Volume 192 Issue 8

Publication deadlines for reporting causes of deaths not yet finalised by coroners and different methods employed by different jurisdictions may have disguised Australia’s true suicide rate Suicide is a topic of public health, public policy and general community interest. Accurate and timely suicide statistics are needed to measure and monitor this cause of death, to guide the development of prevention programs, and to enable evaluation and research.1 The main source of suicide data in Australia is the national mortality database of the Australian Bureau of Statistics (ABS).2 Recently, the ABS data have been used to report reductions in the annual rates and overall numbers of completed suicides since 1997;3,4 another such report, by Large and Nielssen, appears in this issue of the Journal.5 Surely a decline in suicide rates is good news? It is good news if the reported declines have really occurred. However, there are reasons to think that part of the apparent recent decline in suicide, as estimated using ABS data, is the result of changes in the data collection system.1,6-8 The ABS has published cautionary notes concerning suicide statistics in recent years,9,10 and has changed its process for coding deaths registered after 2006, prompted by awareness of the problem of slow finalisation of some cases.1,11 The system underlying cause-of-death statistics is quite complex, and suicide is a particularly challenging cause to record and classify. If a death is suspected to be the result of suicide, an obligation arises to refer it to a coroner. Police, forensic pathologists and staff at the coroner’s office are involved in obtaining and preparing information for the coroner. Sometimes the coroner decides that a formal inquest is warranted, but most cases are dealt with by a simpler administrative process. Details differ between jurisdictions, but the process always results in a conclusion on the cause of death. Coroners are alert to the sensitivity of a finding of “suicide”. Accordingly, they require positive evidence before making a finding of suicide. Findings normally state the means of death (eg, “ligature asphyxiation”), but often remain silent on intent. Coroners’ records are used by ABS officers to guide their selection of a cause of death code. Historically, this information was mainly obtained by ABS officers visiting coroners’ offices and inspecting records. In 2000, an electronic register of coroner cases, the National Coroners Information System (NCIS), commenced operation. ABS officers began to use information in the NCIS, from about 2003, to supplement visits to coroners’ offices; then, from 2006, to replace these visits.11 NCIS records are entered by coroners’ staff. Some information can be entered soon after a death is referred to a coroner, but the record cannot be finished and the finding cannot be entered until the case has been closed by the coroner, sometimes years after the death has occurred. The ABS has operated a system in which all of the deaths registered in a particular year were processed by a deadline, and then reported as final data. For this system to work well, the information that is necessary for coding the causes of all of the deaths registered in that year must be available to the ABS before its deadline. It turned out that the NCIS did not provide complete information on some deaths, including many suicides, in time to meet the ABS deadline.1,9 Often, the mechanism of injury was known by the deadline (eg, gunshot) but the final conclusion on intent was not. Following advice about the use of the International Classification of Diseases codes in this situation, ABS officers assigned to such cases the same codes that are used for unintentional injury deaths.7 Hence, suicide was under-enumerated. The ABS has changed its system for coroner-certified deaths registered after 2006.11 A death registered in 2007 and incomplete in the NCIS at the former ABS deadline (early in 2009) will have been reported in the first release of ABS data on deaths registered in 2007, probably with a code in a range being used as a “holding bay” for incomplete cases (eg, “Hanging, strangulation and suffocation, undetermined intent”), or as unknown cause of death. If the NCIS record for that death closed during 2009, then the ABS reviewed and, if necessary, recoded it for the second release of 2007 deaths data, issued in March 2010.2 Many of the deaths that were initially assigned “holding bay” codes have characteristics suggesting that they will be recoded as suicides when final information is available. As expected, a rise in the number of suicide deaths was observed between the first and second releases of 2007 deaths data, and further rises are likely in subsequent releases. The first estimate of suicides for 2008, based on a further modification of the ABS system, is 2191, which is higher than the first (1881) and second (2054) estimates for 2007. We don’t yet know final ABS suicide numbers for 2007 or 2008. We do know that ABS suicide counts for the several years before that are low. It is likely that this problem reflects the increasing reliance placed on the NCIS by the ABS in the period 2003–2006. Accordingly, a great deal of caution must be employed when interpreting trends in suicide in Australia during the past decade, particularly when making comparisons between jurisdictions (as these have been found to be differentially affected, as a result of differences in coronial processing times1). Unfortunately, it is likely that at least part of the apparent decline since about 2002 shown by ABS statistics and reported by various authors, including Large and Nielssen,5 is an artefact of increased misclassification of suicide deaths. Changes that have been put in place, chiefly by the ABS, are likely to result in materially more reliable suicide statistics in future, providing a better (though still imperfect) basis for efforts to analyse and interpret changes in this important cause of death.

Clare E Bradley PhD · James E Harrison MB BS, MPH · Amr Abou Elnour MB BCh, GradDipPHC

