Letters

To the Editor: The aim of the study by Kennare and colleagues1 was to establish data on home and hospital birth outcomes for the period 1991–2006, before the Policy for Planned Birth at Home in South Australia was introduced in 2007.2 One significant shortcoming of the study was the lack of data regarding the type of birth attendant, the degree of cooperation with the local hospital and the quality of transfer arrangements. Currently, there are virtually no home birth policies in Australia governing women’s access to qualified midwives with hospital visiting rights that enable appropriate transfer. Women who intend to have a home birth are forced to rely on the charity of midwives who provide care without professional indemnity insurance. Failing this, women are known to give birth without a midwife. Kennare et al1 suggested that the Bachelor of Midwifery program will increase the number of midwives planning to offer home birth. However, their study did not examine whether women were attended by registered midwives, non-registered midwives, doulas, untrained birth helpers or a professional of any capacity, and assumed that planned home birth equates to home birth under the care of a qualified registered midwife. This has been a weakness of previous Australian studies.3 Overseas studies which identify the status of the midwives have shown that, for low-risk pregnancies, births at home attended by competent registered midwives in a networked system have outcomes that are comparable to hospital births.4,5 We have previously detailed other limitations of the study, including the inclusion of women who planned a home birth at booking but subsequently developed risk factors and gave birth in hospital, as well as the difficulty of examining the rare outcome of intrapartum death or intrapartum asphyxia in such a sample, as the wide confidence intervals show.6 Kennare and colleagues1 provide useful recommendations about risk assessment, transfer to hospital and fetal monitoring, and rightly highlight that the system must be so terrible for some women that they choose to give birth outside of it, even with risk factors. Despite a malfunctioning system in Australia — where midwives are uninsured and have no visiting rights, and home birth is unfunded and often hard to access — the perinatal mortality rate was no different for home births compared with hospital births. Risk assessment, transfer to hospital and fetal monitoring will be improved when midwives are no longer excluded from mainstream services.

Hannah G Dahlen · Caroline S E Homer · Sally K Tracy · Andrew M Bisits

To the Editor: Kennare and colleagues are to be congratulated.1 Careful, systematic collection and analysis of data on planned home births and planned hospital births creates evidence that women need to make intelligent and safe choices about perinatal care. A central medical cause of concern in the article1 and accompanying editorial2 is a high relative risk of death caused by intrapartum asphyxia in the planned home birth group. But, on closer examination, the underlying cause appears more likely to be a lack of proper integration of home birth midwives into the health care system. Of the nine infant deaths in the study, five were, by definition, unrelated to the place of birth — three were antenatal deaths that occurred after transfer to hospital (all unrelated to type of antenatal care) and two occurred in cases where the baby was born at home but had a fatal congenital anomaly. Three of the other four deaths (two of them due to intrapartum asphyxia) occurred after the parents persisted in their home birth choice despite advice against it, resulting in delayed transfer to hospital, or declined intervention after transfer to hospital — factors thought to have contributed to the deaths. Thus, an underlying contributing cause of the higher risk of intrapartum asphyxia appears to be some parents’ perception that care in hospital was not best for them or their baby. This perception is not entirely baseless, given that the caesarean section rate for planned hospital births in South Australia was 27.1%, 3.7 times the risk associated with planned home births after factoring in differences in maternal characteristics and obstetric conditions between the two groups (adjusted odds ratio, 0.27; 95% CI, 0.22–0.34)1 and about double to triple the 10%–15% rates recommended by the World Health Organization.3 Furthermore, women had seven times the risk of episiotomy for planned hospital births compared with planned home births, and three times the risk of instrumental delivery.1 Recent large, high-quality studies of home birth in Canada4,5 and the Netherlands6 demonstrated that — when home birth midwives are an integral, accepted, insured and funded part of the health care system — home birth is safe and refusal of midwife-recommended care by patients does not appear to be an issue. We suggest that an evidence-based solution to the underlying causes of excess asphyxia and perinatal mortality highlighted in Kennare et al’s study would be to follow the lead of countries such as the Netherlands and Canada — provide state funding for independent home birth midwifery practice, provide professional indemnity insurance and provide home birth midwives with access to hospital privileges as autonomous caregivers. When women can depend on continuity of care during transport, they are less likely to refuse or delay necessary care or transfer to hospital.

Kenneth C Johnson · Betty-Anne Daviss

In reply: Dahlen and colleagues overlooked that we excluded births without professional antenatal care (n = 1217), ensuring that all 1141 planned home births in our study were cared for by registered midwives.1 Nonetheless, we appreciate their acknowledgement that our article contains useful recommendations. Yet, they failed to endorse these recommendations in their letter and in the earlier critique to which they refer. They instead draw attention to a lack of difference in total mortality, but dismiss large differences in intrapartum and asphyxia-attributed mortality through their misinterpretation of confidence intervals. Rare outcomes, such as these, inevitably have wide confidence intervals. However, it is wrong and misleading to use the lack of precision in how much more frequent they are as an argument to dismiss their significantly much higher frequency. We tend to agree with the above correspondents, though, that proper integration of home birth care in maternity services might prevent some avoidable deaths that are a recurrent feature in Australian home birth studies.1-3 Indeed, we postulated this too.1 However, it is fallacious to assume that differences in outcome between Australia and other countries, to which the correspondents refer, are merely an issue of funding and access to hospital privileges for autonomous practitioners. The Netherlands,4 for example, has more than 40 000 home births a year, but only three midwifery academies, with a 4-year curriculum. Australia has less than 1000 home births a year, fewer than it has midwifery students, most of whom learn both nursing and midwifery within 4 years. Midwives in the Netherlands are medical professionals and carefully select only low-risk pregnancies for home birth.4 In Australia, on the contrary, many independent midwives accept home birth for pregnancies that are not low risk.1,2 Adherence to approved policies for planned home birth5 and collaboration with hospital services must be a prerequisite to their integration into maternity services. Unless leaders and teachers of the midwifery profession in Australia unequivocally condemn home birth for women with substantial risks, such as twin pregnancy or previous caesarean section, babies will continue to die needlessly, irrespective of any funding models.

