no de-qi can be elicited. Thus the intervention patients were experiencing de-qi, and the control patients were not. This means that neither the patients nor the therapist were blinded. Consequently, the difference in outcome between the two groups could be unrelated to acupuncture itself, and caused by patient expectation, therapist expectation or both. In addition, the statement of Xue et al that “no other randomised controlled trial of acupuncture in adults with PAR has been reported in the English medical literature”1 was misleading. Our review of this topic2 included no fewer than six randomised controlled trials, all either published in English or, in one case, with an English abstract. Interestingly, three of them suggested acupuncture to be effective, while three failed to do so. I fear that the study by Xue et al does little to resolve this intriguing discrepancy.

Edzard Ernst

In reply: Ernst is concerned about the sham acupuncture procedure used in our trial.1 Although not universally agreed, the sham/placebo control we adopted has been described as best practice.2,3 The assumption that, without de-qi, participants would not be blinded is not supported by the literature. In fact, a sham procedure without de-qi was used in a recent trial reported by Ernst and colleagues on acupuncture for subacute stroke rehabilitation.4 In that study, as in ours, to increase the credibility of blinding, participants with previous experience of acupuncture were excluded, and those assessing the outcomes of treatment were blinded. With regard to previous randomised controlled trials of acupuncture for adults with persistent allergic rhinitis in the English medical literature, Ernst failed to distinguish between seasonal allergic rhinitis (SAR) and persistent allergic rhinitis (PAR).5 Of the six studies included in his review,5 five were on SAR, and the sixth, which was cited in our report (reference 14), was on children with PAR. These reports, therefore, are not inconsistent with our findings.

Charlie C L Xue · David F Story

To the Editor: Cannabis use is implicated in serious social disruption in many Northern Territory Aboriginal communities.1 Rising levels of cannabis use were first reported in Aboriginal communities in Arnhem Land in 2002, along with associated concerns about escalating social impacts and mental health effects compounded by other substance use.2 A random sample of 164 people in Arnhem Land initially interviewed and assessed in 2004 were followed up between October 2005 and June 2006. Their cannabis use was measured using health worker assessments and self-reports from interviews. Ethical approval was granted by the NT Health Department, Menzies School of Health Research, and James Cook University. Despite a modest decline in cannabis use in this population between 2002 and 2004,3 the 2005–2006 data indicate persisting high rates, with 61% of males and 58% of females (aged 13–34 years) using cannabis at least weekly. In a subsample of 60 cannabis users opportunistically recruited for in-depth interviews in 2005–2006 (37 male and 23 female, aged 13–42 years), 92% of males and 78% of females used cannabis daily; 88% reported cannabis dependence symptoms. These figures appear to be far higher than national rates, although national data for similar age groups are not available.4,5 Research has found that, nationally, 6% of males and 3% of females (aged ≥ 14 years) reported using cannabis in the past week; 18% of males and 13% of females smoked cannabis daily;4 and 21% of adults (aged ≥ 18 years) using cannabis were dependent.5 Beyond high rates of cannabis use in Arnhem Land communities, we also found local characteristics and perceptions that illustrate the drug’s distinctive context of use (Box). Quantities of cannabis used appear to be higher than in the general population; unemployment among users is higher; and violence related to diminished supply is common. One Indigenous community leader described attitudes to cannabis use: “... if there’s a bowl of it on the table, it is smoked until gone, morning to night”. Interestingly, some respondents reported that using cannabis prevents them from engaging in criminal activity (Box). While key community members may believe that cannabis is a tool for social control — “good for calming down people” — they are increasingly recognising the significant social and mental health problems it causes: People get chained by [cannabis], they don’t go hunting with family ... lots of fights when they can’t get any ... [Cannabis] becomes the boss. Continued concerns about adverse mental health consequences for Aboriginal people in Arnhem Land who use cannabis seem to be warranted. Cannabis appears to be firmly entwined in these isolated communities in a manner not seen nationally. High levels of concurrent drug use, particularly tobacco, raise additional health concerns. Resources are urgently needed for prevention programs and targeted interventions for chronic cannabis users and those with psychiatric comorbidity. If these patterns of use continue, the implications for compounding of pre-existing mental illness and the potential mental health burden are disturbing. Characteristics and perceptions of cannabis use in Arnhem Land Aboriginal communities (57 males and 49 females, aged 13–42 years*) in 2005–2006 compared with available national data from 1997† and 2004‡ National4,5 Arnhem Land* National4,5 Arnhem Land* Number of cones smoked Per cent unemployed current users / daily users 3.2 (average per day)‡ 7.4 (average per occasion) 25.6%† / nd 60% / Males, 41%; females, 94% Concurrent drug use Motivations for use Alcohol (86.2%); stimulants§ (8.2%–27.9%); none (10.8%); analgesics (6.6%); antidepressants (5.7%); tranquillisers/sleeping pills (4.4%); other (3.9%)‡ Tobacco (100%); alcohol, restricted access (40%); kava (15%); petrol (5%)¶ nd Socialisation (tempted, lonely, copying friends); mood altering (“calms me down”, “gets me going in the morning”, “makes my mind straight”); drug substitution (from alcohol or petrol); prevents criminal activity (stealing or other trouble) Drug substitution (when cannabis unavailable) Motivations for ceasing/moderating use Alcohol (60.4%); no substitution (34.2%); ecstasy/designer drugs (1.3%); painkillers/ analgesics (0.8%); tranquillisers/sleeping pills (0.5%); heroin (0.3%); antidepressants (0.2%); cocaine/crack (0.1%); other (1.1%)‡ No substitution (83%); kava (7%); alcohol (5%); petrol (5%)¶ nd Limited supply; starting a family (females); “sick of fighting when cannabis runs out”; “made me sick”; “mind not straight”; expenses and time spent looking for cannabis; employment (males) * Self-report interview data from an opportunistically recruited sample (using age and sex quotas) of respondents, including people who had never used cannabis as well as current and former cannabis users. † People aged ≥ 18 years.5 ‡ People aged ≥ 14 years.4 § Including ecstasy. ¶ There have been no reliable reports of stimulant, benzodiazepine or barbiturate use in these communities. nd = data not available.