Putting to rest the myth that emergency department overcrowding is due to a lack of primary care services Australia’s emergency departments (EDs) are dangerously overcrowded, but a study by Buckley and colleagues in this issue of the Journal1 should be the last nail in the coffin of the long-discredited myth that the root cause is a lack of primary care services. This study used a time series approach to identify a real — but clinically insignificant — change in ED workload after the opening of an after-hours primary care service in the New South Wales inland rural city of Wagga Wagga. The Australian public are entitled to receive high-quality and available care in both primary care and emergency settings, but the overlap between these services is not as important as many have claimed.2,3 In a rural location without pre-existing after-hours primary care services, the introduction of such a service, which treated 14 patients daily on average, was associated with an adjusted daily reduction in ED presentations of seven patients with an Australasian Triage Scale (ATS) category of 4 or 5 (lower urgency). As the authors note, because non-admitted low-urgency patients tend to have low resource needs, this reduction of 8% of total ED presentations would correspond to a lesser reduction in workload. Based on published Wagga Wagga Base Hospital data and accepted casemix measures, this reduction would translate to around 3% of this rural ED’s costs and no more than 4% of its ED medical and nursing staff time. These figures are higher than some other Australian estimates,4,5 mostly from studies in cities with pre-existing after-hours services. However, they remain consistent with the observation from these studies that the overall weekly primary care workload in an ED amounts to no more than one patient per hour. In Wagga Wagga, few general practices open for more than 55 hours per week, and the after-hours service opens for 27 hours, but the ED is always open and is the only source of medical care in this community for more than half the 168 hours in each week. It is no surprise that some patients who could reasonably go elsewhere will present to the ED. Buckley et al’s results show that the after-hours clinic treated an average of 3.7 patients per hour. During the hours the clinic was open, the reduction in ED presentations was 1.8 patients per hour and, when it was closed (ie, the rest of the week), the reduction in ED presentations was 0.2 patients per hour. It is unlikely that extending the clinic’s opening hours would make much difference: opening during office hours would probably reduce presentations to existing general practices, and opening later at night would likely be uneconomical. Although, as the study authors note, general practitioners working in EDs in the United Kingdom have been shown to be more cost-efficient than junior medical staff in the same environment, the actual cost of emergency medicine is dominated by infrastructure and staff expenses 24 hours per day.6 EDs have a high average cost per patient and a low marginal (incremental) cost for additional low-acuity presentations, especially compared with off-site after-hours clinics, where expenses are dominated by medical labour, and the average and marginal costs are much closer together. Even if patients were 100% interchangeable, a new after-hours service would likely represent an increase in total cost to the community, because it would not reduce the need for the “public good” of a 24-hour service available at the hospital. Despite its limitations, this study confirms that “primary care patients” and “ED ATS category 4 and 5 patients” are not interchangeable. It is to be expected that there is some overlap between patients who might want to present to an ED and those who might want to go to a GP — just as there may be overlap between patients going to a GP or a gynaecologist for a Pap smear, or between those going to a thoracic surgeon or a respiratory physician for investigation of a lung mass. However, the finding that 96% of the weekly workload of an ED cannot be substituted by an after-hours service confirms that patients are largely presenting appropriately. By comparison, at least a third of average ED staff workload (and more than half in some places) consists of providing care to those who have completed their emergency treatment and are waiting for an inpatient bed,7 sometimes for days. Australian EDs are dangerously overcrowded with patients, many of whom should not be in EDs because they would be better managed elsewhere. But it is not the so-called primary care patients who are blocking ambulances from offloading8 — it is the “access block” patients waiting for beds on the inpatient wards who are inappropriately occupying ED space and staff time.

Drew B Richardson MB BS(Hons), FACEM, GradCertHE

Objective: To examine the changes in rates of methods of suicide in Australian states and territories between 1988 and 2007.Design and setting: Meta-analysis of suicide mortality rates and suicide methods (hanging, shooting, gassing, poisoning, jumping from a height, drowning, use of a sharp implement) for males and females in Australian states and territories in the decades 1988–1997 and 1998–2007.Main outcome measures: Changes in use of suicide methods from 1988 to 2007; changes in the overall suicide rates and in rates for each method of suicide in Australian states and territories between 1988–1997 and 1998–2007.Results: There was a decline in rates of shooting, gassing, poisoning and drowning in males and a decline in shooting, gassing, jumping from a heiight and drowning among females, but an increase in hanging by both males and females in the decade 1998–2007 when the compared to 1988–1997. There was significant variation in the rates of and trends in methods of suicide between the states and territories of Australia between 1988–1997 and 1998–2007.Conclusions: The decline in rates of suicide in most parts of Australia coincides with a reduction in the availability of lethal methods. Consideration should be given to further measures to limit the availability of lethal methods of suicide.

Matthew M Large MB BS, FRANZCP · Olav B Nielssen MB BS, FRANZCP

Objective: To estimate the potential health benefits and cost savings of an alcohol tax rate that applies equally to all alcoholic beverages based on their alcohol content (volumetric tax) and to compare the cost savings with the cost of implementation.Design and setting: Mathematical modelling of three scenarios of volumetric alcohol taxation for the population of Australia: (i) no change in deadweight loss, (ii) no change in tax revenue, and (iii) all alcoholic beverages taxed at the same rate as spirits.Main outcome measures: Estimated change in alcohol consumption, tax revenue and health benefit.Results: The estimated cost of changing to a volumetric tax rate is $18 million. A volumetric tax that is deadweight loss-neutral would increase the cost of beer and wine and reduce the cost of spirits, resulting in an estimated annual increase in taxation revenue of $492 million and a 2.77% reduction in annual consumption of pure alcohol. The estimated net health gain would be 21 000 disability-adjusted life-years (DALYs), with potential cost offsets of $110 million per annum. A tax revenue-neutral scenario would result in an 0.05% decrease in consumption, and a tax on all alcohol at a spirits rate would reduce consumption by 23.85% and increase revenue by $3094 million. All volumetric tax scenarios would provide greater health benefits and cost savings to the health sector than the existing taxation system, based on current understandings of alcohol-related health effects.Conclusions: An equalised volumetric tax that would reduce beer and wine consumption while increasing the consumption of spirits would need to be approached with caution. Further research is required to examine whether alcohol-related health effects vary by type of alcoholic beverage independent of the amount of alcohol consumed to provide a strong evidence platform for alcohol taxation policies.

