Letters

To the Editor:We thank Tong and colleagues1 for their report on a patient with schizophrenia and clozapine-induced maculopathy, and for highlighting this under-recognised condition. Both typical2 and atypical3 antipsychotic drugs have been reported to cause widespread retinopathy; more recently, there have been reports of rare cases of retinal damage localised to the macula (maculopathy) due to both typical4 and atypical1,5 antipsychotics. The classical hypothesis for widespread pigmentary retinopathy is that drugs are absorbed by melanin in the retinal pigment epithelium (RPE) and act as photosensitisers to damage the RPE. This results in loss of RPE support functions of overlying photoreceptors, which secondarily degenerate. An alternative hypothesis,2 supported by histological and animal studies, is that the problem begins in photoreceptors, with drug-induced blockade of retinal dopamine receptors followed by photoreceptor and subsequent RPE cell loss. Neuroleptic retinal drug toxicity typically involves pigment disruption in the RPE, but the dopamine hypothesis allows for broader combinations of RPE and/or photoreceptor damage. The reasons for the development of maculopathy in some patients, rather than a widespread retinopathy, are not known. This phenomenon is seen in other ocular drug toxicities, particularly hydroxychloroquine. Most drug-induced retinal toxicities are bilateral and symmetrical; asymmetrical cases have rarely been reported. The patient reported by Tong and colleagues is atypical with apparently unilateral macular changes.1 Significant differential diagnoses for unilateral macular pigment and photoreceptor changes include age-related and secondary to retinal conditions, such as central serous chorioretinopathy, inflammatory retinopathies and trauma. Maculopathy limited to the outer neuroretina may occur with the use of other drugs (eg, poppers maculopathy).6 Also, schizophrenia is known to cause illness-related retinal changes in the neuroretina but not in the RPE.7 We agree that patients taking psychotropic medications benefit from a multidisciplinary approach when ocular symptoms and signs develop.

Heather G Mack · RC Andrew Symons

In reply

Jessica Y Tong · Amy Pai · Stephanie H Young

To the Editor:Whitely and colleagues1 reported that children born in June were more likely to receive treatment for attention deficit/hyperactivity disorder (ADHD) than children born in July. It is unfortunate that they did not measure the year of school intake, and rather made the assumption that all children entered school at the recommended age. The authors concluded that “there are significant concerns about the validity of ADHD as a diagnosis,” which is a large leap not substantiated by the data presented. We are conducting Australia’s first community-based longitudinal study of children with (n = 179) and without ADHD (n = 212), the Children’s Attention Project.2,3 Our design is ideal for examining this research question as children were all recruited across one year of school, enabling us to accurately categorise children as early or late starters. We rigorously assessed for ADHD (ie, via parent and teacher surveys and diagnostic interviews) and also recorded the use of ADHD medications. To investigate the same question within our cohort, we defined early starters as those children with birth months in February, March or April (age at entry, 4 years 9 months to 4 years 11 months; n = 46) and late starters as those children born in May, June or July (age at entry, 5 years 6 months to 5 years 8 months; n = 123). We found no relationship between being an early or late starter and meeting the criteria for ADHD at either age 7 years or age 10 years. Our sample size for these analyses was small because most children with ADHD were born outside the months encapsulating early and late start date definitions (n = 112; 63% of our ADHD sample). Only nine children were prescribed medication across the early and late starter definitions — one early starter and eight late starters. In conclusion, our data show that when school commencement year is considered, there is little evidence to support early versus late school starter status as a predictor of ADHD and treatment in Victoria. The overall rate of ADHD medication prescribing for children aged 6–15 years reported by Whitely and colleagues was 1.9%.1 ADHD has a prevalence of about 5%,4 thus, these data provide further reassurance that the rates of prescribing of ADHD medications in Australia remain moderate.