Marc J N C Keirse · Robyn M Kennare · Graeme R Tucker · Annabelle C Chan

To the Editor: Hudson and colleagues showed that rural patients are a willing teaching resource for medical students, but that there are problems in using this resource.1 My experience shows the problems and opportunities. I have long provided a consultant paediatric service to two rural hospitals and an Aboriginal community in south-east Queensland. Clinical demands are large; resources are minimal. Waiting time from referral to consultation is 4–12 months. Many children with schooling problems lose a year of education waiting for diagnosis and treatment, and many have physical and behavioural conditions seldom seen in city practice. Few families are insured; bulk-billing is the norm. I spend 4 days a month in the area. Hospital staff make the appointments, and I use hospital records for my clinical notes. Hospitals provide clinical and personal accommodation, but not a secretarial service or funds for travel. Facilities are poor by city standards and financial returns meagre. I finish my clinics early then spend 3–4 hours each day typing letters to referring doctors and other paperwork. This is wasteful use of skilled time. Several problems and opportunities regarding medical education in rural specialist practice are evident: The need for more clinical teaching for medical students is real and urgent. As rural patients are available and willing, we should use them. Lack of specialists to meet clinical needs and to meet teaching needs are two sides of the same problem. Specialist clinics and teaching should be done in local hospitals that already have basic facilities, but most rural hospitals are already stretched and cannot take on an extra load. Medical specialists must be used efficiently. Additional administrative staff are needed to organise appointments, type letters and do general paperwork. Suitable clinic space and nursing assistance are also needed. Payments to visiting specialists should be sessional rather than case based, so that teaching carries no financial penalty. Payments for clinical and teaching sessions, travel, and accommodation should be sufficient to attract specialists and consultants. Some costs could be recouped by bulk-billing. Ideally, the specialist or consultant would provide long-term continuity to patients and staff — in contrast to registrars, who tend to be transient. Rural specialist practice is an untapped resource for teaching. Given suitable conditions, senior medical staff could develop its potential while providing a much-needed clinical service.

Alan E Dugdale

To the Editor: Treatment of critically ill pregnant women is challenging, and information on medication use during pregnancy is scant. We describe the case of a pregnant woman who required extracorporeal membrane oxygenation (ECMO), prolonged sedation and paralysis to treat acute respiratory distress syndrome secondary to pandemic (H1N1) 2009 influenza. A 34-year-old pregnant woman (G2P1) at 21 weeks’ gestation presented to a metropolitan hospital with level 1 intensive care unit facilities. She had known Grade 2 placenta praevia, a 5-day history of influenza-like symptoms, and no history of asthma, chronic disease or recent travel. On examination, she was severely hypoxic (PaO2, 27 mmHg on 15 L/min O2), conscious, tachypnoeic and speaking in single words. A chest x-ray showed extensive bilateral infiltrates (Box). She needed urgent endotracheal intubation but remained hypoxic despite maximal intensive mechanical ventilation. The patient was transferred to St Vincent’s Hospital, Sydney, where venovenous ECMO was commenced on arrival. Her oxygenation status improved and remained satisfactory. Mechanical ventilation was reduced (tidal volume, < 6 mL/kg; peak pressure, < 30 cm H2O) to avoid ventilator-induced lung injury. The patient required very high doses of morphine, fentanyl, midazolam, propofol, dexmedetomidine, cisatracurium and heparin during ventilation and ECMO. In addition, empirical treatment with oseltamivir (150 mg twice a day, Days 1–8), azithromycin and ceftriaxone was started on admission, before a bronchoalveolar lavage specimen tested positive for influenza A and pandemic influenza. Furthermore, a multiresistant Escherichia coli caused ventilator-associated pneumonia, which was treated with meropenem (1 g three times a day, Days 17–30). ECMO was discontinued on Day 19, when lung function had improved. No other organ failure developed. On Day 21, a tracheostomy was performed for severe weakness and weaning failure. The patient was weaned from the ventilator on Day 35 and was discharged home 2 weeks later, after making a full recovery. She gave birth by caesarean section at 35 weeks’ gestation. The baby was in good health and the patient recovered well — both left hospital 3 days after the birth. Information on the use of medication in pregnant women who require intensive care is limited, especially the use of neuraminidase inhibitors.1 We found little evidence on the safety of long-term use of neuromuscular blockers and sedation in pregnancy, with or without ECMO.2 Most literature on this topic describes short-term use of neuromuscular blockers and sedation. Dexmedetomidine has a short postmarketing history, and has therefore had limited use. Data from Australia and New Zealand indicate that 9% of patients admitted to an intensive care unit with pandemic influenza are pregnant. An estimated inhospital mortality rate of more than 16% in this population indicates the severity of the infection.3,4 Single-organ lung failure is a common feature of complicated pandemic influenza, and venovenous ECMO should be considered in these circumstances.2,4,5 Our case demonstrates that ECMO and the drugs necessary for its use can be used during pregnancy in a patient with influenza-associated acute respiratory distress syndrome, and that survival of the patient and fetus is possible. Chest x-ray of a pregnant woman with influenza-associated acute respiratory distress syndrome showing extensive bilateral infiltrates