Joshua M Byrnes BComm, MEconStud, MHealthEcon · Linda J Cobiac BEng(Hons), MEngSc, MPhil(Maths) · Christopher M Doran BEcon(Hons), PhD · Theo Vos MSc, PhD · Anthony P Shakeshaft MA(Psych), PhD

Objective: To evaluate the changes in the understanding of the manner and cause of death occurring during the course of coronial investigations.Design: Retrospective analysis of deaths reported to coroners in Australia between 1 July 2000 and 31 December 2007, using the National Coroners Information System.Main outcome measures: (i) Manner of death (natural, external, unknown); (ii) intent classification (eg, unintentional injury, suicide, assault) among deaths with external causes; and, (iii) changes in the manner of death and intent classification between the presumption made at case notification and the coroner’s final determination.Results: The coronial investigation changed the presumption about manner of death or intent classification in 5.2% (6222/120 452) of cases in which a presumption was made. Among deaths with a change in attribution from natural causes to external causes, unintentional falls (442/1891) and pharmaceutical poisoning (427/1891) each accounted for 23%. Among deaths with attribution changing from external causes to natural causes, the leading medical causes of death were cardiovascular compromise (551/842; 65%) and infection (124/842; 15%). Of deaths understood correctly at notification to be due to external causes, but the wrong external cause, 34% (206/600) were ultimately judged to be unintentional injuries, and 22% (133/600) were judged to be suicides.Conclusions: Coronial investigations transform basic understanding of cause of death in only a small minority of cases. However, the benefits to families and society of accurate cause-of-death determinations in these difficult cases may be considerable.

David M Studdert LLB, ScD, MPH · Stephen M Cordner MB BS, BMedSc, DipCrim

Objective: To assess the impact of the opening of an after-hours general practice clinic on the number of daily low-urgency presentations to the nearby emergency department.Design, participants and setting: Retrospective time series analysis of emergency presentation data, from the New South Wales Health Emergency Department Information System, for all patients presenting to the emergency department of Wagga Wagga Base Hospital between January 1998 and October 2008.Main outcome measures: Daily emergency department presentations, before and after the March 2003 opening of the after-hours clinic, of patients triaged as Australasian Triage Scale (ATS) category 4 or 5 (at any time of day, and during the hours of operation of the clinic), and of patients triaged as ATS category 1, 2 or 3 (at any time of day).Results: After adjusting for long-term trends and weekly and annual cycles, the opening of the after-hours clinic was associated with a daily reduction of 7.04 patients (95% CI, 5.39–8.70) in emergency department presentations with an ATS category of 4 or 5. This represented an 8.2% reduction in total presentations (95% CI, 6.2%–10.2%). Presentations of ATS category 1, 2 or 3 patients rose by 1.36 patients a day (95% CI, 0.36–2.35), representing 1.6% of total presentations (95% CI, 0.4%–2.7%). The impact of the after-hours clinic was best modelled by a gradual permanent change.Conclusion: An after-hours general practice clinic was associated with a reduction in low-urgency presentations to the emergency department in Wagga Wagga.

David J Buckley BVSc(Hons), MVSc · Paul W Curtis MB BS, MHA, FRACMA · Joseph G McGirr MB BS, BSc(Med), FACEM

Suicide and intentional self-harm are issues of major importance in public health and public policy, with rates widely used as progress indicators in these areas. Accurate statistics are vital for appropriately targeted prevention strategies and research, costing of suicide and to combat associated stigma. Underreporting of Australian suicide rates probably grew from 2002 to 2006; Australian Bureau of Statistics (ABS) suicide data were at least 11% or 16% undercounted (depending on case definitions) in 2004. In coronial cases with undetermined intent for 2005 to 2007, intentional self-harm was found in 39%. Systemic reasons for undercounting include: (i) absence of a central authority for producing mortality data; (ii) inconsistent coronial processes for determining intent, as a result of inadequate information inputs, suicide stigma, and high standards of proof; (iii) collection and coding methods that are problematic for data stakeholders; and (iv) lack of systemic resourcing, training and shared expertise. Revision of data after coronial case closure, beginning with ABS deaths registered in 2007, is planned and will reduce undercounting. Other reasons for undercounting, such as missing or ambiguous information (eg, single-vehicle road crashes, drowning), differential ascertainment (eg, between jurisdictions), or lack of recorded information on groups such as Indigenous people and gay, lesbian, bisexual and transgender people require separate responses. A systemic coordinated program should address current inaccuracies, and social stigma about suicide and self-harm must be tackled if widespread underreporting is to stop.

Diego De Leo MD, PhD, FRANZCP · Michael J Dudley MB BS, FRANZCP · Caroline J Aebersold BA(Hons) · John A Mendoza DipTeaching, BEd, GradDipHealthSci · Michael A Barnes BA, LLB, LLM · James E Harrison MB BS, MPH, FAFPHM · David L Ranson BM BS, LLB FRCPA

Objective: To evaluate the evidence for and against the effectiveness of homeopathy.Data sources: The Cochrane Database of Systematic Reviews (generally considered to be the most reliable source of evidence) was searched in January 2010.Study selection: Cochrane reviews with the term “homeopathy” in the title, abstract or keywords were considered. Protocols of reviews were excluded. Six articles met the inclusion criteria.Data extraction: Each of the six reviews was examined for specific subject matter; number of clinical trials reviewed; total number of patients involved; and authors’ conclusions. The reviews covered the following conditions: cancer, attention-deficit hyperactivity disorder, asthma, dementia, influenza and induction of labour.Data synthesis: The findings of the reviews were discussed narratively (the reviews’ clinical and statistical heterogeneity precluded meta-analysis).Conclusions: The findings of currently available Cochrane reviews of studies of homeopathy do not show that homeopathic medicines have effects beyond placebo.

Edzard Ernst FMedSci, FRCP, FRCPEd

Recent research has confirmed that Australian children and pregnant women are mildly iodine deficient. A considerable proportion of the pregnant population is moderately to severely iodine deficient. Even subclinical hypothyroidism in the mother, occurring as a consequence of iodine deficiency, can cause irreversible brain damage in the fetus, making it essential to avoid iodine deficiency in pregnancy. The proposal of Food Standards Australia and New Zealand (FSANZ) — Mandatory Iodine Fortification for Australia (P1003) — has been implemented. FSANZ openly admits P1003 is inadequate for covering the needs of pregnant women. Therefore, health professionals and the public must be properly informed about the limitations of this proposal. Views differ about the most effective measures to prevent iodine deficiency in Australia. We propose that women planning a pregnancy, and pregnant and lactating women should be advised to take an iodine supplement. Women with pre-existing thyroid disease should exercise caution and seek medical advice before taking a supplement.