K S Kylie Lee · Alan R Clough · Katherine M Conigrave

To the Editor: I was not surprised by the results published by Fassett et al1 regarding clinical handover. Despite being a crucial part of health care, clinical handover has only recently become a topical issue in the clinical governance arena. In May 2007, the World Health Organization launched the “Nine patient safety solutions” to “help reduce the toll of health care-related harm affecting millions of patients worldwide”.2 Solution number three relates to “communication during patient hand-overs”. Australia is in fact leading the international collaboration on clinical handover through the National Clinical Handover Initiative. This was recently launched by the Australian Commission on Safety and Quality in Health Care to develop and implement standardised solutions to patient safety problems associated with clinical handover.3 At a state level, the Victorian Quality Council conducted a clinical handover survey of Victorian health services in May 2006 to provide an overview of areas of concern relating to clinical handover.4 The Council launched a pilot project in 2007 to look at morning handover processes between junior doctors. Despite these efforts, hospitals are still struggling with the issue of clinical handover at the local level. All health professionals know that clinical handover is good clinical practice, but they need to be provided with the tools to carry it out properly. Clinical handover, depending on your definition, includes referral letters from general practitioners, discharge summaries from hospitals, as well as handover of clinical information between different shifts, treating teams, wards, health professionals and health services. It makes sense that the process of handover of clinical information be carried out in a standardised format, as the minimum dataset required is consistent for most circumstances. While there is a need for standardisation, health organisations must also be able to devise local innovative solutions that work for them. Information technology can assist in developing a solution to this issue. For example, different local health services have already developed in-house systems for electronic discharge summaries that are integrated with an electronic health record. While national quality bodies endeavour to develop national standards and tools for clinical handover, local health services must not sit idly and wait for these, but must continue to innovate and provide workable local solutions for their own health professionals. Otherwise, future surveys of clinical handover will continue to show that a problem still exists in relation to this issue.

Erwin Loh

In reply: Our national survey was specifically confined to medical morning handover report, one of many forms of clinical handover.1 The clinical governance area may have only recently recognised the importance of clinical handover, but it has been a topical issue for many years in the clinical arena, particularly in the United States.2 While Australia may be leading the way in international collaborations, our survey suggests that this is not translating into clinical practice. Rather than commissions and councils providing tools and guidelines to carry out clinical handover, clinical leaders need to participate and conduct clinical handover themselves at the local level. From our previous experience with morning report, we provided simple tips on how to implement clinical handover at the local level,3 and these have been incorporated into Australian Medical Association guidelines.4 Information technology can be employed to help with the clinical handover process. However, when using the all-inclusive definition of clinical handover suggested by Loh, this task is complex, as research has shown that information management needs vary significantly between different clinical environments and would require multiple end-user-defined outputs from a standardised data repository.5,6 Clinical handover needs to be implemented from the bottom up (by clinicians) rather than from the top down (by commissions).