Emma Sciberras · Alisha Gulenc · Daryl Efron

In reply

Martin Whitely · John Phillimore · Leanne Lester · Suzanne Robinson

To the Editor: A 53-year-old woman experienced rapid onset of left eyelid pain, swelling and purulent discharge (Box 1). She presented to our eye hospital 3 days later and, on assessment, the lids were exquisitely tender, inflamed and difficult to open. There was chemosis, microcystic corneal oedema with Descemet membrane folds and moderate inflammation in the anterior chamber. Visual acuity was 6/24 in the left eye and 6/9 in the right eye. Ocular motility appeared normal. The severe inflammation and visual impairment raised concerns for post-septal orbital cellulitis. A computed tomography scan showed severe pre-septal stranding only (Box 2). A diagnosis of left pre-septal cellulitis and keratoconjunctivitis was made. She was given intravenous ceftriaxone 2 g daily, intravenous flucloxacillin 2 g four times a day, topical chloramphenicol 0.5% four times a day and regular eye washings. Microscopy found gram-negative diplococci, and polymerase chain reaction testing was positive for Neisseria gonorrhoeae. The patient denied history of sexually transmissible infection. A urine and serum sexually transmissible infection screen for N. gonorrhoeae, Chlamydia trachomatis and blood-borne viruses was negative. Treatment was rationalised to intravenous ceftriaxone 1 g daily, with a single 1 g dose of oral azithromycin. The patient had dramatic improvement over 4 days, and visual acuity improved to 6/7.5 at discharge (Box 3). One week later, the infection had predominately resolved. N. gonorrhoeae typically produces a hyperacute unilateral conjunctivitis. While the source of infection in this patient is unclear, in most cases infection is acquired via sexual transmission and reaches the conjunctiva through hand–eye auto-inoculation.1,2 The bacteria can invade the corneal epithelium, producing keratitis and corneal melting necessitating therapeutic keratoplasty.1,2 Gonococcal periorbital infection is rare, with only three cases of pre-septal cellulitis and two cases of post-septal cellulitis reported.3 All patients were successfully treated with parenteral antibiotics. N. gonorrhoeae has increasing antimicrobial resistance, creating a therapeutic challenge. The Australian Gonococcal Surveillance Programme has shown an emerging resistance to ceftriaxone — the antibiotic of choice — from 0.6% in 2006 to 5.4% in 2014.4 Azithromycin resistance occurs in 2.4% of strains.4 The Australian Therapeutic Guidelines recommend treatment of N. gonorrhoeae with parenteral ceftriaxone and oral azithromycin, for bactericidal synergy and cotreatment for C. trachomatis. When presented with pre-septal cellulitis and purulent keratoconjunctivitis, the clinician should be vigilant for a sight-threatening N. gonorrhoeae infection. Box 1 – Lid inflammation and purulent discharge at onset, 3 days before presentation Box 2 – Contrast-enhanced computed tomography scan showing significant pre-septal subcutaneous stranding (blue arrow) and severe conjunctival chemosis (yellow arrow) Box 3 – Marked improvement in periorbital inflammation after 3 days of antibiotic therapy, with residual conjunctival injection

Shivesh Varma · Nathan Wong · Jwu Jin Khong

To the Editor:We fully support Colagiuri’s appeal to implement comprehensive, regulatory action to reduce sugar-sweetened beverage consumption.1 Excessive sugar-sweetened soft drink consumption is associated with weight gain, diabetes and dental caries.2 Strikingly, sugary drinks are the single largest contributor of added sugars in the diet of Australians aged 14–50 years.3 In recognition that environmental changes can support healthier consumer choices, the New South Wales government has pledged to remove sugary drinks for sale from all its health facilities by December 2017.4 This follows the lead of 13 health services in Victoria that have also adopted this health-promoting policy. Media coverage of these measures has been positive,4 as communities look to health centres to be leaders in supporting and protecting public health. In contrast, Australian university campuses, including those with medical schools responsible for developing future health leaders, remain saturated in soft drink promotions and sales. Detractors of policy-based approaches suggest that education efforts and offering healthy choices are preferable to “nanny state” restrictions. Health education campaigns that advise people to restrict their consumption of sugary drinks must battle against the ubiquitous advertising and availability of these products. In the United States, it is well documented that the university food environment is shaped by purveyors of unhealthy food and drink.5 “Free choice” arguments ignore the realities of sales contracts that include exclusively selling certain brands and products. Similarly, in Australia, exclusive sales contracts offered to suppliers may restrict the choices of staff and students on campus. The real issue appears to be the unfounded fear that banning the sale of soft drinks on campuses may have negative revenue implications. This fails to acknowledge that replacement beverages that are not sugar-sweetened could still be sold. Australian university campuses have readily banned smoking and the sale of tobacco without experiencing financial hardship as a consequence. Universities, especially those training future health professionals, need to flex their collective muscle and be part of the momentum towards creating healthy environments. Initiating healthy beverage policies is a significant step forward.