Gisselle Gallego BPharm, PhD · Stephen Goodall BSc, MSc(Health Econ), PhD · Creswell J Eastman MD, FRACP, FAFPHM

In the United States, policy experiments over a 20-year period have demonstrated that road crash deaths among young adults can be substantially reduced by raising the minimum legal drinking age to 21 years. A recent evaluation of the cost-effectiveness of policies for reducing alcohol-related harm in Australia found that, if the US experience were to be replicated in Australia, raising the minimum legal drinking age would be more cost-effective than random breath testing and drink-driving campaigns. Given the major political obstacles to increasing the minimum legal drinking age, we propose another policy that could achieve a similar reduction in road crash deaths — requiring licensed drivers to maintain a blood alcohol concentration (BAC) of zero until at least the age of 21 years (close to the current policy of zero BAC until age 22 years in Victoria), and preferably until 25 years. This would allow young Australians to drink or drive but not to combine these activities for at least the first several years of driving. If all Australian jurisdictions had adopted this policy in 2003, 17 deaths could have been be averted among young Australians as they aged from 18 to 21 years and many more serious injuries could have been prevented each year. If we had enforced a zero BAC until age 25, the number of deaths averted until age 25 years could have been as high as 50.

Wayne D Hall PhD · Angela L Wallace BSc, MPH · Linda J Cobiac BEng, MEngSc, MPhil · Christopher M Doran PhD · Theo Vos MSc, PhD

Alcohol consumption is a major risk factor contributing to the burden of disease in Australia. The National Preventative Health Taskforce recommends the long-term goal of reshaping Australia’s drinking culture to produce healthier and safer outcomes. A study of the cost-effectiveness of interventions to reduce alcohol-related harm in Australia suggests that policymakers could achieve over 10 times the health gain if they reallocated the current level of investment. The optimal package of interventions identified in the study comprises, in order of cost-effectiveness, volumetric taxation, advertising bans, an increase in the minimum legal drinking age to 21 years, brief intervention by primary care practitioners, licensing controls, a drink-driving mass media campaign, and random breath testing. Australia has a window of opportunity to significantly expand activities to reduce alcohol-related harm. It is important that federal and state governments take this opportunity to reform alcohol policy in Australia.

Christopher M Doran PhD · Wayne D Hall PhD · Anthony P Shakeshaft PhD · Theo Vos MSc, PhD · Linda J Cobiac BEng, MEngSc, MPhil