Susan A Welch · Leone N Snowden · Hergen Buscher

To the Editor: Hydroxychloroquine is used infrequently (in less than 0.1% of Australians) for the long-term management of chronic conditions (eg, rheumatoid arthritis).1 Hydroxychloroquine retinopathy is a rare but sight-threatening side effect that is usually not reversible.2-5 Various eye screening recommendations for hydroxychloroquine toxicity have been proposed overseas,3-5 but there is no recommended consensus for eye screening in Australia. As a result, screening is currently not uniform or universal, and this sometimes leads to significant consequences. A 36-year-old woman with a longer than 10-year history of hydroxychloroquine therapy (400 mg/day; body weight, 62–67 kg) for rheumatoid arthritis presented to her general practitioner after a year of central visual disturbance and photopsias (a sensation of flashes of light). She was referred to the Medical Retinal Clinic at the Royal Victorian Eye and Ear Hospital in August 2009 with suspected hydroxychloroquine toxicity. She had undergone screening by her optometrist for an initial period, but had not been screened within the past 4 years because she failed to attend; she appeared unaware of the potential serious side effect of the medication on her vision. On examination, her visual acuity was 6/9 in the right eye and 6/12 + 2 letters in the left. Her colour vision (assessed by Ishihara plates for colour blindness) was normal. She had left vortex keratopathy (a whorl-like corneal epithelial deposit) and examination of her fundus revealed subtle macular pigment change and retinal arteriolar attenuation (Box, A). Fundus autofluorescence showed significant changes at the level of the retinal pigment epithelium (Box, B). Dense bilateral paracentral field defects were detected on visual field testing. The rheumatologist was notified of the hydroxychloroquine retinal toxicity, and therapy with the drug was ceased. At 6-month eye review, the patient’s vision was stable. Recommendations on the timing of eye screening vary.3 The manufacturer’s product information recommends quarterly ophthalmological examinations, but this is impractical and not cost-effective.3,5 The Royal College of Ophthalmologists (RCO) in the United Kingdom found no evidence-based justification for a systematic screening program.4 They recommend ophthalmological referral only when there are visual symptoms (eg, distorted or patchy central vision, reading difficulties), or eye disease is detected at baseline and confirmed by an optometrist. In contrast, the American Academy of Ophthalmology (AAO) suggests a systematic approach, determined by risk status, that is based on factors such as hydroxychloroquine dose and duration of intake.5 Despite their differences, these protocols both aim to detect toxicity early and minimise the degree of visual loss, rather than to prevent visual loss. This is because there are currently no established criteria to identify toxicity at a reversible stage.4 We recommend adoption of the AAO or RCO protocols and alerting patients to the symptoms of toxicity. Careful counselling of patients at commencement of hydroxychloroquine treatment and on an ongoing basis is essential to promote early presentation and minimise toxicity. Hydroxychloroquine toxicity, although rare, can lead to severe loss of vision if therapy is not stopped. By stopping treatment, the condition may stabilise, and further irreversible vision loss can potentially be avoided. Hydroxychloroquine retinopathy in a 36-year-old woman A: Subtle macular pigment change (black arrows) and some arteriolar narrowing (white arrows). B: Autofluorescence imaging showing symmetrical changes at the level of the retinal pigment epithelium. Mottled loss of autofluorescence (black arrows) indicates loss of retinal pigment epithelium cells, and the adjacent increased autoflourescence (white arrows) indicates cell abnormality.

Elvis Ojaimi · Robyn H Guymer · Tien Y Wong · C Alex Harper

To the Editor: In their letter in the 1 February 2010 issue of the Journal, Rashid and Grant reported the first Australian case of hepatotoxicity associated with the weight-loss product Hydroxycut.1 They noted that, in May 2009, the United States Food and Drug Administration (FDA) advised consumers to stop using Hydroxycut products on the basis of 23 reports linking them to serious injury, including one fatal case of liver failure. In response, the Australian sponsor, Export Corporation (Australia) Pty Ltd told the Therapeutic Goods Administration (TGA) that there were differences between the US and Australian formulations of Hydroxycut products. As the TGA had received no reports of adverse reactions similar to those reported in the US, they allowed local marketing to continue. The TGA website advised consumers to exercise caution when using Australian Hydroxycut products;2 however, no such warnings appeared in local promotional material. In contrast, despite also being told that products marketed in the United Kingdom had different formulations, the UK Food Standards Agency (FSA) said: The specific ingredient or dosage which might be causing health problems has not yet been identified. However, as a precautionary measure, the FSA is warning people not to take them. There are no reported illnesses in the UK related to these products. . . . Hydroxycut products have been withdrawn from sale in the USA, Finland and Canada. Ireland has also advised retailers to withdraw the product and consumers to discontinue use of the products.3 Meanwhile, there have been three complaints upheld about the promotion of Australian Hydroxycut products, with another in progress.4 In 2008, the Complaints Resolution Panel (CRP) requested that the sponsor, retailers and website publishers withdraw any representations that the advertised product(s) has benefits in relation to fat-burning, weight loss, or weight management. Regardless, these claims continue to be made by numerous Australian internet pharmacies, and supplement and health food sites. This highlights the impotence of the CRP (which lacks the power to impose sanctions), the ineffectiveness of the TGA (which can impose sanctions, but apparently declines to do so) and the need for regulatory reform.5 A reformulated Hydroxycut is back on the shelves in the US. An FDA spokesperson said: “The only ingredient left in from the original formulation is caffeine. We do not have any evidence that caffeine causes liver toxicity.”6 However, on 14 February 2010, I had no difficulty in purchasing Hydroxycut (AUST L 154243) from a local pharmacy. This product has a similar formulation to products withdrawn overseas. Rashid and Grant called on the TGA to re-examine the continued availability of these products in Australia.1 I reiterate their call. Why is the TGA out of step with other regulators? Why are these products still on the Australian market if their benefits are negligible or absent, if unethical promotion continues despite CRP determinations, and when the risks are clear?

Ken J Harvey

To the Editor: In the December 2009 issue of the MJA, I came across an interesting article by Dr Paul Zimmet, “A lifetime pursuit of diabetes through chance”.1 This is an account of his impressive achievements in medicine. However, I disagree with the statement that describes his father’s situation in 1930s Poland: “He returned to an unpaid position in the Tarnopol Hospital — unpaid because Jewish doctors could not be ‘officially’ employed in Poland.” I argue that, in Poland at that time, there was no discrimination against national minorities, and this applied to the Jewish minority as well.2 I have done some research on the subject. There were 3.5 million Jewish people in Poland before the war — 10% of the population. According to numerous historical sources, Jewish doctors represented 34% of doctors in Poland in 1938. In the Polish capital, Warszawa, this percentage was 66%. The same sources quote the percentage of lawyers of Jewish origin as 55%.3,4 These numbers are a tribute to the talents and assertiveness of Polish Jews; however, they do not support the statement by Zimmet that I am disputing. In Polish archives, I have discovered statistical documents containing alphabetical lists of all doctors registered in Poland between 1936 and 1938.5 According to these documents, there were two hospitals in Tarnopol at that time: the General Hospital and a Jewish hospital. In the official register of all Polish doctors practising between 1936 and 1938, I have not found the name of Dr Jacob Zimmet. He was not registered as a doctor, and therefore could not legally be employed as a doctor in Tarnopol or any other Polish hospital.