Becky Freeman · Kieron Rooney · Eloise Howse

To the Editor:Recent reports from the World Health Organization1 and from Australian agencies2,3 emphasise the urgency of improving health service response to family violence. Understanding the victim and survivor experience and perpetrator patterns is essential to improving health practitioners’ capacities for recognising and responding appropriately to family violence.1,3 Although there is an increasing awareness of the severity of health consequences of family violence,1,4 there is little standardisation of terminology within the national and international literature. The Royal Australian College of General Practitioners recognises physical, emotional, economic, social, sexual, psychological, verbal and spiritual abuse as forms of family violence.4 Family violence includes any violence or abuse that occurs within a family,4 including between partners, parents, children, siblings, uncles or aunts, cousins, grandparents and in-laws. Complexities arise because of the pervasive nature of violence when trying to differentiate the types of violence and individual victims. For example, studies show that 50% of children who experienced physical abuse and 40% of children who experienced sexual abuse have a mother who experienced intimate partner violence.5 “Domestic violence” emphasises the place of the violence, whereas “family violence” emphasises the relationships between the victim and the perpetrator. “Intimate partner violence” refers to the “behaviour within an intimate relationship” of current or former partners (including same-sex relationships) causing “physical, emotional, sexual, economic and social harm to those in the relationship”.4 Family violence (Box) encompasses domestic violence, intimate partner violence and sibling violence. Cases of child neglect, child abuse, child sexual abuse, sexual assault and rape may occur in the context of family violence; however, these forms of violence may also occur outside the context of the family, such as institutional abuse or stranger violence. Likewise, older people abuse, which can include sexual abuse and rape, may occur in the context of family violence and also in institutional contexts, in the context of service provision or between people who have no familial or institutional relationships. An increased understanding of the terminology used in the research literature enhances the capacity for delivering high quality care to women, children and men experiencing the health impacts of family violence. Box – Terminology for family violence Figure by Debbi Long and Serena Lee.

Debbi Long · Serena Lee · Jan Y Coles

To the Editor: We note with interest the recent review of challenges in the management of maturity onset diabetes of the young associated with glucokinase gene mutations (GCK-MODY).1 In Box 2, Bishay and Greenfield reported a prevalence of gestational diabetes mellitus (GDM) of 5–10%. Indeed, in 2010 we reported an estimated prevalence of 10–11% of GDM in south-western Sydney;2 however, the prevalence is now almost double that figure (18.5% of births at Bankstown-Lidcombe hospital in 2015). Bishay and Greenfield also summarised the findings of Chakera and colleagues3 for a population of predominantly European descent: A lower body mass index (BMI, < 25 kg/m2) and a fasting glucose level greater than or equal to 5.5 mmol/L have sensitivity and specificity of 68% and 96%, respectively. It is estimated that among lean women with mild fasting hyperglycaemia, the number of women needed to test is 2.7 to detect a single case of GCK-MODY.1 In contrast, in our recent study of women with GDM, we found that at least 8.1 women would need to be tested to identify one case of GCK-MODY.4 Given our interest in the management of women with GDM, we sought to determine whether these criteria were applicable in a large multi-ethnic cohort of women with GDM. Analysing de-identified, prospectively collected data from all women with GDM in our ethnically diverse population, diagnosed using the Australasian Diabetes in Pregnancy Society (1998) criteria at our institution between 1993 and 2013, we categorised the women into two groups: those with body mass index ≤ 21 kg/m2 (group A1) and those with body mass index > 21 kg/m2 and < 25 kg/m2 (group A2). We collected complete data, including post-partum oral glucose tolerance test results, for 171 women (54, group A1; 117, group A2). The oral glucose tolerance test and post-partum glycated haemoglobin results identified few women (< 14%) in either group who still had possible GCK-MODY. Testing all 171 of these women in pregnancy would have been a costly exercise with a low yield. In testing data in different ethnic groups, we therefore recommend caution regarding the number suggested by Chakera and colleagues.

