Letters

To the Editor:Legislation mandates that all adult medical records be retained for a minimum of 7 years from the time of last patient contact, after which they can be destroyed. Exceptions to this requirement exist for young patients, and there are state-by-state variations, but there is no legislative requirement to retain records of patients who have implantable, high-risk devices. This is disturbing because many of these devices have an in vivo lifespan that exceeds 7 years. Of particular concern are patients with breast implants whose records may have been destroyed before a diagnosis of breast implant-associated anaplastic large cell lymphoma, which has an average latency period from implant to diagnosis of 9 years.1 Later presentations of this lymphoma are not uncommon, with latency intervals up to 23 years;2 therefore, it is imperative that implant details are retained to enable us to better understand the pathophysiology of this potentially fatal disease, which has been strongly associated with deeply textured surface implants. While the Australian Breast Device Registry (ABDR) is a safe repository for secure information on patients who are registered, those patients who are not may be at risk of losing important information about their implants. Furthermore, the expected lifespan of in vivo breast implants is at least a decade,3 so records may have been discarded at the time of patients presenting with serious implant-related problems. In our efforts to improve the safety of patients with breast implants, 30% of whom are breast reconstruction cases for cancer or congenital deformities, we encourage all practitioners to ensure that their patients are registered with the ABDR so their implant details are securely stored.4 In an effort to preserve the details of all Australian patients with breast implants, the ABDR can also store patient implant details retrospectively and will accept information from Australian patients having cosmetic tourism surgery overseas, after which significant complications can arise.5 It may be time, however, for legislation to be enacted to lengthen the mandatory retention period for patients with high-risk devices or to make it legally compulsory for practitioners inserting high-risk devices to enrol all patients into a clinical quality registry such as the ABDR.

Rodney D Cooter · Ingrid Hopper · John J McNeil

To the Editor:The National Bowel Cancer Screening Program will reduce the burden of colorectal cancer, saving lives and money.1 The benefits of the program, however, rely on both public and private sectors to deliver colonoscopy, surgery and, if necessary, advanced cancer care. Public confidence in the whole program is likely to be affected by the affordability, ability and availability of these frontline services. Some public hospitals are unable to reliably deliver timely colonoscopy (ie, within 120 days).2,3 Private practice is an efficient and, for many, affordable option, but there is considerable variation in price. Furthermore, pricing information is often not readily available before referral and can be complicated by multiple separate fees. In contrast, the public hospital system is affordable (free), but there may be issues of availability due to waiting times. The ability of the colonoscopist is relevant to both settings, with adenoma detection rate a well validated quality indicator.4 To test the performance of a discounted, anaesthetist-assisted, private colonoscopy service for high-risk public patients, we conducted the following observational study in a metropolitan practice. Through efficiencies and cost sharing, we provided colonoscopy for a discounted out-of-pocket fee of $310 ($300 for the colonoscopy plus $10 for the bowel preparation kit). We performed 100 colonoscopies and diagnosed seven cancers, with an adenoma detection rate of 66% and a median wait of 29 days. These colonoscopies, if performed publicly, would have cost the state budget over $190 000, at approximately $1900 per colonoscopy (Margaret Clark, South Australia Health, personal communication; July 2018). In contrast, the total cost of this program was about $94 895, comprising the total patient payment of $31 000 plus the total combined bulk-billed fee for clinicopathological services of $63 895. This program did not cost-shift, it cost-saved about $95 105. Private and public services should provide current information to general practitioners, patients and government concerning their affordability (total out-of-pocket fee), ability (http://recert.gesa.org.au/recertified.php) and availability (waiting time from GP referral to colonoscopy). The $310 out-of-pocket fee is unlikely to be the equilibrium price for self-funded colonoscopy in Australia and investment in public colonoscopy remains important. Nevertheless, we suggest that patient autonomy and access would be improved by real time accurate information about their colonoscopy options to allow them to make a rational choice. This would help optimise the benefits of the National Bowel Cancer Screening Program and allow public and private sectors to work together to eradicate bowel cancer death in Australia.