Matthew J Fassett · Terry J Hannan · Iain K Robertson · Steven J Bollipo · Robert G Fassett

To the Editor: I was part of a review of the Therapeutic Goods Administration (TGA)-approved product information (PI) monographs contained in MIMS (Monthly index of medical specialties) annual with respect to their poisoning management advice.1 We looked at the 10 most common poisonings presenting to Westmead Hospital and another 15 clinically important poisonings as determined by two of the authors, and compared the poisoning management advice given in MIMS to a “gold standard” derived from a consensus of five pharmacological resources. For the 25 drugs examined, 14 monographs contained inaccurate information, one contained a recommendation for ineffective treatments, and 14 omitted specific treatments or antidotes. Many of these errors could delay or even prevent patients receiving currently accepted and effective therapies for life-threatening poisonings if MIMS were used as the primary resource. The omission of sodium bicarbonate for ventricular conduction delay and hypotension in amitriptyline, quinine and thioridazine poisonings is particularly problematic. Ventricular conduction delay and hypotension is often refractory to other therapies, and delay in bicarbonate administration could result in avoidable deaths. The recommendation of sodium bicarbonate for ventricular conduction delay and hypotension was included in the TGA-approved monograph for amitriptyline in 1984, but was subsequently removed without qualification in 1990 and remains absent. Cyproheptadine, an important therapy for serotonin syndrome, is not included in the TGA-approved monograph for sertraline, and its delay could result in avoidable morbidity. Atropine for verapamil-induced bradycardia is a simple and intuitive therapy; however, its omission from the TGA-approved monograph could again result in avoidable morbidity and mortality. We also found potentially dangerous treatments recommended in the TGA-approved monographs not covered by the consensus opinion. These included intravenous amphetamine or intramuscular ephedrine to counter the sedative effects of promethazine poisoning, administration of enteric-coated ammonium chloride tablets to increase urinary excretion in chloroquine poisoning, and forced osmotic diuresis using a urea or mannitol infusion for lithium poisoning. These treatments are out of the Dark Ages, and their use should be considered negligent. Based on this and other reports in previous editions of the Journal, the TGA-approved PI monographs contain inaccurate, inadequate, out-of-date or potentially dangerous information relating to poisoning management advice, paediatric drug dosages,2 drug interactions,3 breastfeeding mothers,4 and various thyroid medications.5 How can we use MIMS for anything other than simple drug formulation information? Surely, to anyone who wishes to practise up-to-date, safe, evidence-based medicine, the answer must be that we cannot. It is time for the TGA to take up its role as regulator and insist on updated and accurate PI monographs from the pharmaceutical companies.

James L Mallows

In reply: An article by Stockigt1 and follow-up correspondence from Mallows raised concerns about the limitations of approved product information (PI). The purpose of PI needs to be realised. The document is not intended to act as a textbook of medicine or general management of patients, but is intended to contain sufficient information to allow a health professional, in average circumstances, to use the specified medicine safely and to refer to other sources of information and expertise should they be required. The PI covers uses of the medicine evaluated and approved by the Therapeutic Goods Administration (TGA). The sponsor of the medicine is responsible for maintaining the PI, and the TGA has procedures in place to support their timely updating. On occasions, the TGA initiates reviews of PI when a need is identified. Health professionals, especially specialists, are important in identifying possible improvements in PI, based on their experience, knowledge or awareness of current medical practice. The TGA encourages physicians who have suggestions to approach the sponsor of the medicine or the TGA. It is not possible to address in detail the article by Stockigt1 or the letter by Mallows. The thyroid PI documents have been reviewed by the sponsor companies, and changes have been made where evidence supports this. However, as indicated above, there are limitations on the role of PI. Mallows raises the issue of complex management instructions on overdosage, including the specifics of bicarbonate administration for potential metabolic acidosis. The PI documents for the named products do mention that overdose patients are likely to develop such complications, and that they require admission to hospital and management by appropriate specialists; intensive care admission is recommended in several of the documents. It is arguable how much further detail is required. The PI cannot replace careful consideration of the individual circumstances of the patient combined with expert knowledge of patient management. PIs are complex documents. The TGA is currently considering the format of the PI and whether it can be rearranged to better balance provision of basic messages and more complex material in separate presentations.