Jeff R Flack · Glynis P Ross · N Wah Cheung

In reply

Ramy H Bishay · Jerry R Greenfield

Modern digital radiological techniques include “stitching” together multiple x-ray images. This provides one overall image of the area of interest, such as the entire spine or lower limbs, for deformity assessment. Dedicated software automatically combines separate exposures and allows for overlap. Image acquisition is rapid, minimising patient motion artefact and reducing distortion.1 However, if images are inappropriately put together (digitally stitched), stitching errors may occur with this computer-driven process. If not manually corrected by the radiology technician, the supplied image may hide pathology or give the false impression of abnormality. Four cases of digital stitching error have recently occurred in our tertiary referral paediatric hospital. Digitally stitched x-rays from the lower limbs were obtained for routine assessment of a child with skeletal dysplasia, and fractures of the left tibia and fibula were apparent (Box, A). This did not correlate with the clinical findings, including the child dancing in the waiting room. The radiology department was contacted and they re-issued corrected images (Box, B). Spinal x-rays in two patients after scoliosis surgery incorrectly showed broken surgical rods. In the context of ongoing symptoms, the option of revision surgery was discussed with the family in the first case. Repeat x-rays, obtained as part of the pre-operative planning, showed the rod was in fact not broken. A stitching error was immediately recognised by the spinal surgeon when a second similar case occurred. In a fourth case, comparison of the anteroposterior and lateral views of a child’s spine showed different numbers of vertebrae in the two views (11 vertebrae on the frontal view and 12 on the lateral). Digital radiology is commonplace and allows rapid image acquisition and ease of digital measurement.2 However, technical errors — digital stitching errors — may occur. Although rarely reported, these may be relatively common, with one study identifying stitching errors in 14 out of 86 reviewed scoliosis studies.1 Despite ongoing technological refinements,3 clinicians should always carefully check digitally stitched images: look for soft tissue mismatch, correlate with source images and clinical presentation, and avoid digital stitching in certain patients, such as people with movement disorders. Box – Digitally stitched long leg images of a paediatric patient, showing the stitching error and apparent fracture (A),* and corrected image with resolution of the stitching error and no fracture (B) * Note the mismatched soft tissue shadow (A).

Clare Faurie · Nicole Williams · Peter J Cundy

To the Editor: Intensive care is a finite and costly resource with nine beds per 100 000 population in Australia and at a cost of $4000 per bed-day. From 1999, the demand for intensive care unit (ICU) beds has increased at an average rate of 2.5% annually.1,2 Faced with increased demand and capacity restraints, fiscal sustainability is dependent on efficient use of limited ICU resources. ICU bed availability varies significantly across countries and creates a threshold for clinicians to admit patients.3 The availability of beds may be influenced by the number of patients well enough for ward discharge but who are exit blocked. ICU access block is a significant safety concern for critically ill patients, and ICU exit block (the inability to discharge a patient who is medically fit for discharge) may contribute significantly to ICU access block.4,5 Using a single-day point prevalence study, we obtained an estimate for ICU exit block in 39 Australian and ten New Zealand adult ICUs in 2014. Across all sites, 13% (median value of exit block across the sample hospitals, 8.1%; interquartile range, 0–23%) of patients in the ICU on the study day were awaiting a ward bed. Patients in Australian ICUs were twice as likely to be exit blocked compared with patients in New Zealand ICUs (14.9% v 7.6%). Hospital and ICU size and location (rural v metropolitan) did not influence levels of exit block, but ICUs with > 80% occupancy had higher levels of exit block (Box). Our results were similar to those of the 2007–14 Australian Council on Healthcare Standards clinical indicator report, which found that about 25% of ICU discharges were delayed for more than 6 hours.5 Using an ICU bed for a patient who no longer needs it represents an inefficient use of resources and risks creating delays in admitting other acutely unwell patients. In the emergency department setting, we have seen the 4-hour rule improve hospital access and outcomes by prioritising transfer of emergency department patients to ward beds. Monitoring ICU access and exit block provides a comparable metric for understanding the effects of prohibiting ICU patient flow and for determining how to safely and efficiently allocate limited resources for critically ill patients. Box – Intensive care unit (ICU) bed occupancy and exit block Bed occupancy No. of ICUs* Median percentage of patients experiencing exit block (IQR) 0–50% 6 0 (0–28.6%) 51–80% 20 0 (0–10.8%) 81–100% 21 13.0% (5.5–25%) IQR = interquartile range. * Two sites did not provide bed occupancy rates so were not included in our analysis.