Peter Bampton · Tarik Sammour · Gregor JE Brown · David G Hewett · Daniel L Worthley

To the Editor:Lichen planus is an autoimmune mucocutaneous inflammatory disorder. Diagnosis is often made clinically and confirmed on biopsy.1 Hypertrophic lichen planus is a distinct subtype characterised by pruritic, hyperkeratotic plaques. Histopathological findings may not have the typical features of lichen planus and can mimic squamous cell carcinoma (SCC).2 Distinguishing between hypertrophic lichen planus and SCC can be difficult for clinicians and pathologists. In our dermatology practice, we encountered three patients initially diagnosed with SCC, but on review, the cases were consistent with lichen planus. One patient was a 52-year-old woman presenting with asymmetrical, raised and violaceous lesions to her lower legs. She was referred to a skin cancer clinic that performed biopsies of these lesions, which were reported as well differentiated SCC. These lesions were excised, but they were recurrent and were excised again. The second patient was a 54-year-old man who presented with a one-year history of eruptive raised, violaceous lesions to his chest and legs. Biopsies were reported as SCC and multiple lesions were excised by a general surgeon. The third patient was a 77-year-old woman with a 2-year history of pruritic lesions to the lower legs (Box). Biopsies were reported as well differentiated SCC. Each of these patients underwent numerous excisions before being referred to our practice. The patients were reassessed and new biopsies taken, and the clinical picture was discussed with a dermatopathologist. Hypertrophic lichen planus was confirmed as the diagnosis in each of these patients, and they responded well to prednisone, acitretin and topical steroid treatment. SCC may arise in long-standing hypertrophic lichen planus, but it should be emphasised that cases of supposed SCC with atypical history should not be treated without consideration of the many mimics of SCC, including pseudoepitheliomatous hyperplasia, irritated seborrhoeic keratosis, coral reef granuloma, hypertrophic lupus erythematosus and hypertrophic lichen planus. Clinicians should provide clinical description and a list of potential differentials when referring to a pathologist. Adequate biopsy depth is important, as lichenoid activity may only be present at the tips of the rete ridges, which may be missed on a superficial biopsy. These cases highlight the difficulties in distinguishing hypertrophic lichen planus from SCC. In the cases we described, correct diagnosis was made after re-evaluation and clinicopathological correlation. Box – Figure showing violaceous hyperkeratotic patches on the patient’s lower leg, with original biopsies reported as squamous cell carcinoma (A). Histopathology showed a lichenoid inflammatory infiltrate confined to the tips of the rete processes (B)* * Infiltrate is composed of predominantly lymphocytes with few eosinophils and plasma cells. While these features are typical of hypertrophic lichen planus, superficial shave biopsies may not capture the lichenoid infiltrate at the rete processes.

Emily X Shao · Benjamin Carew · James Muir

To the Editor:Calabria and colleagues1 report that, overall, 9.8% of Aboriginal and Torres Strait Islander adults are at high absolute cardiovascular disease (CVD) risk, reflecting how poorly Australia supports the social and cultural determinants of health for the First Australians. However, this is a different nuance from their statement: “Absolute CVD risk is high among Aboriginal and Torres Strait Islander people”. Aboriginal and Torres Strait Islander people have median age of 23 years,2 and only 1.1% of those in the 18–24 age group are at high risk. The authors note undertreatment with lipid-lowering therapies of Aboriginal and Torres Strait Islander people at high CVD risk; many Aboriginal and Torres Strait Islander people who would benefit are not offered best practice care. However, 13% of people at low CVD risk are on lipid-lowering medication,1 which may be unnecessary treatment, with costs and side effects. As health professionals we need to beware of tendencies to emphasise pathology and risk among Aboriginal people.3 Many health professionals hold ideas of “the passivity, dependency, and non-compliant nature of [the Aboriginal] mob … The perception of Aboriginality as … a health risk, and predictor of unhealthy behaviours … reinforces stereotypical ideas of Aboriginality… and disconnects Aboriginal people from their own identities … [and] stories of strength and survival”.3 There is a tension between our desires to prescribe behaviour to reduce risk and enabling and empowering people to make decisions for themselves. Well intentioned efforts to manage Aboriginal and Torres Strait Islander people may have iatrogenic side effects. For example, health professionals may develop assumptions about people’s behaviour and worthiness to receive treatment,4 while Aboriginal and Torres Strait Islander people themselves may be disconnected from their sense of self-efficacy and community and cultural strengths and identity, contributing to disengagement from health care.3 Like other procedures in health care, absolute CVD risk assessment has costs as well as benefits. Educating community members about absolute CVD risk would promote health literacy and enable people to give informed consent to assessment of this statistic. Numbers hold both face and cultural values, so it is important that Aboriginal and Torres Strait Islander people have control of their statistics.5