Wladyslaw W Smolilo

In reply: Dr Smolilo has challenged my claim that my father, the late Dr Jacob Zimmet, worked in a hospital in Tarnopol, Poland, and without salary, in the pre-World War II period.1 I am pleased to refute Smolilo’s inaccurate claims. Smolilo argues that “. . . in Poland at that time, there was no discrimination against national minorities, and this applied to the Jewish minority as well”. I accept his statement that there was not an official policy as such. There are, however, ample historical records of discrimination against Jews in many areas.2 Smolilo questions the specific instance relating to my late father. I have a letter in Polish from the Director of the Government Hospital in Tarnopol and its 1939 official translation by the Polish Consul-General in Sydney, copies of which I have provided to the Editor of the Journal. This letter not only confirms my father’s employment from 1935 to 1938, but also the fact that he was not paid. The very fact that Smolilo could not find my father in the official records also stands as confirmation! Clearly, there were many Jewish doctors and other professionals employed in Poland from earlier years who retained their positions during the period from 1935 to 1939. However, even before that time, a quota was imposed on Jewish students and many had to go overseas for medical training.3 On return, like my father, they were unable to find gainful employment and eventually left Poland, many emigrating to Australia. My father provided loving care to many Polish immigrants in his medical practice in South Australia.

Paul Z Zimmet

To the Editor: In your recent column, you drew attention to the “limitations of psychiatry’s scientific foundations for disorders of the mind”.1 This was despite psychiatry’s recent high profile, and the very large sums of money being thrown at the problem. The limiting factor for a scientific psychiatry is that there isn’t one. Extensive research has shown that orthodox psychiatry does not yet have a formal, articulated model of mental disorder to guide its practice, its teaching and its research.2,3 Moreover, not one of the models used today, including the biological approach, can be developed to the point where it would meet the minimum criteria for a scientific model. Confections such as the “biopsychosocial model” do nothing but conceal the problem under yet another layer of jargon. Releasing another Diagnostic and statistical manual of mental disorders (DSM) will achieve nothing because it does not address mental disorder within the framework of an agreed model. In the absence of science, there is scope for non-scientific pressures (such as politics and finance) to have an inordinate influence on the many DSM committees. Needless to say, this conclusion is most unpopular among many in the psychiatric establishment but, sooner or later, they will have to come to grips with the problem; otherwise, psychiatry as a profession will cease to exist.4

Niall McLaren

To the Editor: We read the article by Gibson and colleagues on the assessment and management of cough1 with some concern, specifically regarding the authors’ classification of levels of evidence for current therapies for allergic rhinitis. We would agree that a trial of antihistamines, intranasal corticosteroids and allergen immunotherapy is unlikely to help non-specific cough in the absence of allergic rhinitis. This consensus should be distinguished from the beneficial impact of these modalities on symptoms of allergic rhinitis, for which the authors misquote their main source of information2 and suggest that evidence of benefit from these is “weak”. Although evidence of benefit from allergen avoidance to help manage allergic respiratory disease is controversial,3 a large number of double-blind placebo-controlled trials of all other modalities show Level I evidence of benefit and category A strength of recommendation specifically for treatment of allergic rhinitis, as recently reviewed2,4-6 — evidence consistent with “strong” recommendations using the GRADE (Grading of Recommendations Assessment, Development and Evaluation) criteria.7 We do our patients and colleagues a disservice to suggest otherwise.

Raymond J Mullins · Constance H Katelaris · Janet Rimmer

To the Editor: We read with interest the Australian Cough Guidelines summary statement by the CICADA multidisciplinary group.1 However, we feel that the role of direct examination of the upper aerodigestive tract in assessing cough was underemphasised. Flexible nasal endoscopy (FNE) is a quick, relatively straightforward examination performed under topical anaesthesia as part of an ear, nose and throat (ENT) consultation. It allows direct visualisation of the nasal cavities, postnasal space, oropharynx and larynx, and can be performed on adults and older children and also some younger children.2 Nasal causes of cough, and hence the potential role of FNE, appear to have received more emphasis in previous chronic cough management strategies, including those proposed by the American College of Chest Physicians in 20063 and the European Respiratory Society task force in 2004.4 The diagnosis of chronic rhinosinusitis or upper airway cough syndrome (postnasal drip syndrome) is enhanced by direct examination. The presence of mucopus in the middle meatus of the nasal cavity is associated with a positive diagnosis of chronic rhinosinusitis.1 FNE can also provide direct evidence of the presence of gastro-oesophageal reflux affecting the larynx (laryngopharyngeal reflux), and plays a significant role in the clinical diagnosis of laryngopharyngeal reflux.5 FNE should be used in patients with alarm symptoms for serious underlying disease (as suggested by the CICADA group1), particularly those potentially related to laryngeal causes (hoarseness, haemoptysis, feeding difficulties, stridor or smoking). As part of a complete examination, FNE can help in targeting therapy for two of the three most common causes of cough in adults (gastro-oesophageal reflux and rhinosinusitis), and in excluding some of the significant causes of cough in both adults and children. It is particularly recommended in patients with a suspected nasal or laryngeal cause, in those with alarm symptoms, and in those for whom initial therapy fails.

Nicholas J Potter · Eduard I Pudel

In reply: The recently published CICADA cough guidelines1 draw attention to the important role of systematic assessment of chronic cough in children and adults, and provide an appraisal of the evidence that treating specific conditions will improve cough. Mullins and colleagues raise a key point that requires emphasis, and is relevant beyond the instance of allergic rhinitis that they cite. Chronic cough is associated with several common conditions, such as allergic rhinitis, asthma, gastro-oesophageal reflux disease and sleep apnoea. For each of these conditions, there are well established treatment guidelines that describe the effectiveness of treating that primary condition. However, in developing the CICADA guidelines we were considering the effect of the treatments on the symptom of cough, not on the primary condition. It was stated at the bottom of Box 1 (page 2661) that “The final GRADE recommendations were based on [the] votes [of committee members] and considered cough in the context of the respective conditions”. We agree that the evidence for treating symptoms of allergic rhinitis per se is strong, as published.2 But in the case of a patient presenting with cough and associated rhinitis, the CICADA group determined that the evidence that treating allergic rhinitis would resolve the cough was weak. It is often not possible to determine from successful trials of immunotherapy for rhinitis the outcome for cough. For example, trials of injectable or sublingual immunotherapy both mention cough only once, and it is not possible to determine the effect of the treatment on this symptom.3,4 We welcome the comments by Potter and Pudel giving more specific details of the role of FNE in assessing the upper airway in people with chronic cough. We agree that this is a quick and useful examination. We believe we have placed greater emphasis on upper airway disorders compared with other cough guidelines. Specifically, we have identified vocal cord dysfunction and sleep apnoea as relevant upper airway disorders that are associated with chronic cough. These conditions are not featured in previous guidelines, yet they respond well to specific therapy. We also devote comparatively more space to upper airway disorders that to lower airway disorders.