David T Graham

To the Editor: The recent conference report by Knight and Taruscio highlights the need for a coordinated effort to fill knowledge gaps and improve service provision for Australians with rare diseases.1 Although, by definition, individual rare diseases occur infrequently, there are about 6000 rare diseases affecting 6%–10% of the population.2,3 This equates to 1.2 million Australians, 30 million people in Europe and 25 million in the United States. By comparison, diabetes affects 1.4 million Australians.4 It is increasingly acknowledged that low prevalence does not equate to low impact. Rare diseases often have their onset in childhood, continue throughout life, are difficult to diagnose, are disabling, and have significant impact on patients, their families, the community and health services.2,5 However, rare diseases receive such scant attention that they have been dubbed “orphan” diseases. Lack of epidemiological and scientific data has hindered development of evidence-based practice, policy and services. To tackle the problem of rare diseases, the European Union, the US, Canada and New Zealand have established policies and agencies to foster research, and develop resources for clinicians, community information services, and appropriate health facilities. The National Institutes of Health in the US established the Office of Rare Diseases because: . . . rare disease research requires the collaboration of scientists from multiple disciplines and the capacity to share access to geographically distributed national research resources and patient populations . . . knowledge about rare diseases may offer leads for scientific advancement in other rare diseases and in more common diseases.6 There is no coordinated national effort or policy in Australia. Currently, there are 14 national paediatric surveillance units, including the Australian Paediatric Surveillance Unit (APSU), to which paediatricians contribute epi-demiological, clinical and outcome data on rare conditions of childhood.7 These data inform development of health policy and improved diagnosis and clinical management, and result in the establishment of cohorts, thereby enabling further research.7 The APSU is developing information resources for clinicians and the community on rare infections, genetic disorders, mental health conditions and injuries in children. In Australia, the APSU is the only provider of prospective national data on up to 16 rare childhood diseases concurrently, but it receives no ongoing core funding. Sound evidence is needed to underpin development of policy and services. Sound evidence requires sound research into the causes, management and effects of rare diseases. Australian clinicians, researchers and, most importantly, patients and their families deserve the benefits of a coordinated national plan to address the common burden of rare diseases.

Yvonne A Zurynski · Katie N Reeve · Elizabeth J Elliott

To the Editor: In recent years, there has been an increase in the use of highly mobile three-wheel strollers that facilitate parental activities such as jogging. Unfortunately, the very design feature that enables fast transit over uneven ground also makes it possible for unsupervised strollers to move rapidly into situations that may be highly dangerous. Within the past year in South Australia there have been two separate incidents where infants, one aged 5 months and the other aged 10 months, died after being immersed in the Torrens River. They had both been strapped into three-wheel strollers. In both instances, carers, who had been walking or jogging in the park along the banks of the river, were momentarily distracted — one by a mobile phone call and the other while attempting to use a plastic bag dispenser. The strollers had not had their front wheels locked or their brakes engaged, or been attached to the carers by wrist straps and so were unrestrained, enabling them to roll rapidly forwards into the water. Police re-enactments confirmed the scenarios described by the carers. While three-wheel strollers have safety features, such as brakes and sometimes wrist straps, these are not always used. Although consumer organisations have listed a series of recommendations for users of these strollers, this advice is not always being followed. The recommendations include never leaving a child unattended in one of these strollers, always using a wrist safety strap, always engaging the brake when stationary, and locking the front wheel when jogging to prevent swivelling. In addition, specific warnings are issued about stopping on slopes, being distracted by mobile phone calls, and being particularly careful near water, roads and railway lines.1 Drowning of infants and toddlers in rivers is an uncommon event, with only two cases documented of a total 32 drowning deaths of children under the age of 2 years in South Australia over the 35 years from 1963 to 1998 (rate, 6.25%).2 Thus, the occurrence of two drowning deaths within 4 months associated with three-wheel stroller use in parks next to a river is of concern. While mandatory requirements for safety devices such as parking brakes and tether straps will take effect on 1 July 2008,3 this legislation will have little effect if the devices are not used. Parents and carers must be made aware that infants or toddlers in three-wheel strollers near water are at risk of immersion and drowning. Such warnings should be clearly specified on these products.