Rosalie Schultz

In reply

Raymond W Lovett

To the Editor: Primary meningococcal conjunctivitis (PMC) is a rare presentation of Neisseria meningitidis.1 Before antibiotics, N. meningitidis conjunctivitis was a recognised harbinger of cerebrospinal meningitis due to systemic infection.1-3 Secondary N. meningitidis conjunctivitis is now uncommon.1 PMC seeds exogenously from mucosal secretions, causing a primary infection of the ocular surface without systemic infection,4 and it is characterised by purulent conjunctivitis and periorbital oedema.3,4 Untreated PMC spreads systemically in 10–18% of cases,1,3,5 and early diagnosis is essential to prevent visual loss and life-threatening complications.1,3,5 In September 2017, the Northern Territory experienced an outbreak of N. meningitidis serogroup W strain. Presentations were atypical and, consequently, the threshold was low for empirical treatment. We report the case of a 4-year-old girl who presented to a remote clinic with a 24-hour history of rapidly progressive pain, erythema and discharge from both eyes. Her medical history was unremarkable. She had bilateral conjunctival injection with profuse yellow mucopurulent discharge (Box, A). Systemic examination was unremarkable. Considering the meningococcal outbreak, conjunctival swabs were sent for urgent Gram stain, which showed gram-negative diplococci with characteristic N. meningitidis appearance (Box, B). Ceftriaxone and topical ofloxacin were commenced as empirical meningococcal treatment. Ocular culture and polymerase chain reaction (PCR) were positive for N. meningitidis-W. Three blood cultures and serum PCR were negative. After 48 hours, the purulent discharge and eye pain resolved. On Day 4 of treatment, her conjunctivae normalised and she was asymptomatic (Box, C). Her family members received prophylactic treatment with ciprofloxacin. She was discharged from hospital on Day 6 and had an unremarkable follow-up. To our knowledge, this is the first reported case of N. meningitidis-W PMC. Since presentations of PMC in contemporary society are rare,1,3,4 clinicians may overlook PMC as a differential diagnosis to the patient’s detriment. Given the highly virulent nature of the N. meningitidis-W, the importance of early treatment and contact tracing is paramount, so that antimicrobial prophylaxis can be offered to close patient contacts, especially direct household members. To preserve vision and prevent systemic infection, a high suspicion of atypical microorganisms must be entertained, especially during an outbreak. Box – Primary meningococcal conjunctivitis due to Neisseria meningitidis: bilateral conjunctival injection with profuse yellow mucopurulent discharge (A), gram-negative diplococci with characteristic Neisseria appearance (B), and normalised conjunctivae (C)