Peter G Gibson · Anne B Chang · Andrew S Kemp

To the Editor: From 30 September 2009, the Australian Government began offering free pandemic (H1N1) 2009 influenza vaccine (Panvax, CSL Limited, Melbourne, VIC), using either 10-dose (5 mL) or 20-dose (10 mL) vials.1 Multidose vials are not used routinely in Australia, and are designed for high-volume vaccination clinics.2 Once pierced, a Panvax vial must be used within 24 hours or discarded.3 We investigated vaccine wastage in general practice during the first month of the vaccine’s availability. We randomly selected 300 of 697 known general practices within the Sydney South West Area Health Service. A one-page audit of vaccine vials received and consumed, and of patients vaccinated to 31 October 2009 was faxed to practices. One reminder fax was sent. Faxes were successfully delivered to 271 practices and 146 (54%) responded. Twelve responses (4%) were substantially incomplete, leaving 134 (49%) for analysis. Practices reported vaccinating 28 445 people. A median of 70% (interquartile range, 50%–90%) of people immunised belonged to a priority group. An estimated 49 130 doses were consumed, indicating that 20 685 doses (42%) were wasted. A median of 40% of doses were wasted per practice. Three practices (2%) had administered only one dose per multidose vial. There was significantly less wastage in practices with access to 5 mL vials (median wastage, 30%) than practices that had only 10 mL vials (median wastage, 50%) (P < 0.001; Wilcoxon rank-sum test). There was no significant difference in the proportion of doses wasted between the 70 practices that organised vaccination clinics and the 63 practices that did not (median wastage, 43% v 40%; P = 0.9; Wilcoxon rank-sum test). There was also no statistically significant difference in the proportion wasted between solo and multidoctor practices (median wastage, 43% v 34%; P = 0.2; Wilcoxon rank-sum test) although the absolute wastage level was lower for multidoctor practices. These results provide evidence that multidose vials (discarded within 24 hours of first use) are an inefficient method of presenting pandemic influenza vaccines for general practice use. Wastage was substantial. This study is limited to the program’s first month, so initial results may not reflect results over the whole program. However, if similar wastage occurred nationally, over 7.5 million of the 19 million doses available to Australians could be wasted. Nevertheless, the low unit cost and rapid production advantages of multidose vials may justify their use when faced with an urgent threat, and if used in mass vaccination clinics. Wastage could be reduced by increasing the availability of 5 mL multidose vials, but not (according to our data) by organising general practice vaccination clinics. Extending the vaccine shelf-life from 24 hours to 28 days, to align with licence conditions in the United States,4 could decrease wastage, as it may be that the short shelf-life results in more wastage than does supplying the vaccine in multidose vials. No rationale for the shorter shelf-life in Australia has been found, but we surmise it was set as a precaution to reduce the risk of contamination. Doses saved through reduced wastage could be used to increase Australia’s donation of vaccine to developing countries.5

Caroline E Turnour · Stephen J Conaty · Michelle A Cretikos

To the Editor: In their recent article, Beaman and Leung raised a number of important and pertinent issues about what we can learn from the influenza pandemic of 2009.1 However, we would like to correct a number of misconceptions on their part, including claims that Western Australia’s central public reference laboratory, PathWest Laboratory Medicine WA, (i) unreasonably favoured polymerase chain reaction (PCR) testing over antigen testing; (ii) rationed and prioritised testing primarily because of inability to cope with the high demand; (iii) rarely achieved the benchmark turnaround time of 48 hours; and (iv) spent excessive time processing a large number of specimens, of which 96% were reported as negative. State reference laboratories had to provide tests that would best guide individual patient management and the most effective use of hospital beds, as well as informing the public health response. The decision to avoid antigen detection tests was supported by the World Health Organization from the beginning of the pandemic2 and confirmed by subsequent published data showing that PCR testing was more reliable than antigen testing.3,4 Inaccurate test results hinder rather than help the pandemic response,5 especially in the early stages. From very early in the pandemic, we prioritised samples from hospitalised patients, health care workers, people at higher risk of severe disease and cases of special public health importance. For these urgent samples we aimed for, and largely achieved, a 48-hour turnaround time. Beaman and Leung did not allow for the substantial delays in transport and processing of samples before testing, which contributed 2–3 days to the turnaround time. A similar experience was reported in Victoria.6 This has highlighted the need to improve the way in which samples are handled at all stages between collection and testing. Rationing of services was a decision made in consultation with our public health colleagues, to ensure sustainable testing capacity for essential clinical and public health needs. In the end, PathWest tested 24 310 samples, representing 92.8% of the samples received, which included all of the high-priority and/or critical samples. It is misleading to suggest that a 96% negative rate was inefficient, and is a misunderstanding of the purpose of testing in the different phases of the pandemic. In the early phases, the yield of positive test results was expected to be low, as there was active case-finding at a time when no or very little virus was present in Australia. Across the course of the pandemic, the positive rate at our laboratory was 23% overall and 40% during the peak week. The response of public and private laboratories to the pandemic throughout Australia was impressive, and has now been the subject of state and national debriefings to identify potential improvements and the highest priorities for action. As part of that, we should all look at how we could improve our own laboratory’s performance and how we could make the best contribution to dealing with future pandemics and other emerging infectious diseases, both as individuals and as members of organisations. We would like to take this opportunity to acknowledge all the people within and outside laboratories who made a huge effort to save lives and reduce the impact of the pandemic.