Roger W Byard · Neil Matthews

To the Editor: A 30-year-old man presented with pain, swelling and discharge from lesions on his left arm. He had undergone extensive tattooing on the arm 3 days earlier at a commercial tattoo operation, where single-use needles were used, with initial drawing of lines followed by additional shading. The patient complained of severe neuropathic pain in the arm, which was greater than would be expected from uncomplicated bacterial cellulitis. He did not give a history of oral or genital herpes and had previously been tattooed without complication. On presentation, the patient had a low-grade fever (37.9°C), a heart rate of 80 beats/min and blood pressure of 130/80 mmHg. He had no neurological deficit. Vesicular lesions were visible in the region of the tattoo marks, predominantly affecting areas of shading and with minimal spread outside tattooed areas (Box). A bacterial swab of the lesions grew methicillin-sensitive Staphylococcus aureus, and a polymerase chain reaction test of vesicular fluid was positive for herpes simplex virus type 1 (HSV-1). The patient was commenced on intravenous flucloxacillin (1 g four times daily) and oral famciclovir (250 mg three times daily). He required ongoing inpatient management for pain relief. Five days after development of the lesions, HSV-1 serology demonstrated positive results for IgM and IgG. An HIV test was negative. The patient’s lesions slowly resolved, and he was discharged 7 days after admission. Most concerns regarding infectious complications of tattooing have focused on transmission of blood-borne viruses, but superficial infections with other pathogens have also been described.1 The personal care and body art industries are regulated in Australia to minimise the transmission of blood-borne infection,2 and most state and territory authorities also publish infection control guidelines. Herpes dermatitis is often confused with bacterial infection, although co-infection may occur. This distinction is clinically important, as antibiotics and surgical debridement are not usually required for herpetic infections, and herpetic lesions may recur. Secondary herpetic infection complicating skin disease is most commonly associated with eczema (eczema herpeticum) or other skin diseases (Kaposi’s varicelliform eruption), and minor skin trauma, such as in herpetic whitlow or herpes gladiatorum.3,4 We are not aware of any previous reports of herpetic infection complicating tattoo placement. The distribution of herpetic lesions in our patient suggested that the needle used for tattoo shading became contaminated with HSV-1 during the course of tattoo placement, but it is also possible that superinfection occurred through damaged skin after the procedure. We propose the term “herpes compunctorum” to describe this condition. Vesicular lesions on patient’s tattooed forearm

Catherine S Marshall · Felicity Murphy · Shannon E McCarthy · Allen C Cheng

To the Editor: Helping patients who have had a stroke return to driving when possible should be an important focus in rehabilitation wards. The National Stroke Foundation supports a three-stage approach to assessing ability to drive, comprising physical and cognitive assessment, an off-road driving test and an on-road driving test.1 Austroads is the association of Australian and New Zealand road transport and traffic authorities, which aims to improve road and road transport outcomes. It provides clear guidelines on criteria for licence and assessment after stroke, but the implementation of these guidelines varies in practice.2 We conducted a review of 53 consecutive patients with a primary diagnosis of stroke admitted to a specialised rehabilitation ward over a 6-month period between January and July 2007. The mean age of the sample population was 77.0 years (SD, 10.7 years), and cognition score (Functional Independence Measure) on discharge was 28.3 (SD, 7.1) (maximum possible score, 35). Each patient completed a survey on driving history. Case notes were reviewed for medical factors associated with admission, any notations about driving, and actions taken regarding driving. Patients were telephoned 6 months after the date of the stroke to determine whether they had resumed driving and, if not, to explore the reasons. At the time of admission, 26 of the 53 patients held a current drivers licence, a proportion higher than the South Australian state rate of less than 10% for people aged 75 years and over. At the time of discharge, 12 of the 26 patients had their licences cancelled, 11 were referred for medical review after discharge without formal suspension, two were referred for occupational therapy driving assessment, and one was advised not to drive for 6 weeks. At 6 months, only five of the 26 patients (19%) had resumed driving, with one having regained a cancelled licence; six patients cited “lack of confidence” as the reason for not resuming driving. Reasons for the doctors’ decisions regarding driving were poorly documented in the case notes, and the time frame proposed for medical review ranged from 1 to 4 months. Austroads requires a minimum time of 4 weeks post-stroke before patients can resume driving, but does not specify a time frame for medical or on-road reassessment. Commonly, patients undergoing acute rehabilitation are still within the 4-week period, and assessments regarding return to driving are premature. The low rate of referral to available occupational therapy on-road driving assessment may reflect poor awareness of available hospital resources and online guidelines. While overseas studies of post-stroke populations indicate a return-to-driving rate between 30% and 58%,3-5 our rate was 19%. This low rate may represent a lack of formal assessment and driver rehabilitation opportunities. The benefits of formal driving assessment and training are supported by recent studies which found that licensed drivers post-stroke did not have an increased incidence of either car accidents or driving violations.6 While most doctors in the rehabilitation ward seemed to have understood the need to address the issue of driving, more formal training in this field is required for doctors.