James Sterrey · Farshad Abedi · Tim RM Henderson

To the Editor: Behavioural and psychological symptoms of dementia can manifest as aggression directed towards staff or other residents,1 often culminating in recourse to the local emergency department as a “permanent solution”. What does the law say? Under Division 2, User Rights Principles 2014 (section 96-1, Aged Care Act 1997), the only circumstances in which a provider may ask a care recipient to leave a residential care service are if (i) the service is closing; or (ii) the service no longer provides suitable accommodation and care (as assessed by an aged care assessment team or at least two medical or other health practitioners chosen by the recipient who are competent to assess their care needs) and the provider has not agreed to provide the care that the recipient presently needs; or (iii) the recipient no longer needs the care provided, as assessed by an aged care assessment team; or (iv) the recipient has not paid any agreed fees for a reason within their control; or (v) or the recipient has intentionally caused serious damage to the service or serious injury to staff or another care recipient; or (vi) the recipient is away continuously for 7 days or more from the service for reasons not permitted by the Aged Care Act or an emergency. The approved provider must neither imply nor take action to make the care recipient leave, unless suitable alternative accommodation is available that is affordable and meets the care recipient’s needs. Written notice must be given of the decision and reasons for it. A person cannot be asked precipitously to leave a nursing home or, in practical terms, hospital staff or family cannot be told that a bed is no longer available without adhering to the guidelines above. Intention regarding injury and behavioural and psychological symptoms of dementia is complex and cannot be used as grounds for discharge without proper assessment. An alternative is to use the Dementia Behaviour Management Advisory Service and Severe Behaviour Response Teams (24-hour helpline: 1800 699 799), which provide clinical support for carers of people with behavioural and psychological symptoms of dementia. Aged care consumers need to be aware of their rights around security of tenure, and facilities should be resourced sufficiently to fulfil their commitments under the Aged Care Act to care for residents with behavioural and psychological symptoms of dementia.

Carmelle Peisah · Tiffany Jessop · Henry Brodaty

To the Editor:The Reflection article by Bravery1 reminded us of the disability rights movement slogan “Nothing about us without us” and prompted us to reflect on the ways in which expert patients, carers, health and patient advocates, and community members contribute to medical student teaching at the School of Medicine at the University of Notre Dame Australia, Fremantle. Their partnership is crucial to the School being able to meet the standards — (2.1.4) “the medical education provider relates its teaching, service and research activities to the health care needs of the communities it serves,” and (4.6) “learning and teaching methods in the clinical environment promote the concepts of patient centred care and collaborative engagement” — of the Australian Medical Council’s Standards for Assessment and Accreditation of Primary Medical Programs.2 From the School’s inception in 2005, academic staff and community members have worked collaboratively, in the spirit of reciprocity, to teach students. First-year students engage with teenage mothers, expert patients and their families, older people in community-based physical activity classes, and patients in general practice settings, and they live with a family in the Wheatbelt region in Western Australia to learn first-hand about the social determinants of health and the health needs and priorities of Australians in rural settings — a program undertaken in collaboration with the medical students from Curtin University.3 By the end of the pre-clinical years, students have been taught by sex workers, people of diverse sexualities, and children with cancer via panel discussions and in clinical skills sessions, and they have shadowed a patient to witness their lived journey in a community radiology clinic. A one-week Kimberley placement provides insight into health issues in remote areas by living and working in community settings such as Indigenous communities, pastoral stations, art galleries and sporting organisations. These opportunities pave the way for collaboration between the School and other professions and industries — two-way interprofessional learning in real-world settings. As stated by Bravery,1 the impact on students is palpable. They appreciate the opportunity to understand people’s personal perspectives4,5 and apply this understanding to their medical practice — “the [rural or remote placement] guides my work now … It comes back to me; it helps me understand rural people’s lives”.6