David W Smith · David J Speers · Rodney A Bowman

To the Editor: We report the case of a child who presented with intussusception due to heterotopic pancreas. A 10-year-old girl presented with right iliac fossa pain and nausea. She was febrile (38.4°C) and had right iliac fossa tenderness with guarding. When she started vomiting, she was taken to theatre with a provisional diagnosis of acute appendicitis. During the diagnostic laparoscopy, her appendix did not appear inflamed and she was found to have intussusception due to a 10 mm tumour in the ileum, about 80 mm from the ileocaecal valve. The tumour was resected, and microscopic examination showed the presence of ducts and lobules of exocrine acini, with occasional foci of islet cell tissue extending into the muscularis propria. These features were consistent with heterotopic pancreas. Heterotopic pancreas is defined as the presence of pancreatic tissue outside its usual location and without anatomic relation either of continuity or of vascularisation with the pancreas.1 Its overall surgical incidence has been estimated as one case in every 500 abdominal explorations at Mayo Clinic.1 During embyrogenesis, the normal pancreas arises from several evaginations originating from the wall of the primitive duodenum. If one or more evaginations remains in the wall of the bowel, it may be carried away from the rest of the gland by the developing gastrointestinal tract and give rise to heterotopic pancreas.2 In adults, the most common locations for heterotopic pancreas, in descending order of frequency, are the stomach, duodenum and jejunum.3 However, in children, the most common location is within a Meckel diverticulum.3 Heterotopic pancreas is usually asymptomatic, and most cases have been found coincidentally at laparotomy performed for other abdominal conditions.4 However, in some people, pathological changes such as inflammation, abnormal hormone secretion and cystic degeneration within the heterotopic pancreas have been reported to cause abdominal pain and discomfort.3,4 Isolated heterotopic pancreas in the ileum is very rare and usually asymptomatic. The lesion within the wall of the ileum may act as a lead point,3,5 and this is thought to be the mechanism of intussusception. It has also been postulated that intussusception arises from local disturbance in the motility of the small intestine caused by the heterotopic pancreas.3

Narotam R Jootun · Hock P Cheah · Siddath C Fernando · William S Munro · Martin Veysey

To the Editor: The recent article by Davis and colleagues reported that the SMART-COP score underestimates the severity of pneumonia in tropical northern Australia, but can be improved by using locally relevant additions.1 The authors’ revised scoring system, SMARTACOP, increased the score for an albumin level < 35 g/L and added Aboriginal or Torres Strait Islander status as a variable. While these additions are useful, the reason for adding ethnicity was not fully clarified. A factor overlooked was low serum 25-hydroxyvitamin D [25(OH)D] levels among dark-skinned Australians.2 Smoking, identified as a marginally insignificant risk factor,1 is also associated with lower serum 25(OH)D levels.3 Vitamin D enhances the innate immune system through induction by 1,25-dihydroxyvitamin D of cathelicidin and defensins, which combat several types of bacterial and viral infections including upper respiratory tract infections.4 In the 1918–1919 influenza pandemic in the United States, many deaths were due to pneumonia that occurred as a complication of influenza infection. An ecological study found that indices for levels of vitamin D production from solar ultraviolet-B irradiance explained 50% of the variance in pandemic case-fatality rates among 12 communities.5 The mechanisms proposed for the beneficial effect of vitamin D were reduced proinflammatory cytokine production, which would reduce damage to the epithelial lining of the lungs, and induction of cathelicidin and defensins to fight the secondary bacterial pneumonia infection. If sera are available for those included in the Australian SMART-COP study,1 they could be analysed for 25(OH)D levels to test this hypothesis.

William B Grant

In reply: We thank Grant for his interest in our study on pneumonia severity assessment in tropical Australia. Our revised scoring system included increased weighting for hypoalbuminaemia, as well as adding a point for Indigenous status, because these two factors had the strongest association with the need for intensive respiratory or vasopressor support on univariate analysis.1 Unlike vitamin D status, these and the other factors included in the scoring system are readily available measures that can be used in the clinical setting to rapidly predict the need for intensive support. The scoring system was not intended to identify underlying aetiology or risk factors for severe pneumonia. For example, Indigenous status is likely to be a surrogate measure for undiagnosed comorbidities, lack of access to health care, and socioeconomic disadvantage. We agree that vitamin D is important in immune function and that the levels of insufficiency that result in impaired resistance to infection are not well defined.2 Most data on vitamin D deficiency in dark-skinned populations in Australia come from temperate areas,3,4 and the reference offered by Grant to support the concern about vitamin D deficiency does not cite any data from Australian populations north of southern Queensland.5 Further studies are needed on the prevalence of vitamin D deficiency in Indigenous Australians in tropical areas, and the additional contribution of vitamin D deficiency independent of known risk factors of severity and outcome.

Joshua S Davis · Allen C Cheng · Bart J Currie · Nicholas M Anstey

To the Editor: Newby and Robertson’s study of the effect of computerised prescribing on the frequency of repeat prescriptions for antibiotics is important in highlighting unnecessary repeat prescribing.1 However, their work has highlighted another issue — researchers’ growing habit of using the prescription of selected antibiotics to infer indication, and then to measure appropriateness of care. When using the term “upper respiratory tract infections” (URTIs), do the authors mean viral infections or all URTIs, including bacterial infections? They state: While we did not include data on the indication for treatment in our study, the antibiotics we chose are those commonly used for respiratory tract infections. Therefore, the continued high rate of repeat ordering for these antibiotics remains a concern.1 We support the latter statement wholeheartedly, but the inference that the antibiotics examined in the study were used to manage URTIs (because these antibiotics are “commonly used to treat URTIs”) is inappropriate and incorrect. A media report misguidedly described Newby and Robertson’s study as examining “how GPs’ use of computerised prescribing systems affects antibiotic prescribing for upper respiratory tract infection.”2 The study was not about prescribing of antibiotics for URTIs, but this implication is apparent in their article. From the national Bettering the Evaluation and Care of Health (BEACH) program 2006–2009,3 we examined 20 011 general practitioner prescriptions for Newby and Robertson’s selected antibiotics: amoxycillin, amoxycillin/clavulanate, roxithromycin, and cefaclor. We would usually include cephalexin, because it is prescribed as often as cefaclor for URTIs at BEACH encounters, but we have limited our comparison to the above four antibiotics. In the BEACH program, GPs link the prescription to the problem being managed so we can determine the indication for which these antibiotics have been prescribed. Over the 3-year period of the 2006–2009 BEACH program, only 21.1% of these antibiotics were prescribed for URTIs (adults [≥ 15 years], 20.6%; children [0–14 years], 22.7%). In four out of five cases, the prescriptions were for acute bronchitis, sinusitis, acute otitis media or myringitis, tonsillitis, urinary tract infections, skin infections, pneumonia, and a variety of systemic infections. It cannot be assumed that a URTI is the indication simply because these antibiotics are most commonly used for its management, and by inference, that GPs are prescribing inappropriately. Newby and Robertson are not alone — the 2010 Productivity Commission report used the number of prescriptions for “antibiotics most commonly used to treat URTI” as one indicator of the appropriateness of GP services.4 These antibiotics are, in most cases, prescribed for indications other than URTI. The appropriateness of this prescribing cannot be assessed without knowledge of the indication, and without clear guidelines as to what level of antibiotic prescribing for each indication is “best” quality.