Zoe A Allen · Julie Halbert · Lydia Huang

To the Editor: The Australian Pharmaceutical Benefits Scheme records 35 657 prescriptions (for either one or two devices) for EpiPen autoinjectors (CSL Limited, Melbourne, VIC), the self-injectable form of adrenaline, in 2006. This is a 650% increase on the 4758 prescriptions for EpiPens in 1998. The increase is much greater than the increase in the rate of food allergy. It is not enough to merely prescribe an EpiPen. It is vital that carers (of children), patients and prescribers understand its use. A previous South Australian study of children who had been prescribed an EpiPen at an allergy clinic found that, in 71% of severe reactions, the parents failed to use the device appropriately. Another study found that only two of 100 doctors in a major Australian paediatric teaching hospital could correctly demonstrate EpiPen use. In 2006, we surveyed EpiPen use by 120 parents of children attending the allergy clinic at the Children’s Hospital at Westmead. Children with egg allergy who were aged under 5 years when seen in 2003 were selected. Seventy per cent (84/120) of the children were prescribed an EpiPen. Half of the children had additional food allergies. Of those prescribed an EpiPen, 69% always carried it, 13% often carried it, 13% sometimes carried it and 5% never carried it. Ten per cent of parents had ever used the device, and 86% stated they were confident that they knew how and when to use it. Despite this, almost 40% stated they had concerns about using the EpiPen in an emergency. These included doubting their ability to correctly administer the EpiPen, whether they would have enough time and would inject correctly, concerns they may hurt their child, concern for the child in the event they needed it, doubt about the effectiveness of the EpiPen, and concern about appropriate timing. In the United Kingdom, 69% of parents were found to have problems using the EpiPen.4 Where, when and how to use the EpiPen was recently identified as one of 12 core parental information needs in our clinic.5 The findings that, even for parents of children attending a specialist allergy clinic where education strategies for EpiPen use are in place, 30% did not always carry the EpiPen, and 40% had concerns about its use in an emergency situation highlight the facts that just providing the device is an inadequate measure and that education and reinforcement, both in EpiPen use and in avoiding relevant allergens, are critical.