Donna B Mak · Jelena Maticevic · Brian D Power

To the Editor:In less than 12 months, voluntary assisted dying (VAD) will become a reality in Victoria. The recent past has seen much passionate debate on both sides of this issue, covering aspects of its impact on society, public health, the law, medicine and an individual’s right to self-determination. Public health interventions have provided our society with significant benefits in many areas; however, for most physicians in clinical practice, our care is focused on each individual patient. To date, little attention has been placed on the implications of VAD for each doctor–patient encounter in which a request is made. For a clinician, the most challenging aspect of VAD now is how to support our patients. How do we balance the fundamentals of our professional and personal beliefs with our clinical and therapeutic responsibilities in practice? The legislation allows doctors the choice to participate in VAD or not; yet, we wonder how we may navigate this therapeutic space. While we believe that directly ending life is a boundary we cannot cross, we also know we cannot abandon our patient at what would clearly be a time of need. Can the doctor–patient relationship survive when electing not to participate? No amount of debate in Parliament will answer this question. We believe we need to derive collective wisdom to craft our compassionate response in this setting — in a considered and thoughtful manner. We believe we must recognise our own distress and anxiety and, nevertheless, remain focused on how we best care for patients. We need to remember our critical role as scientists to learn how to accurately assess, measure and report risks and benefits, to improve care for patients requesting VAD and to inform public health policy. In Victoria, VAD will soon be available. As doctors we must consider our response to our patients and assess the resulting impact on our relationship, here and now. This is a conundrum we had hoped we would never need to face. And it is what keeps us up at night.

Brian H Le · Jennifer Philip

To the Editor: Due to the adverse effects of modified release (MR)-oxycodone/naloxone in patients with moderate to severe liver impairment as a result of advanced cirrhosis or with spontaneous or artificially created portosystemic shunts (Box), its use in this patient population is contraindicated.1 In our clinician roles, we have observed both poor analgesic efficacy and opioid withdrawal in such patients, and similar observations are reported in the literature.2,3 There are clear pharmacological and physiological bases for these outcomes. MR-oxycodone/naloxone is an oral combination opioid analgesic. The naloxone component is subject to a significant first-pass metabolism, and bioavailability is less than 2%.4 The benefit of low level oral bioavailability of naloxone is reduced opioid-induced constipation due to antagonism of opioid receptors in the gut while permitting the desired analgesic opioid effects. The recommended dose of MR-oxycodone/naloxone ranges from 2.5/1.25 mg to 80/40 mg twice daily — the upper limit guiding prescribers to avoid further opioid dose escalation.1 In patients with compensated cirrhosis (mild hepatic impairment) (Box), MR-oxycodone/naloxone may cautiously be prescribed.1 Satisfactory analgesia without significant adverse effects has been observed in selected patients with compensated cirrhosis and pain from hepatocellular cancer.5 In moderate to severe liver impairment, the first-pass (hepatic) metabolism of both medications are markedly but disproportionately reduced, thereby increasing the systemic relative exposure to naloxone (Cmax > 5000% of control) compared with oxycodone (Cmax > 200%).1 The mechanisms are hepatocellular dysfunction and spontaneous portosystemic shunting.3 Artificially created surgical or transjugular intrahepatic portosystemic shunts also reduce hepatic extraction. Hepatic infiltration due to malignancy similarly reduces the liver’s ability to metabolise MR-oxycodone/naloxone effectively.2 The relative increase in exposure to naloxone reduces analgesic efficacy through increased antagonism of opioid pain receptors. Escalating doses of MR-oxycodone/naloxone (or other opioid) may not achieve improved analgesia.2 The relatively high systemic naloxone exposure may also induce opioid withdrawal symptoms.3 Switching from MR-oxycodone/naloxone to oxycodone immediate-release in a patient with hepatic impairment contributed to opioid toxicity due to the sudden loss of the high level systemic naloxone exposure.2 In patients with moderate to severe liver impairment due to advanced cirrhosis or with portosystemic shunts, clinicians should be aware of the contraindication of MR-oxycodone/naloxone. Box – Severity of liver impairment in cirrhosis Liver impairment Clinical features of portal hypertension/portosystemic shunting Biochemical signs Mild Early, compensated cirrhosis No ascites or hepatic encephalopathy Albumin ≥ 35 g/L Bilirubin < 34 μmol/L INR < 1.7 Moderate to severe Advanced, decompensated cirrhosis Portosystemic shunting Presence of: Oesophageal/gastric varices Portal vein thrombosis Ascites Hepatic encephalopathy Hepatorenal syndrome TIPSS Surgical portosystemic shunt Albumin < 35 g/L Bilirubin ≥ 34 μmol/L INR ≥ 1.7 INR = international normalised ratio. TIPSS = transjugular intrahepatic portosystemic shunt.