Matthew H Anstey · Kelly Thompson · Ian Seppelt

To the Editor:I thank Kritharides and colleagues1 for their review Cardiovascular disease in patients with schizophrenia. I agree with them and support their work, which seeks to improve the physical health of patients living in the community with a chronic mental illness such as schizophrenia, through an innovative, coordinated and multidisciplinary model of care. Clozapine side effects, including risks of myocarditis and cardiomyopathy, hypercholesterolaemia and weight gain, reduce years of life and require medical attention. But the management is not always straightforward. One challenge is patient compliance with often demanding allied health therapies. How do we keep our patients motivated to continue with prescribed regular exercise most days of the week? How do we encourage compliance with a weight-reducing, low salt, low glycaemic index diet? Multidisciplinary primary care and specialist teams may consider a rehabilitation approach to complement the model of care. Two essential elements are goal setting and measurement of function.2 Some patients will be motivated by their personal goals (eg, getting back to weighing 80 kg or playing a game of table tennis) and other patients will appreciate their gain in terms of function (eg, walking up the stairs without a rest or shopping for groceries independently) more so than in terms of presented data (eg, cholesterol levels or absolute cardiovascular risk reduction). For motivating patients with schizophrenia and significant cardiovascular risk, a rehabilitation approach may be worth a try.

David Skalicky

In reply

Leonard Kritharides · Vincent Chow · Tim JR Lambert

To the Editor: We read with interest the recent study by Freed and Allen on the cost to patients of consulting a private specialist physician.1 Although not the main focus of the study, we were intrigued by the disproportionately low bulk-billing rates by physicians in Western Australia. This was highlighted in the local media,2 with an implication that WA physicians are out of step with interstate colleagues on billing practices. We acknowledge there was no such assertion in the article by Freed and Allen.1 The study findings are based on Medicare data supplied by the Commonwealth Department of Human Services.1 However, the data do not appear to differentiate between Medicare billing in private physicians’ rooms (which is the intended target of the study) or elsewhere. Hence, the bulk-billing findings may be confounded by occasions of Medicare billing occurring in outpatient clinics run by public hospitals. Public hospital services are usually funded by state governments. Nevertheless, Commonwealth (ie, Medicare) funded clinics are permitted under an interpretation of the Health Insurance Act 1973 that allows private services to be rendered by specialists within a public hospital.3 Anyone with a Medicare card is eligible to be considered a “private patient”. If bulk-billed, the patient will not suffer any financial disadvantage — or notice any difference — compared with attending an ordinary state government funded clinic. In most cases, revenue from Medicare is not retained by the specialist, but donated to the hospital to defray clinic costs.4 This model permits the creation of new fee-free hospital outpatient services that would otherwise be unsustainable within the existing state funding. In view of the large number of outpatient visits to public hospitals, there could be an inflation of statewide physician bulk-billing rates where Medicare funded hospital clinics are widespread. In our experience, such clinics are rare or non-existent in WA. It would be interesting to reappraise bulk-billing rates if billing episodes occurring at public hospitals could be excluded. We suspect that bulk-billing rates occurring entirely within private specialist rooms are not significantly different between jurisdictions.