Two Australian blood donors were diagnosed with relapsing Plasmodium vivax malaria 5 and 15 months, respectively, after their most recent travel to a malaria-endemic country. Common features included travel to Papua New Guinea (specifically, the Kokoda Trail); full compliance with recommended malaria chemoprophylaxis; and negative results on malaria antibody testing at the time of donation. Although all fresh blood components from the two donors issued on the basis of these negative results were recalled before transfusion, these cases underscore the increased potential for relapse of P. vivax in donors returning from malaria-endemic countries, as well as the inability to identify the potential for relapse using current malarial screening tests. Clinical recordPatient 1A 63-year-old man donated blood to the Australian Red Cross Blood Service (the Blood Service) 12s7 days after returning from an organised trek on the Kokoda Trail, Papua New Guinea (PNG). An enzyme immunoassay (EIA) for Plasmodium falciparum and Plasmodium vivax antibodies was non-reactive at donation. Twenty-six days later, the donor’s wife notified the Blood Service that her husband had been admitted to hospital with fever and rigors; he was subsequently diagnosed with P. vivax malaria based on visible P. vivax parasites in a blood film (13 800 parasites/μL), and a positive result on a (non-P. falciparum) malarial antigen test (Box). He was successfully treated with primaquine. After his discharge from hospital, he was interviewed by a Blood Service medical officer and reported that he had no history of malaria; complied fully with malarial prophylaxis (doxycycline 100 mg daily, starting 2 days before entering PNG and finishing 14 days after returning home); had 2 months of lethargy after his return and developed febrile symptoms 20 days after donation; and had not travelled outside Australia after his donation. He also reported that seven of his 15 trekking companions were diagnosed with malaria after the trek. Patient 2A 39-year-old man donated blood 13 months after returning from PNG. He had made three previous donations, the first 5 months after returning from PNG, all testing negative for malarial antibodies. During the trip, the donor walked the Kokoda Trail and complied fully with prophylaxis (atovaquone–proguanil, 250 mg/100 mg daily, starting 1 day before and finishing 7 days after travel). He did not recall any recognisable malarial symptoms during the trek, but noted that a trekking companion had malaria on return to Australia. Approximately 66 days after his latest donation, the donor notified the Blood Service that he had recently been admitted to hospital with a febrile illness subsequently diagnosed as non-P. falciparum malaria; P. vivax was later confirmed from the blood film (0.5% parasitaemia) (Box). He was treated with atovaquone–proguanil (250 mg/100 mg four times daily for 3 days), made a full recovery and was discharged from hospital. He later confirmed that he had not travelled outside Australia after his return from PNG. Results of diagnostic testing of the two donors are summarised in the Box. DiscussionMalaria is transmitted predominantly through the bite of an infected female Anopheles mosquito, but, because the parasite invades and multiplies in red blood cells (RBCs), it can also be transmitted by transfusion of any blood component containing RBCs.1 Although malaria is not endemic in Australia, between 500 and 900 cases are notified annually, constituting an ongoing risk of transfusion-transmitted malaria (TTM).2 However, this risk is well controlled — the most recent recorded case of TTM occurred in 1991, involving a donor infected with P. falciparum.3 Notably, the transfusion recipient died, an outcome observed in about 10% of TTM cases caused by P. falciparum.4 To minimise TTM risk in Australia, each potential donor is asked questions to elicit if he or she has spent time in malaria-endemic countries or is at risk of having had malaria. Those identified at risk of infection are tested with an EIA for P. falciparum and P. vivax antibodies (Malaria EIA, NewLabs, Newmarket, United Kingdom). When the EIA is negative, the RBC component of the donation is considered for transfusion if at least 4 months have elapsed since the donor’s risk exposure. The 4-month waiting period minimises the possibility of false-negative test results that arise from testing within the putative 7–14-day “window period” before a complete antibody response is detectable. The Blood Service implemented serological testing of donors for malaria in 2005, replacing the previous strategy of restricting manufacture of fresh blood components from at-risk donations (ie, donations from people who had visited malaria-endemic countries in the previous 12 months or from those who had resided in an endemic country for a cumulative total of 6 months or more in the previous 3 years).5 While effectively minimising the risk of TTM, the older strategy resulted in significant loss of transfusible components (estimated in 2001 at about 5% of the Blood Service’s annual RBC production). This loss was considered unacceptable in the face of mounting demands on supplies of blood and blood products. The feasibility of serologically testing at-risk donors to reduce the period of restriction and consequent component loss had been established in Europe, where serum tests had been implemented in France6 and the UK.7 Furthermore, the use of a validated antibody test to reinstate donors after a minimum of 4 months is permitted by the applicable regulatory standard used by Australia.8 The predominant TTM risk is associated with so-called “semi-immune” individuals born or resident for extended periods in malaria-endemic countries.9 In the semi-immune person, the infection may take the form of an “equilibrium” in which very low parasite loads (generally undetectable by microscopy, and even polymerase chain reaction [PCR] testing) coexist with malarial antibodies without producing overt symptoms. Most recently recorded cases of TTM have resulted from the failure to detect and exclude the RBC-containing components of donations from semi-immune donors infected with P. falciparum.4,6 When parasite loads are extremely low, even the best plasmodial PCR assay is unable to interdict all potentially infectious donations, given that a transfusion contaminated with as few as 10 parasites can transmit infection.1 This underpins the rationale for antibody-based testing as the optimum donor-screening test, underscored by the Australian regulatory standard’s explicit exclusion of the use of molecular tests to screen donors.8 Another potential TTM risk is that both P. vivax and Plasmodium ovale have a hypnozoite form that can persist in the liver and lead to relapses after successful treatment of the primary infection.10 The interval from primary infection to relapse ranges from 1 month to 4 years.11,12 Chemoprophylactic agents are prescribed based on their efficacy against blood-stage parasites, but they are, with the exception of terminal (ie, postexposure) primaquine prophylaxis, ineffective against hypnozoites.13 Thus, they cannot prevent relapse but may delay its onset.11 Our two cases were strikingly similar, and the evidence strongly implicates PNG (specifically, the Kokoda Trail) as the site of primary infection for both. This is consistent with published evidence showing that, among non-immune travellers and soldiers returning to Australia, those from PNG and neighbouring countries were more likely to have relapsing malaria.13-15 These two cases of apparent relapse associated with P. vivax malaria in non-immune donors are, to our knowledge, the first reported cases detected by antibody testing. Further, they were unexpected because the perceived TTM risk is predominantly associated with P. falciparum infected semi-immune individuals. This either indicates that malarial antibody titres in individuals harbouring hypnozoites decline to undetectable levels 4 months or more after infection or, alternatively, that levels of parasitaemia during a “suppressed” primary infection may be too low to stimulate a significant antibody response. Thus, the current testing strategy cannot be relied on to discriminate donors at risk of relapse. This should not be seen as a reason to reject antibody testing per se, as no other available laboratory test for parasitaemia can reliably identify these individuals. Notably, the strongly positive EIA results in samples taken from the two donors at the time of admission to hospital support a robust antibody response and are consistent with the high sensitivity of the Newmarket EIA observed in samples taken from patients with acute disease.1 The TTM risk posed by relapsing P. vivax infection occurs during the asymptomatic period because symptomatic individuals would be prevented from donating. Although not precisely known, this period is expected to be short, perhaps several days. The TTM risk posed by our two patients was contained. One RBC component had been issued (Patient 1), based on its non-reactive malarial antibody test result, 20 days before symptom onset. This was successfully recalled, avoiding any potential risk to recipients. Considering the 20-day period between donation and symptom onset, it is highly likely that the donation was made before the onset of parasitaemia and, therefore, the RBC component would not have been infectious. No fresh blood components from Patient 2 were issued. What do these two cases suggest about the safety of the current Blood Service testing strategy? They certainly raise concern given that their late detection could have resulted in transfusion of potentially infectious blood components. However, such cases appear to be exceedingly rare — these are the only two reported in Australia in more than 4 years of testing. Furthermore, the contribution of such cases to overall TTM risk appears to be minute, as no TTM cases have been reported since testing began We recently published a comprehensive review that supports the existing strategy — it concluded that the current TTM risk was less than 1 in 3.3 million and had not measurably increased after implementing the testing strategy.16 Importantly, the Blood Service achieved this level of safety while recovering over 70 000 fresh blood components that would otherwise have been unavailable annually. Nonetheless, recognising the limitations of the testing strategy and the imperative to reduce recipient risk where possible, the Blood Service is considering mitigation options. As these two cases suggest travel to PNG carries a disproportionately high risk, the Blood Service is considering the feasibility of excluding donors returning from PNG from the testing protocol, and restricting fresh component production from their donations for appropriate periods of time. Blood testing for relapsing Plasmodium vivax in the two patients Place Time Pf/Pv antibody EIA* Pf/Pv antigen ICT† PCR‡ Blood film Patient 1 Sample 1 Blood Service At donation (127 days after return from PNG) Non-reactive (S/Co 0.28) Not tested Not tested Sample 2 Blood Service At hospital admission (26 days after donation) Reactive (S/Co 4.2, 3.6§) Positive Pf band negative Pan malaria positive Plasmodial DNA detected (4415 parasites/μL) Pv parasites visible (13 800 parasites/μL) Sample 3 Blood Service In hospital after treatment (33 days after donation) Reactive (S/Co 4.8, 3.7§) Negative DNA not detected Patient 2 Sample 1 Blood Service At donation (13 months after return from PNG) Non-reactive (S/Co 0.27) Not tested Not tested Sample 2 Hospital At hospital admission (66 days after donation) Reactive (S/Co > 19, 18.8§) Positive Pf band negative Pan malaria positive Plasmodial DNA detected (1861 parasites/μL) Pv parasites visible (0.5% parasitaemia) Blood Service = Australian Red Cross Blood Service. EIA = enzyme immunoassay. ICT = immuno-chromatographic test. PCR = polymerase chain reaction. PNG = Papua New Guinea. Pf = Plasmodium falciparum. Pv = Plasmodium vivax. S/Co = sample-to-cut-off ratio (this test relates to the level of antibodies in each sample compared with a predetermined cut-off level). * Malaria EIA, NewLabs, Newmarket, United Kingdom. † Binax NOW Malaria assay, Inverness Medical, United States. ‡ artus malaria RG PCR, Qiagen, Hilden, Germany. § Two values were reported because repeat testing usually requires a double check to ensure accuracy.