Venessa Pattullo · Gavin G Pattullo · Simone I Strasser

To the Editor: The recent guideline review by Almeida and colleagues1 coincides with an international call for action to address the burden of low back pain.2 Low back pain is a major societal problem and the number one cause of disability internationally. Recent guidelines prioritise advice, reassurance and self-management as first line care. Implementing these simple, high value interventions is important in populations, such as Aboriginal Australians, where there has been limited previous recognition of low back pain as a problem. A recent systematic review of musculoskeletal pain among Aboriginal Australians3 summarised that the prevalence of low back pain is higher among Aboriginal Australians and has disproportional impacts. Qualitatively, low back pain has multidimensional effects, including functional, cultural and emotional. Access to both primary and specialist level care is lower for some musculoskeletal pain conditions such as osteoarthritis, and there may be parallels for low back pain. Worryingly, there is evidence that the health care that Aboriginal people receive for low back pain is worse than that received by non-Aboriginal Australians, including care with the potential to cause iatrogenic harm. These include higher rates of opioid prescribing and unhelpful low back pain information. Low back pain is associated with a higher number of comorbid health issues, psychological stress and income poverty, and may contribute to the complex milieu of health burden and disadvantage for some Aboriginal communities. The implementation of effective, high value, first line care described by Almeida and colleagues1 is critical for Aboriginal people with low back pain; however, it needs to be adapted so that it is acceptable, accessible and appropriate. For example, advice and education to reassure patients and encourage self-management may need to be supported by culturally appropriate low back pain information. This could include visual, story-based information that has been developed with input from Aboriginal people.4 Implementing successful self-management requires doctors to develop trusting relationships with patients in services that are culturally secure for Aboriginal people. Effective communication is critical.5 The provision of evidence-informed low back pain care to Aboriginal patients requires better recognition of low back pain as a health issue affecting Aboriginal Australians, and a greater understanding of how such care can be best implemented in Aboriginal communities.

Ivan Lin · Donna B Mak · Juli Coffin · Peter O'Sullivan

In reply

Matheus Almeida · Bruno Saragiotto · Chris G Maher

To the Editor: As Clay-Williams and colleagues,1 we have also experienced frustration at the time-consuming, expensive2 and protracted processes required as a prerequisite before undertaking research involving identified patient data across Australia. Ironically, in the case of clinical quality registries, we collect data designed to measure quality of care so that patients may benefit from improved clinical processes. Yet, the system conspires to delay and undermine these efforts. There are lessons we have learned in developing clinical quality registries that deal with some governance issues identified by Clay-Williams and colleagues. They describe developing a legal agreement, which 21% of hospitals refused to accept. The Southern Eastern Border States (SEBS) Committee was developed with representatives of health departments from Victoria, New South Wales, Queensland and South Australia to streamline and prevent duplication of legal agreements.3 We worked with a SEBS Committee representative to develop special clauses and conditions to include in the Medicines Australia Clinical Trials Research Agreement schedule, subsequently endorsed by the SEBS Committee. Participating sites, both public and private, recognise and routinely accept this agreement. This same committee, or one with a similar construct, could determine nationally whether research is low risk to address the confused and contradictory advice given by ethics committees. We agree that standardisation of forms and processes is required — participating sites should not be permitted to introduce their own forms, causing confusion to researchers and introducing additional delays. A national information portal and repository for protocol amendments which governance officers can access to review or approve changes would be welcomed. However, while Clay-Williams and colleagues recommend that there should be no requirement for principal investigators to be employees of the participating site, we believe that for clinical quality registries, having a local principal investigator provides a vital link between researchers and local staff. As previously suggested,4 limits should apply on an acceptable time period to provide a definitive determination on study conduct within an institution, as occurs in Europe with clinical trials.5 It is unacceptable that this process lasts more than 60 days. As researchers usually have no capacity to have an impact on institutional authorisation processes, greater accountability should vest with governance offices. The current costly and dysfunctional system is stifling research in Australia.