Gregory SY Ong · Senq J Lee · Dejan Radeski

To the Editor: The demand for human leukocyte antigen (HLA) typing in the diagnostic work-up of coeliac disease (CD) in Australia has driven a 14-fold rise in testing since 2003 (Medicare Benefits Schedule data, item 71151). Although HLA typing offers limited specificity for CD, its clinical utility results from its exceptional negative predictive value (> 99%) when the specific HLA susceptibility genotypes are not detected.1 Unlike traditional tests for CD, HLA typing results are informative even when the patient is following a gluten free diet. While the accuracy of HLA typing in CD has not been reported, HLA test results are assumed by clinicians to be definitive. Our findings challenge this view. Discrepancies between several patients’ clinical diagnosis of CD and their negative HLA-DQ2 and -DQ8 typing results in AJD’s practice led to repeat HLA testing with another laboratory. The subsequent reporting of a genotype consistent with CD prompted a clinical audit (2013–2016). Of 211 patients with HLA typing results, nine had been coperformed by two separate laboratories (laboratories 1 and 2), either deliberately or inadvertently. Of these nine patients, six returned conflicting results. An additional DNA sample from all six patients was sent for HLA genotyping by a reference laboratory, where genetic susceptibility for CD was confirmed in five patients (Box). Laboratories 1 and 2 differed in the detection of risk alleles and in the interpretation of or reporting of the results in all six cases. Laboratory 2 identified an at-risk allele in only two of the six patients, and of the four patients with a reported negative genotype, two were subsequently confirmed to have definite CD. These preliminary findings raise serious concerns about CD HLA testing errors that adversely affect patient care. Although identified in Queensland, these laboratories routinely outsource their HLA typing to laboratories in New South Wales and Victoria, indicating that several Australian states are involved. We are particularly concerned about laboratories new to HLA testing or laboratories that are not participating in stringent quality assessment programs as the sourced reference laboratory does. Therefore, we suggest that an assessment of the performance and quality control measures of all laboratories offering HLA typing is urgently needed. Consistent adoption of evidence-based guidelines that describe optimal HLA testing and reporting1 should form part of the solution. Box – Human leukocyte antigen (HLA) typing results from three laboratories† Patient Laboratory 1 Laboratory 2 Reference laboratory Confirmed CD “Consistent with DQ2 phenotype; susceptible for CD” Genotype not supplied; “Not susceptible for CD” HLA-DQ2.2/2.5; susceptible to CD Incorrect Confirmed CD “Consistent with DQ2 phenotype; susceptible for CD” Genotype not supplied; “Not susceptible for CD” HLA-DQ2.2; susceptible to CD Incorrect CD excluded “Consistent with DQ2 phenotype; susceptible for CD” Genotype not supplied; “Not susceptible for CD” HLA-DQ2.2; susceptible to CD Incorrect CD not excluded; on GFD “Consistent with DQ8 phenotype; susceptible for CD” Genotype not supplied; “Not susceptible for CD” No susceptibility to CD detected Incorrect Normal CD serology “DQ2 and DQ8 not identified; no genotype susceptibility for CD” “DQA1*0505 has been detected; small percentage susceptible to CD” DQA1*05 (HLA-DQ7); low risk susceptibility to CD Incorrect CD excluded “DQ2 and DQ8 not identified; no genotype susceptibility for CD” “DQA1*0505 has been detected; small percentage susceptible to CD” DQA1*05 (HLA-DQ7); low risk susceptibility to CD Incorrect CD = coeliac disease. GFD = gluten free diet. ND = not detected. † The reference laboratory was in the Victorian Transplantation and Immunogenetics Service in Melbourne. In addition to the incorrect typing results, laboratory 2 failed to report the specific alleles detected and laboratory 1 failed to distinguish between HLA-DQ2.5 and DQ2.2.

A James M Daveson · Michael Varney · Kate E Jackson · Jason A Tye-Din

To the Editor:I thank Byard and colleagues1 for their review of risks of herbal products to the Australian community, which highlighted the high rates of use in younger women with a tertiary education and in patients with chronic diseases or comorbidities. Refugee and migrant women represent a group with potentially high rates of use of herbal products as well as other traditional practices, particularly during pregnancy. Ethnobotany surveys found that 90% of women in eastern Ivory Coast and 80% of women in Mali used medicinal plants during pregnancy.2 A prospective cohort study found that 45% of women in China consumed Chinese herbal medicine during pregnancy and the postpartum period.3 The ingestion of soil, clay or chalk has been observed in up to 84% of pregnant women in African countries, and may be complicated by hypokalaemic paralysis, iron and zinc deficiency, lead poisoning, intestinal obstruction and parasitic infestation.4,5 It is commonly reported that migrant women transfer cultural practices to their new country. In the United Kingdom, geophagia is associated with immigrants from South Asia and West Africa.6 Likewise, Congolese and Zimbabwean women commonly consume clay during pregnancy after migrating to Cape Town.7 In addition, the use of skin lightening creams has been reported in 69% of pregnant women on their third-trimester attending a standard maternal centre in Dakar, which may result in maternal Cushing’s syndrome and adrenal insufficiency and in fetal intrauterine growth restriction. Most case reports in the literature describing Cushing’s syndrome due to skin lightening creams have been on African women who had migrated to Australia, the United States or Europe.8 Skin lightening creams may also contain mercury, with the risk of birth defects and irreversible neurological damage to the child. These products are usually obtained over the counter in African shops, and thus are not subject to any form of safety regulation. A further difficulty is that migrant women may not disclose their use of herbal medicines or other traditional products, even when questioned specifically. Therefore, health professionals in Australia should be aware of the risk of use of herbal and other natural products and practices by migrant women, particularly during pregnancy. Engagement with matriarchal figures, nurses and doulas within migrant communities may be valuable in identifying the extent of these practices.