Clare W Allen · Dianne E Campbell · Andrew S Kemp

To the Editor: A 5-year-old girl with known peanut allergy presented with an acute allergic reaction after ingesting “nut-free” butter containing sunflower seeds (85%), sugar, emulsifier and antioxidant. The label on this product stated that it was processed in a peanut-free facility, and that each batch was tested for traces of nuts and peanut protein. The child had a history of atopic eczema, asthma, allergic rhinitis and egg allergy. At age 17 months, after eating a small amount of Thai satay containing peanut, coconut and chicken, she developed generalised urticaria, vomiting and marked angioedema. Skin prick tests at the time showed a negative reaction to sunflower seed (Box). The patient continued to avoid all nuts and egg. At the age of 5 years, within minutes of first eating a few mouthfuls of sunflower seed butter on toast, she developed generalised urticaria and angioedema of the lips. (The toast was made from the bread she usually ate, both before and after the reaction.) Skin prick tests at this time showed a strong positive reaction to sunflower seed (Box). She was thus diagnosed with generalised allergic reaction secondary to sunflower seed ingestion. Allergic reactions to sunflower seed are rare, with fewer than 30 published cases.1 Here, we report a child with peanut allergy who developed an allergic reaction after eating “nut-free” sunflower seed butter. The marketing by online and specialty shops of sunflower seed butter as a safe alternative to peanut butter for those with peanut allergy raises concerns, because allergic reactions can still occur, possibly through the development of new sensitisation. Our patient may have been sensitised through eating foods containing sunflower seeds, such as muesli bars and breads. There was no evidence of sensitisation through inhalation — for example, of seeds in bird feeds — although this has been reported.2 Another potential cause of allergic reaction is a previously unknown co-allergy to sunflower seed. This co-allergy was reported by 9.5% of patients with peanut allergy in one study.3 Yet patients with peanut allergy are often not tested for sunflower seed allergy because of its rarity. The promotion of sunflower seed butter as a safe alternative for those with peanut allergy raises concerns. As medical practitioners, we should carefully consider the safety of sunflower seed butter in individuals with peanut allergy. Skin prick test results,* by patient age Weal diameter (mm) Test extract 18 months 5 years Histamine (10 mg/mL) 3 8 Glycerosaline Negative Negative Dermatophagoides pteronyssimus 4 10 Cat Not done 13 Dog dander 4 Negative Egg white 6 15 Egg yolk Not done 10 Peanut 6 21 Almond Not done 6 Hazelnut Not done Negative Cashew Not done Negative Coconut 2 6 Sunflower seed Negative 16 * Skin prick tests were performed with a Microlance lancet using HollisterStier allergen extracts (HollisterStier Laboratories, Spokane, Wash, USA). Weal size was expressed as the average of two diameters. Average diameter ≥ 3 mm (with negative glycerosaline control) was considered positive.

Denise C Hsu · Constance H Katelaris

To the Editor: I refer to the recent letter by De Costa and Calcutt1 about diagnosis and management of possible Down syndrome pregnancies in remote areas of Queensland, and more specifically the lack of abortion facilities and cost of travel to larger centres for this service. Nowhere in the letter was impartial counselling mentioned. The following anecdote may be anathema to an academic journal, but I think it is relevant. Thirty years ago I took my 7-year-old son, who has Down syndrome, to a hospital cricket match. He had enormous fun trying to play cricket, as kids do. Watching was a young doctor whose wife fell pregnant not long after. The tests of those days suggested that the child might have Down syndrome. With memories of our son, they decided to go ahead with the pregnancy. As it happened, the child did not have trisomy 21. Children with Down syndrome, given a normal family life and lots of stimulation and love, may be able to achieve normal school levels and even work outside sheltered workshops. And they give lots in return. At a World Down Syndrome Conference in Sydney some years ago, adults with Down syndrome took part in the presentations, and notably present were a number of babies with Down syndrome whose mothers seemed quite happy with their lot. I am not against free choice, but people making that choice should be fully informed of the positive side of having a child with Down syndrome.

Kevin B Orr

To the Editor: Coory and colleagues revealed a disturbing attitude to children with Down syndrome in their recent report in the Journal on trends in Down syndrome birth rates in Queensland.1 The authors inform us that, of the 70 children with Down syndrome who would have been born without a particular form of “antenatal care” (selective termination), 21 were aborted, but another 22 could (and, by implication, should) have been aborted, had the recommended “antenatal care” by private obstetricians been replicated across the whole of Queensland. The United Nations Committee on the Rights of the Child has condemned selective termination as discrimination against children and “a serious violation of their rights, affecting their survival”.2 The Committee’s recent General comment on the rights of children with disabilities affirmed that these children have a right to positive antenatal care.3 The concluding comment of Coory et al that “When the costs of screening are offset against the life-time costs of caring for a person with Down syndrome, screening is less costly . . .” is deeply disturbing. Surely a person with Down syndrome is entitled to the same recognition of inherent dignity and worth as are all other members of the human family. The authors acknowledge that their view may be regarded by some as “distasteful”, but offer the defence that they are merely advocating that “. . . all expectant parents should be provided with the same information and have the same access to services so that they all have the same choices”. But termination is not a value-free choice. By suggesting that the best outcome of screening is a reduction in the births of children with Down syndrome by cutting these children’s lives short, the authors make a moral judgement that steps outside medicine and contravenes universal human values. The human rights of children have been recognised by the international community since the 1924 Geneva declaration of the rights of the child4 and continuously re-affirmed to the present day. It is frightening to see how much progress we have still to make when authors such as Coory and colleagues can argue that reducing the births of children with Down syndrome by the practice of selective termination is a positive thing.

Mary C Joseph