Joan V Henderson · Christopher M Harrison · Helena C Britt

In reply: We accept the evidence presented by Henderson and colleagues that the antibiotics examined in our study are not used exclusively for upper respiratory tract infections (URTIs), and we acknowledge in our article the lack of information on indication for treatment. However, data from the Bettering the Evaluation and Care of Health (BEACH) program have been used by others to suggest that the four antibiotics represent over 60% of the prescribed antibiotics for URTIs.1 Our study does not assess the appropriateness of the antibiotic choices, focusing instead on duration of therapy as implied by the issuing of repeat prescriptions. Irrespective of indications for use of these antibiotics, our data still support our primary conclusion that computerised prescribing is associated with increased repeat ordering for these, and probably other, antibiotics. The increase in repeat ordering could possibly be explained if doctors who use computers to prescribe see “sicker” patients or a significantly different case-mix from those who write prescriptions by hand. However, the size of the difference (70% v 40% of prescriptions with repeats, respectively), the consistency across the antibiotics examined, and the identical rate of repeat ordering on handwritten prescriptions in both surveys, makes this conclusion unlikely.

David A Newby · Jane Robertson

To the Editor: In April 2009, a registered nurse at the Sydney Medically Supervised Injecting Centre (MSIC) overheard two clients warning others about the effects of injecting from a particular glass vial, believing it had given them a “dirty shot” (bacterially contaminated injection). Seeing an unlabelled, discarded vial containing cloudy fluid, the nurse was concerned that it may have contained insulin, and assessed all four clients who reported injecting from similar vials. Three clients were sweaty, nauseated, and looked unwell, while only two (who had subsequently injected heroin) showed the pin-point pupils and hypoventilation typical of opioid use. Blood glucose levels confirmed likely insulin use, with the lowest reading being 1.5 mmol/L. MSIC staff made sweet drinks available, but one client became unconscious and required intramuscular glucagon and hospital admission. She was subsequently discharged without complications. Staff were concerned that insulin from an unknown source and of unknown concentraion was for sale in the local area, and immediately informed the local police and health and social welfare agencies. Thankfully, no further cases were noted, and no permanent harm resulted from this incident. The vial found at the injecting centre was later identified as Humulin 30/70 (Eli Lilly Australia, Sydney, NSW). Insulin-induced hypoglycaemia may result in brain damage and death.1 To our knowledge, this is the first case of inadvertent insulin injection in an injecting facility reported in the scientific literature. Given the unlikely nature of the substance, and that two clients showed physical signs consistent with opioid use because of subsequent heroin injection, their presentation in another setting could well have been confused with opioid overdose. We believe the MSIC was able to avert serious morbidity and possible death because of the presence of experienced staff able to provide immediate medical attention. The MSIC opened in 2001 in Kings Cross, Sydney, the first of its kind in the English-speaking world. The centre reduces morbidity and mortality from drug overdose, enhances access to health and social welfare services, reduces transmission of blood-borne viruses and reduces the incidence of drug injecting in public places.2 The main drugs injected at the MSIC include heroin, other opioids, cocaine and methamphetamines. There are now 70 such facilities around the world; these are legally sanctioned sites where people may inject previously obtained drugs under the supervision of qualified personnel. There is growing scientific evidence internationally to show that supervised injecting facilities reduce the harms associated with illicit drug injection.3-5 This case highlights their role in preventing harm associated with more unexpected drug injections.

Marianne E Jauncey · Anita P Trevan · Richard P Sulovsky

To the Editor: Optimism about our growing ability to recognise coeliac disease (CD) is tempered by a worrying trend towards misuse of genetic testing for CD risk, as illustrated by this salutary case. A 42-year-old woman with nausea and lethargy attended her doctor, concerned that she may have CD, because her niece had the condition, and she knew it was “genetic”. A laboratory representative had told her doctor that a test for the HLA-DQ gene was the best test for CD; this test was performed, and detected genotype susceptibility for CD (HLA-DQ2 and HLA-DQ8 alleles). The patient was told she had CD and was referred to a dietitian to commence a gluten-free diet. She contacted the Coeliac Society of Australia and learned that this was an unusual way of diagnosing CD. This led to her being referred to a gastroenterologist. Further testing showed normal IgA and IgG transglutaminase antibody (TGA) levels (8 enzyme-linked immunosorbent assay [ELISA] units [reference range, 0–20 ELISA units]), and normal iron, folate and IgA levels. Mild nausea and diagnostic ambiguity prompted gastroscopy and duodenal biopsy. Findings of these tests were normal, showing no intraepithelial lymphocytosis. CD is common, affecting up to 1% of Australians,1 and causing a spectrum of complaints from classic malabsorption to more subtle problems (eg, osteoporosis and iron deficiency). It is clarified by sensitive serological detection methods (TGA levels).2 This gluten-triggered autoimmune disease represents one of the best characterised models of gene–environment interaction, in that an “at-risk” genome is needed to provide disease predisposition.3 However, CD genotyping (looking for HLA-DQ2 and HLA-DQ8 alleles) is increasingly requested under the misconception that a “genetic” test must be a more reliable detector of disease than other tools. The HLA risk genotype is necessary but not sufficient for development of CD: 20% of Australians share this risk factor, but only 5% of these express CD. Serological testing (TGA) provides approximately 90% sensitivity and specificity for CD in the appropriate clinical setting, but the diagnostic “gold standard” still involves biopsy confirmation of gluten-responsive tissue changes to justify the life-long social and financial costs of gluten avoidance. CD genotyping should be considered when: gluten challenge is not possible or acceptable; serological–histological discrepancies exist; or endoscopic biopsy is difficult or potentially non-diagnostic (eg, certain paediatric cases, or patients being treated with anticoagulants or immunotherapies [eg, prednisolone] that may normalise biopsy appearances). Our group is seeing more misuse of CD genotyping, with some practitioners using a positive result to confirm CD. As a centre of expertise in CD, we recommend that CD genotyping be confined to its negative predictive role: negative CD genotyping indicates a substantially reduced likelihood of CD (< 1%).4