Adam Morton

To the Editor:The recent review by Byard and colleagues1 highlighted the need for tighter regulation and monitoring of traditional herbal products sold in Australia to minimise the risk of exposure to preparations containing toxic substances, including heavy metals. Use of imported Ayurvedic medicines containing high levels of lead is a concerning exposure source among Victorians and elsewhere in Australia.2 Between 2010 and 2015, 1530 incident cases with blood lead levels above 10 μg/dL were notified to the Department of Health and Human Services under the Public Health and Wellbeing Act 2008 (Vic). Eight patients, aged 26–41 years, reported Ayurvedic medicine use, including one case of occult lead poisoning described previously.3 The median blood lead levels were higher in patients using Ayurvedic medicines (median, 79.5 μg/dL [range, 26.1–102.9]) compared with other non-occupational lead exposures (n = 184; median, 16.4 μg/dL [range, 10.0–63.6]). For patients reporting Ayurvedic medicine use, testing was often prompted by clinical symptoms, including abdominal pain and vomiting. All patients obtained different products directly from India (n = 7) or Pakistan (n = 1). Analysis at an independent laboratory revealed that these products had 2000–15 000 times the maximum amount of lead allowed in complementary medicines by the Therapeutic Goods Administration under the Poisons Standard (ie, 10 mg/kg or 0.001%).4 The ease by which these Ayurvedic products were obtained via the internet or by travellers to non-regulated countries means that they remain a difficult product to monitor. It is also concerning that all female patients (n = 3) reported using these products as fertility therapies or for the treatment of morning sickness, as high blood lead levels may be passed onto babies during pregnancy and while breastfeeding.5 We support the assertion that clinical vigilance is necessary in monitoring lead and other heavy metal levels in patients reporting traditional medicine use.2,3 Difficulties may arise if the health-seeking behaviours of people using Ayurvedic therapies result in fewer contacts with health services, reducing opportunities to test individuals at greatest risk. Public health messages about the potential risks of traditional and Ayurvedic medicines were distributed using targeted media for at-risk communities, Chief Health Officer alerts and the Victorian Government’s Better Health Channel.

Tanyth de Gooyer · Rohani Savage · Nicola Stephens

In reply

Roger W Byard · Garth Maker · Michael Bunce

To the Editor: In Adelaide, which comprises 78% of the population of South Australia, municipal wastewater has been subject to bimonthly analysis since 2009 to measure trends in substance use. Beginning in October 2015, there was a precipitous decrease in the detection of oxycodone residues in wastewater samples (Box). This decrease was counter to the long term trend of increasing amounts of this opioid in previous samples. Prescribing data show a continuing increase in the use of prescription opioid analgesics (POAs), including oxycodone, nationally and in SA, during the period between 1992 and 2011.1 There is a strong relationship between the amount of POAs used in a community and the amount of harm from opioid dependence and overdose.1 The cause of this regional trend change in oxycodone use has not been established. On 1 July 2015, there were some significant changes in the regulation of work injuries in SA which led to a decrease in the number of complex long term claimants, and there was also a similar change in South Australian motor vehicle injury regulation in July 2013. Complex injury claims are strongly correlated with POA use;2 however, the role of these factors is highly speculative and there may be many other factors that contributed to the results. The methods used for the bimonthly wastewater analysis in Adelaide have been published before,3 and another group used this process to report changes in population methamphetamine use in Queensland.4 From October 2015, there was a change in the established temporal trend for oxycodone residues detected in Adelaide wastewater (Box). However, over the same period, there is no such trend change for national Pharmaceutical Benefits Scheme (PBS) and Repatriation PBS data for the number of oxycodone prescriptions dispensed (not total doses),5 or for Adelaide wastewater residues of methadone, which is predominantly dispensed for treatment of severe opioid use disorders via a specific program. A limitation of our investigations was that no regional oxycodone prescription or wastewater data from other jurisdictions were available for comparison. Nonetheless, our findings suggest that wastewater analysis could potentially be used to rapidly monitor changes in substance use on a regional basis. Box – Oxycodone and methadone residue in Adelaide wastewater compared with national data for the total number of oxycodone prescriptions supplied, December 2011 – February 20175 PBS = Pharmaceutical Benefits Scheme. RPBS = Repatriation Pharmaceutical Benefits Scheme.