Sue M Evans · John R Zalcberg · Ri Scarborough

In reply

Jeffrey Braithwaite · Robyn Clay-Williams · Natalie Taylor

To the Editor: In their recent article, Shulruf and colleagues1 concluded that prior academic achievement constituted the most effective means of predicting timely graduation. This outcome measure overlooks a more important graduate attribute: professionalism — the values and skills that the profession and society expects of doctors. This attribute is identifiable at admission, and it is possible to test for and select for this.2 When considering the desired outcome of satisfactory performance at junior medical officer level, the authors state that the “outcome of subsequent workplace performance, while important, is moderated by influences beyond the undergraduate environment”.1 This statement contradicts extensive literature suggesting otherwise. An erosion of vicarious empathy during medical education programs is well documented and is evident across other health care professions.3 Medical school education fails to consistently foster the development of advanced moral reasoning in medical students, with particular problems developing during the period of clinical immersion, when the influence of the “hidden curriculum” becomes evident to students.3 The above have been linked to the experience of burnout in students, which can manifest as professionalism lapses in both pre-clinical and clinical rotations.4 Papadakis and colleagues5 suggested that disciplinary action by a medical board was strongly associated with prior unprofessional behaviour in medical school. Most complaints against doctors are due to conduct, not competence. Many organisations have developed guidelines to ensure medical students adhere to professional standards. Academic and intellectual qualities alone cannot predict the ideal candidate for admission to medical school, and facets of professionalism such as moral orientation, resilience and self-control are acknowledged to contribute to one’s efficacy as a doctor. Furthermore, prioritising timely completion may promote students not seeking help, perpetuating poor performance in an effort to ensure timely completion. This perpetuates a workplace culture where people do not feel able to seek help, with significant repercussions as seen in the recent suicides of young doctors. Timely completion may indeed be predicted by prior academic success; however, attitudinal and behavioural factors are highly relevant at selection and throughout subsequent careers. An overemphasis on prior academic achievements may de-emphasise student characteristics associated with the development of professionalism.

Mark H Arnold · Jennifer Smith-Merry · Andrew S Lane

To the Editor: We are concerned about the emergence of antibiotic-resistant gonorrhoea in Australia. On 17 April 2018, the Commonwealth’s Chief Medical Officer Brendan Murphy released a statement about two cases of multidrug-resistant gonorrhoea that had recently been detected in Australia1 — at least one of these patients acquired the infection in Southeast Asia. These particular cases were similar to the one recently reported in the United Kingdom,2 where the patient was reported3 as having high level resistance to azithromycin and to ceftriaxone — the cornerstone of treatment. Also notable in that case was treatment failure using spectinomycin, with ongoing detection of the bacterium on throat swab. Treatment with intravenous ertapenem was successful. It should be of concern that gonorrhoea may only have the option of intravenous treatment, but the real problem here is that we may be on the precipice of untreatable gonorrhoea. With almost 750 000 short term resident returns every month,4 and over 200 000 of these being returns from Southeast Asia, the likelihood of repeated introductions is real. In the current context of rising gonorrhoea rates in Australia,5 further importation, transmission and spread of these resistant organisms will add substantial challenges to the disease control, especially in men who have sex with men and in Indigenous Australians. Such spread will incur significant health and health care costs for the sexual and reproductive health of Australians. There is an urgent need for all treating doctors to ensure that swabs for culture are taken for all symptomatic patients, as well as for those with an initial positive polymerase chain reaction result; for travellers to be aware of the risks of having unprotected sex; and for any multidrug-resistant patients and contacts to be referred for expert advice to ensure testing and treatment.