Clive R Seed BSc · Jacqueline T Coughlin MB BS, FRACGP · Anne M Pickworth MB BS · Robert J Harley MB BS, BMus, FRACGP · Anthony J Keller FRACP, MRCPath, FRCP

An Eritrean-born man observed over an extended period had upper gastrointestinal symptoms, fever, hepatosplenomegaly and pancytopenia in the setting of advanced HIV infection and poor adherence to antiretroviral therapy. Despite thorough investigation, it was not until a repeat gastroscopic examination and gastric biopsy were performed 18 months after initial presentation that Leishmania infection was diagnosed. The species was identified by polymerase chain reaction assay as L. donovani. Physicians managing HIV-infected patients from regions where Leishmania is endemic should consider visceral leishmaniasis, even in patients who have not lived in a Leishmania-endemic region for many years. Clinical recordA 42-year-old Eritrean-born man who had previously lived in Sudan arrived in Australia in 1995. He had not travelled overseas since that time. He was diagnosed with HIV infection in 1996. He presented in 2005 with a 2-month history of odynophagia, dysphagia and vomiting. The patient was non-adherent to antiretroviral therapy and his CD4 count was 40 cells/μL (reference range [RR], 410–1590 cells/μL). He had low-grade fever, hepatosplenomegaly and pancytopenia (haemoglobin level, 118 g/L [RR, 130–180 g/L]; white cell count, 3.2 × 109/L [RR, 4.0–11.0 × 109/L]; and platelet count, 111 × 109/L [RR, 150–400 × 109/L]). A computed tomography scan confirmed hepatosplenomegaly, but there was no intra-abdominal or pelvic lymphadenopathy. A bone marrow biopsy showed hypercellular marrow with no granulomas or malignancy. Bone marrow fungal and mycobacterial culture and a polymerase chain reaction (PCR) assay for parvovirus DNA were negative. No abnormality was visible on gastroscopic examination. Histological examination of oesophageal biopsies showed chronic inflammation, but no fungal elements were detected by fungal stains, and fungal cultures were negative. A herpes multiplex PCR assay (capable of detecting herpes simplex virus types 1 and 2, cytomegalovirus and varicella-zoster virus) was negative. No Leishmania amastigotes (the non-flagellate, intracellular form of Leishmania) were identified. Symptoms improved after treatment with omeprazole and a period of improved adherence to antiretroviral therapy. Odynophagia, dysphagia, weight loss, intermittent fever and mild pancytopenia recurred and continued over the next 18 months. Despite changes to the antiretroviral therapy regimen and efforts to improve adherence, the patient’s CD4 count remained below 50 cells/μL and the HIV viral load was consistently > 750 000 copies/mL. A repeat gastroscopic examination 18 months after initial presentation demonstrated pseudomembrane formation over the upper stomach, and histological examination of a gastric biopsy showed a florid inflammatory cell infiltrate. Within histiocytes, numerous intracellular organisms 1–3 μm in diameter were identified as Leishmania amastigotes (Box). A PCR assay confirmed the presence of L. donovani, leading to a diagnosis of visceral leishmaniasis (VL) in the setting of advanced HIV infection. Induction treatment was commenced with daily liposomal amphotericin B 4 mg/kg for 1 week, followed by weekly doses for a further 4 weeks. The odynophagia, dysphagia and pancytopenia resolved over the following 4 months. Secondary prophylaxis with monthly doses of liposomal amphotericin B continued, but the patient missed three doses over the next 6 months and symptoms recurred. When repeat endoscopy, biopsy and histology showed that Leishmania was still present, therapy was recommenced and the symptoms resolved. Further unsuccessful attempts were made to optimise the antiretroviral therapy regimen. After 12 months of intermittent adherence to treatment, the patient again developed symptoms. He subsequently returned to East Africa and was lost to follow-up. DiscussionLeishmaniasis is a protozoal infection caused by species of the genus Leishmania, an intracellular parasite transmitted by sandflies of the genus Phlebotomus. Clinical presentations include visceral, cutaneous and mucocutaneous forms, depending on the infecting species and the strength of the host’s cell-mediated immunity. The Leishmania donovani complex, composed of L. donovani and L. infantum/chagasi, is responsible for most cases of VL. Where co-infection with HIV is present, deteriorating immune function may delay the clinical presentation of VL for many years after the initial infection.1 Although documented in 70 countries, most cases of VL occur in southern Asia (particularly north-eastern India, Nepal, and Bangladesh) and East Africa (mostly Sudan, Ethiopia and Eritrea). In these regions, L. donovani is the predominant species. About 15 000 to 20 000 cases of VL occur annually in Sudan, particularly in the eastern region bordering Ethiopia and Eritrea, and VL–HIV co-infection rates are as high as 29%–40%.2-4 In southern Europe, especially in urban coastal regions, where the less virulent L. infantum is the predominant organism, high rates of VL–HIV co-infection have also been described.5 The usual incubation period of VL is 2–6 months, but a proportion of patients will remain asymptomatic after primary infection, and immunosuppression can lead to reactivation of the disease many years later. The classic presentation of VL includes fever, weight loss, hepatosplenomegaly, pancytopenia and hypergammaglobulinaemia. HIV co-infection does not dramatically alter this presentation.6,7 Gastrointestinal tract involvement is evident in 7%–40% of VL–HIV co-infected patients, and may be accompanied by odynophagia, dysphagia, chronic diarrhoea, malabsorption or abdominal pain.6,8 Most patients with HIV who present with VL are in a state of advanced immunodeficiency: up to two-thirds of patients with concomitant HIV and L. donovani infection have CD4 counts < 200 cells/μL.3 Serological tests for VL are of low sensitivity and thus have limited diagnostic value for VL–HIV co-infected patients.2 Demonstration of amastigotes in tissue or blood is the preferred method of diagnosis. Examination of a bone marrow smear is often the most useful diagnostic test (sensitivity, 67%–94%),2,4,8 and aspirates from other sites can be considered depending on the clinical presentation. A PCR assay for Leishmania DNA may improve the diagnostic yield and allow identification to a species level. Treatment of VL in patients with underlying HIV infection is associated with lower cure rates, higher rates of drug toxicity, higher relapse rates and greater mortality than treatment of VL in immunocompetent patients.2,9 Optimal treatment regimens have not yet been developed, as there is a paucity of clinical data on patients with VL–HIV co-infection. Treatment options include pentavalent antimonials such as sodium stibogluconate, standard and lipid formulations of amphotericin B, miltefosine, paromomycin and pentamidine.2,9 Although liposomal amphotericin B has not been formally assessed in VL–HIV co-infected patients, it has the highest therapeutic index of all antileishmanial drugs and a superior safety profile, making it the first choice for treatment in resource-rich countries. Although there has been recent interest in miltefosine because of its oral administration, an Ethiopian study showed that miltefosine was less effective than intramuscular sodium stibogluconate for treating HIV-infected patients.10 Maintenance secondary prophylaxis and initiation of effective antiretroviral therapy is required to prevent relapse.9 In a study conducted in a resource-limited setting in Ethiopia, antiretroviral therapy was shown to reduce the risk of VL relapse by about 50%.3 The increasing rate of VL–HIV co-infection in Africa and India is a major concern, but so far, very few cases have been reported in Australia. The case described here highlights the importance of considering the diagnosis of VL in a patient with immunodeficiency and a history of travel to, or residence in, a Leishmania-endemic region; the value of tissue biopsy combined with PCR testing; and the need for ongoing secondary prophylaxis and immune restoration. Section of gastric biopsy showing a florid inflammatory cell infiltrate and numerous Leishmania amastigotes Amastigotes appear as non-flagellate, intracellular, ovoid bodies (1–3 μm in diameter) within histiocytes (haematoxylin and eosin stain, original magnification × 300).