Philip Crowley · Jason M White · Benjamin J Tscharke · Cobus Gerber

To the Editor:We read with interest the excellent review by Scott and colleagues1 on the contribution of sarcopenia to type 2 diabetes in the ageing Australian population. In a prospective Australian cohort of community-dwelling men, we recently found that muscle grip strength and muscle quality, but not muscle mass, were associated with incident type 2 diabetes at 5 years follow-up.2 These associations were not mediated by serum interleukin 6 or tumour necrosis alpha. As we did not examine sarcopenia, nor appendicular lean mass adjusted for body mass index (ALM-BMI), we have undertaken further analysis in 1180 participants with valid sarcopenia data. Their mean age was 56.9 years (standard deviation [SD] ± 10.9), mean ALM-BMI at baseline was 0.950 (SD ± 0.135) and mean peak hand grip strength at baseline was 48.7 kg (SD ± 9.9 kg). At 5 years follow-up, incident type 2 diabetes occurred in 119 participants (10.1%). Baseline ALM-BMI of less than 0.789 occurred in 9.2% of patients (n = 109) and baseline grip strength of less than 26 kg occurred in 1.4% of patients (n = 16), thus only six participants (0.5%) had sarcopenia as defined by the Foundation for the National Institutes of Health Biomarkers Consortium Sarcopenia Project (both ALM-BMI < 0.789 and peak hand grip strength < 26 kg).3 Hence, in our middle-aged Australian cohort of men, the prevalence of sarcopenia was very low. Moreover, while there was an unadjusted association between baseline ALM-BMI of less than 0.789 and incident type 2 diabetes (odds ratio [OR] 2.54; 95% CI, 1.49–4.17; P < 0.001), this attenuated to non-significance after adjustment for age, subcohort, income, fasting plasma glucose, physical activity, family history of diabetes, triglycerides and hypertension (OR 1.73; 95% CI, 0.95–3.05; P = 0.06). However, when analysing ALM-BMI as a continuous variable, the adjusted association was significant (OR per 0.1 unit decrease: 1.33; 95% CI, 1.13–1.58; P < 0.001). Overt sarcopenia may not have a large contribution to type 2 diabetes in community-dwelling Australians. Rather, reduction of skeletal muscle strength, ALM-BMI and muscle quality across the spectrum of healthy values may have greater population level significance. Our previous population-attributable fraction calculations suggest that a substantial proportion of incident type 2 diabetes may be prevented if muscle strength in the Australian community was generally increased.2

Joule J Li · Jonathan W Newbury · Robert J Adams

In reply

David Scott · Barbora de Courten · Peter R Ebeling

Editor’s note: The Lancet recently published an important Australian randomised controlled trial of robotic and open prostatectomy. We publish the following non-commissioned correspondence by Hutchison and colleagues together with an invited response from the corresponding author of the trial, Robert Gardiner, because of the relevance of the debate to Australian health care. To the Editor: Robotic prostatectomy took off quickly, despite the cost. In Australia, most prostatectomies are now done with a robot that costs almost $10 000 in capital and maintenance per procedure, or between $442 and $3548 more than an open prostatectomy.1 The robotic option was meant to reduce side effects relating to impotence and incontinence; however, preliminary findings from the world’s first randomised controlled trial suggest that this is not the case.2 Uptake of innovative surgery tends to outpace evidence because it is hard to design and run randomised studies. In addition, placebo surgery is rare and controversial, and recruitment is challenging, as surgeons and patients often prefer one option. Trial results may also be difficult to interpret: if the same surgeon performs both operations, they may be better at one; or if different surgeons operate, one may be superior.3 Australia is not immune to these challenges, despite local initiatives to improve quality of care4 and evaluate the benefits of the robotic procedure.5 The industry understands this. Intuitive Surgical aggressively marketed its robot while the jury was still out on its comparative benefits. Celebrity stories have also driven demand; for instance, radio personality Alan Jones has been an outspoken advocate.6 But even when evidence commends a surgical innovation, introducing it to the public health care system may create or exacerbate inequity. Suppose that the robot, or some successor, eventually proves superior to alternatives. Expensive equipment and difficult procedures require high patient throughput to justify the costs and maintain surgeons’ skills, so they tend to be concentrated in the biggest, busiest hospitals. Therefore, patients in regional areas are often expected to travel for treatment, with little or no financial support; and the barrier is even higher for people who do not have the social and economic resources to get themselves to a big city hospital.7 We should resist the hype of a new technology and wait for good evidence before expending scarce health care dollars. This will sometimes mean lagging behind other countries and saying no to patients. However, it will also mean safeguarding patients and the public purse from innovations that turn out to be no better, or maybe worse, than existing options. Moreover, when a new technology is introduced, we should also fund the supports that people need to access it.

Katrina Hutchison · Drew Carter · Jane Johnson

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Mark Frydenberg · Robert (Frank) A Gardiner

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Rosalie Schultz

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Pamela Palasanthiran · Asha C Bowen