Neil J Porter · Huy A Tran · Glenn E M Reeves

To the Editor: A 59-year-old woman presented with acute bilateral deafness, ataxia, and pyrexia. She had no significant past medical history and was taking no medications or antibiotics. Examination revealed normal tympanic membranes. Audiology and fundoscopy were not performed. Full blood examination results, electrolyte levels and renal function were normal. A plain chest x-ray was unremarkable, but a computed tomography scan showed lobar consolidation. The patient had microscopic haematuria but no pyuria, and negative urine culture. Blood cultures were repeatedly negative. She was commenced on a third-generation cephalosporin, as well as corticosteroids on suspicion of vasculitis. Her condition improved initially, but relapsed on weaning from the steroids. Further history-taking revealed that 3 weeks before the onset of her illness, the patient’s pet budgerigar had a prolonged diarrhoeal illness and subsequently died. On suspicion of Chlamydophila infection, she was commenced on doxycycline, and the fever resolved within 24 hours. Doxycycline was continued for 14 days, and the patient remained well thereafter. Her hearing returned to normal over 3 days. Autoimmune markers, and serological tests for Legionella species, Mycoplasma species and respiratory viruses were negative. However, her Chlamydophila psittaci IgG titre was > 512 and Chlamydophila pneumoniae IgG titre was > 2048, consistent with a recent infection with either C. psittaci or C. pneumoniae. Convalescent serological tests were not performed. To our knowledge, acute hearing loss has been reported only four times as an extrapulmonary feature of Chlamydophila infection. Puolakkainen and colleagues reported the case of a 49-year-old man who presented with otitis media in one ear and sudden deafness in the other after a severe influenza-like illness thought to be due to psittacosis.1 Crosse performed a retrospective study that looked at the clinical and epidemiological features of cases in which there was a fourfold rise in C. psittaci titre. One patient developed deafness, although no further detail was given.2 Brewis and McFerran reported the case of a 61-year-old pig farmer with sudden bilateral hearing loss associated with C. psittaci pneumonia. The hearing loss resolved with antibiotics and prednisolone.3 Finally, Darougar et al reported the case of a 15-year-old girl who presented with chronic relapsing sensorineural hearing loss, uveitis, keratitis and vertigo.4 In this case, chlamydial antibody titres were raised, and C. psittaci was isolated from the conjunctiva. She had no respiratory involvement. Her only animal exposure was to a cat with conjunctivitis, which tested negative for chlamydial and viral infections. Interestingly, Dünne et al have recently found an epidemiological association between sensorineural hearing loss and elevated C. pneumoniae IgA titres.5 This case represents further evidence that acute deafness may be a component of atypical pneumonias, and especially of Chlamydophila infection.

Andrew F Whyte · Richard Yu

To the Editor: The comments about health literacy by Adams and colleagues1 and Nutbeam2 are timely, given findings that 60% of Australians lack basic health literacy skills.2 Despite attention given to health literacy by the National Health and Hospitals Reform Commission, current discussions remain worryingly limited. In the 1990s, Nutbeam was prominent among those who recognised both the individual and the larger environmental settings of health literacy, as well as its relevance to prevention. “Health literacy and health skills” was included as a category in a landmark health goals and targets framework, as “personal health knowledge and positive attitudes towards changing behaviour demonstrably influence people’s ability to adopt healthy lifestyles”.3 Significantly, the goals of improving health literacy were expressed as enabling people to make more informed choices about their health and to take an active role in bringing about changes in environments that influence health. Since then, surprisingly scant attention has been given to health literacy in the context of coping with everyday life, including new situations4 — surprisingly, given that “nearly every choice we make throughout the day is relevant to health in some way — what we eat, how much we move, what products we buy”.5 Most discussions focus on the skills and knowledge individuals need to navigate the health system. Studies of health literacy in broader health contexts remain comparatively rare and frustratingly dispersed throughout numerous disciplines.6 It is time for greater recognition of health literacy as both a consumer issue and a public health issue relevant to disease prevention. (It is perhaps no coincidence that the Newest Vital Sign test for health literacy involves the comprehension of nutrition information about ice cream.) Nutbeam’s suggestions for building health literacy and consumer engagement in health services could easily be expanded. Why not, for example, develop a national plan with specific objectives and approaches, and definitions and indicators to measure health literacy progress? There are obvious tie-ins with the “prevention agenda” and with Australia’s new national policies on men’s and women’s health, and just bringing together the scattered articles on health literacy and gender would be a major task.7 Australian health initiatives aimed at reducing the burden of chronic and preventable disease should consider the role and challenges of health literacy beyond its application to health services use. Our growing understanding of the complex behavioural, social, systemic, and ecological forces that influence health and wellbeing should help guide these efforts.

Margo H Saunders · Anita Peerson

To the Editor: A recent editorial about health literacy and a research article on the prevalence of low health literacy in a South Australian population sample2 highlight the potential negative impact of low health literacy on treatment outcomes. Adams and colleagues also suggest a need to assess health literacy in clinical practice.2 Although calls for the introduction of screening to identify patients with low health literacy appear frequently in such articles, we urge caution in taking such a step at this time, because of a lack of sound evidence to support such a recommendation. High-level evidence related to health literacy screening is scarce. One randomised controlled trial found that making physicians aware of patients’ health literacy status led to greater use of recommended strategies, but did not translate to expected improvements in patient self-efficacy.3 An unanticipated outcome was that physicians who received advice about their patients’ health literacy status reported significantly lower satisfaction with the consultation and felt marginally less effective than those not given such information. The authors caution against health literacy screening in clinical practice unless system-wide training and support for both health practitioners and patients is in place. A fundamental principle of screening is that it should not be introduced without an effective intervention — to do so offers no advantage to patients and may be harmful.4,5 Health literacy screening raises the potential for harm due to high levels of stigma and shame that may be experienced by those with poor literacy. In Australia at this time, it is uncertain whether effective intervention strategies suitable for use in clinical settings are readily available. Moreover, we do not have reliable information about the skill levels of practitioners to address low health literacy. Published studies consistently show that 40%–60% of clinical and population samples have low or marginal levels of health literacy. This means that one of every two people attending a medical consultation can be expected to have suboptimal health literacy. Therefore, a universal approach to the assurance of comprehension in every consultation, supported by practitioner training in health literacy communication and evidence-based tools to enhance patients’ encounters with health services, may offer a more effective and efficient alternative to screening.

Robert A Bush · Frances M Boyle · Remo Ostini