Samuel C Hume MB BS(Hons), FRACP · Craig A Aboltins MB BS(Hons), FRACP · Karin A Thursky MB BS, FRACP, MD · John R Daffy MB BS, FRACP · Peter A Stanley MB BS, FRACP

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

To the Editor: Pregnancy following aorto-iliac bypass or replacement grafting is uncommon, as most patients requiring this operation are beyond childbearing age. However, conditions may occur at earlier ages that necessitate such a procedure and, as the case described here illustrates, the surgery is no bar to pregnancy. In 1982, a 13-year-old girl presented to hospital after two episodes of abdominal pain. Ultrasound examination showed a large dumbbell-shaped retroperitoneal tumour widely separating the aorta and vena cava. Laparotomy revealed a large tumour firmly adherent to the inferior vena cava and completely surrounding the aorta. Biopsy showed it to be a ganglioneuroma. It was possible to separate the tumour from the vena cava but not the aorta, as no plane could be defined, and during the dissection a hole was made in the vessel. The involved aorta was resected and the tumour was able to be completely removed. The removed segment was replaced with a 10 mm woven dacron tube graft (compatible with the host aorta) from the infrarenal level to the aortic bifurcation. Five years later, the aortic graft thrombosed. Exploration showed no evidence of recurrence of the tumour, and the previous graft was replaced with a 14 × 7 mm gelatin-impregnated, knitted dacron bifurcated prosthesis from the infrarenal aorta to each common iliac artery. The patient had regular follow-up, including ultrasound and magnetic resonance imaging scans. In June 2007, after I had retired from vascular surgery, I was contacted by the patient (now aged 39 years), who was seeking information about her previous operations because she was 14 weeks pregnant and her obstetrician was concerned about the uterine blood supply. She had approached the hospital, but was told that her records had been destroyed. Fortunately, I still had my personal records of her previous surgery. The patient had required in-vitro fertilisation for conception because her uterine tubes were blocked. The pregnancy proceeded normally until the 36th week, when signs of eclampsia developed. Caesarian section was performed at 37 weeks and a healthy infant was delivered. A review of the literature revealed six other reported cases of pregnancy occurring in patients who had had previous aortic grafting for aneurysmal or atherosclerotic disease.1-6 Two patients had caesarean section and the others were delivered vaginally; all infants were viable. Possible concerns expressed by clinicians in cases such as this include compromise of the pelvic circulation, affecting foetal development; compression of the graft by the fetal head during delivery; uterine contractions contributing to graft occlusion; reduction of blood flow through the graft because of the patient’s position during labour; and false aneurysm formation at the anastomotic sites, with an increased risk of rupture. With adequate assessment and supervision by obstetric and vascular surgical teams, the outcome of pregnancy in women with a history of aortic grafting should be favourable.

H Reginald Magee

Mosby’s dictionary of medicine, nursing & health professions, 2nd Australian and New Zealand edition . Peter Harris, Sue Nagy, Nicholas Vardaxis, editors. Sydney: Elsevier Australia, 2009 (xvi + 2015 pp). ISBN 978 0 7295 3909 8. The first Australian and New Zealand edition of this popular American dictionary was published in 2006. It was a landmark achievement, with its Asia-Pacific orientation in both content and style. For instance, entries included the “bluebottle jellyfish”, common to Australasian waters. Local spelling and phonetic pronunciation guides were also provided. However, almost as soon as it was published, the need for a continuing process of review and revision was recognised. And so, editors-in-chief Peter Harris, Sue Nagy and Nicholas Vardaxis led a team of 60 specialists to produce further refinements, which resulted in this second edition. The language of medicine is constantly evolving to keep up with the latest developments in research and technology. Thus, some of the new terms in the second edition include Hendra virus, Nipah virus, swine flu and vancomycin-resistant enterococcus. There were some 40 000 entries and 2400 colour images in the first edition. More than 500 images, 300 drug entries and 73 tables have been added or updated in this edition. The many useful appendices cover areas such as nutrition guidelines, immunisation schedules, infection control and herb–drug interactions. Charts and graphs range in content from lung sounds and burn depths to contraceptive effectiveness and cardiac arrhythmias. Simple devices such as extensive cross-referencing and a thumb-style index make navigation easy. The bonus “Evolve” website access provides many free online resources, such as all the images from the book, directories of key health organisations and health promotion information. This strategy has enabled the dictionary to be confined to a single volume that is still kept current through the website. This dictionary can help health professionals and students become familiar with new medical terminology and techniques, and thus improve their communication and outcomes. Certainly, as a proofreader for the Journal, I’m sure to refer to it at least once a week.

Gita Sankaran

BABY BONUS Since the introduction of the federal government’s “baby bonus” the annual hospital birth rate in New South Wales has risen by over 11 000. This rise has also had an important and possibly unexpected impact on maternity services and related costs, with the extra births increasing costs by $60 million/year. In 2008, there were over 8700 more vaginal deliveries, over 1000 more preterm births and over 45 000 extra infant hospital days/year. The increase in numbers of deliveries was observed in tertiary, urban and rural public hospitals but, interestingly, no increase was seen in private hospitals. Aust NZ J Obstet Gynaecol 2010; 50: 25-29 A STITCH IN TIME Using staples for wound closure in orthopaedic surgery is more likely to be associated with superficial wound infection than traditional sutures, according to a recent UK meta-analysis of six studies. The review included outcomes for 683 surgical wounds and found that the overall rate of wound infection was over three times greater (RR, 3.83; 95% CI, 1.38-10.68) when staples were used, and that this was even more likely after hip surgery (RR, 4.79; 95% CI, 1.24 -18.47). There was no significant difference between the two closure methods for development of inflammation, discharge, dehiscence or allergic reaction. However, the authors note several problems with the quality of the studies included in the review and call for further trials to reappraise the issue. BMJ 2010; 340: c1199 doi: 10.1136/bmj.c1199 SNOW SAFETY Does wearing a helmet while skiing or snowboarding reduce the risk of head injury? A recent meta-analysis of 12 studies indicates that wearing a helmet can reduce the risk of head injury by 35% (95% CI, 21%- 46%). However, the benefits of wearing a helmet for snow sports has been a topic of debate due to concerns about the potential for an increased risk of neck injury during a fall (which may be more evident among young children due to a greater head:body ratio). According to an analysis of six of the studies in the meta-analysis, there was no overall increase in the risk for neck injuries (OR 0.89; 95% CI, 0.72-1.09), but only two of these studies included children under 13 years of age. CMAJ 2010; 182: 333-340 MOVIE MARKETING Until now, restriction of junk food advertising targeting children has mainly focused on children’s television, with little attention paid to movies as a potential avenue for advertising. However, US researchers who analysed 200 popular movies found a surprisingly high prevalence of “brand appearances”, with two-thirds of the movies containing at least one food, beverage or retail-establishment brand, mostly for energy-dense, nutrient-poor foods. One-third of G-rated, more than half PG-rated and almost three-quarters of PG-13 rated movies included such material. Of particular concern was the high number of sugar-sweetened drinks appearing in PG and PG-13 rated movies, which are geared to older children and teenagers who are gaining independence with their food choices, and who may not even be aware of the advertising. Indeed, other researchers in the area have suggested that movie product placement is “on a par with subliminal advertising”. Pediatrics 2010; 125: 468-474 COUCH POTATOES “Get off the couch” and turn off the TV appears to be the message from a recently published analysis of data from AusDiab (Australian Diabetes, Obesity and Lifestyle study), which included 8800 adults followed up for a median of 6.6 years. Watching more than 4 hours of television per day was reported to be associated with an 80% increase in the risk of cardiovascular death, compared with viewing less than 2 hours per day. Interestingly, this was independent of leisure-time exercise and other traditional risk factors such as smoking, blood pressure, diet and cholesterol. Excessive TV viewing was also associated with a 46% increased risk of death from any cause. Circulation 2010; 121: 384-391

Alison Williams