Brett Sutton · Mihaela Ivan

To the Editor:I read with interest the article by Brukner and colleagues1 on traumatic cricket-related fatalities in Australia, which describes two autopsy-confirmed deaths due to subarachnoid haemorrhage following vertebral artery dissection, with a further 11 deaths suspected to be secondary to this condition. Two recent articles described a total of 230 cases of carotid or vertebral artery dissection temporally related to 45 different sports or recreational activities.2,3 The majority of episodes of arterial dissection were related to non-contact sports, including jogging, walking, swimming, golf, basketball, tennis and scuba diving. The mean age of patients was 35 years. The mechanism of non-traumatic dissection is thought to relate to shearing stress on the arterial wall with sudden neck rotation. Thus arterial dissection in golfers affected the right side in 11 of 14 patients (79%), and involved the posterior circulation in 12 of 14 patients (86%).4 Controversy regarding the association between neck manipulation and arterial dissection persists, although a retrospective case–control study found an odds ratio of 12.8 for prior neck manual therapy in individuals aged 55 years or less presenting with craniocervical arterial dissection.5 Arterial dissection may also occur spontaneously, the risk being increased in the setting of systemic lupus erythematosus, other connective tissue disorders, migraine and in the postpartum period. It is important that health professionals recognise that arterial dissection may occur spontaneously or as a result of non-contact sports and activities, and that persons of any age presenting with symptoms suggestive of anterior or posterior circulation ischaemia require urgent review and neuroimaging.

Adam Morton

To the Editor:A recent article by O’Brien and colleagues1 highlights the worsening epidemic of Buruli ulcer in Australia. The steep rise in both the incidence and severity of the disease is associated with estimated health care costs of over $2.5 million per year in Victoria.1 The increase in Buruli ulcer cases in Australia parallels the increase in non-tuberculous mycobacterial (NTM) infections, especially lymphadenitis and Buruli ulcer, reported worldwide. Although this rise might be partly attributable to improved awareness and diagnostic methods, it might also be related to the discontinuation of universal bacillus Calmette–Guérin (BCG) vaccination in settings where the rate of tuberculosis has declined. Routine vaccination with BCG through the school program was discontinued in Victoria in the mid-1980s. The live-attenuated strain of Mycobacterium bovis contained in BCG vaccine shares epitopes with NTM, which makes cross-protection plausible. Our recently published meta-analysis indicates that BCG vaccination has a protective effect against NTM.2 In particular, two randomised controlled trials provide strong evidence for protection against Mycobacterium ulcerans.3,4 However, immunity might only be short lived, as the highest protection was observed in the first year after vaccination. Nevertheless, studies also report that compared with BCG-naive individuals, those who have received the BCG vaccine have smaller skin lesions,4 a shorter duration to healing5 and protection against severe forms of Buruli ulcer with multiple skin lesions.6 Buruli ulcer is a serious condition, which, despite prolonged antibiotic treatment and surgical intervention, can lead to complications such as osteomyelitis and other crippling sequelae. In light of the worsening epidemic, the protective effect of BCG vaccination should not be overlooked.

Petra Zimmermann · Adam Finn · Nigel Curtis

To the Editor:Salmonella infection manifests as enteritis and enteric fever, predominantly acquired overseas. When required, therapy with azithromycin, ciprofloxacin or ceftriaxone is recommended by the Therapeutic guidelines: antibiotic;1 however, reduced susceptibility to fluoroquinolones in Asia limits the use of ciprofloxacin unless susceptibility is confirmed.2 The Australian Bureau of Statistics recorded a 546% increase in short term departures to Indonesia over 10 years, with 1.2 million nationally in 2016.3 A 31-year-old man was taking long term azithromycin 250 mg daily to prevent bronchiolitis obliterans syndrome after a bilateral lung transplant several years earlier for cystic fibrosis. Three weeks after returning from Bali, he was admitted with fatigue, fever, diarrhoea and abdominal pain. He had acute kidney injury. His C-reactive protein level was 190 mg/L (reference interval [RI], < 5 mg/L) and procalcitonin concentration was 3.5 μg/L (RI, < 0.05 μg/L). A single set of blood cultures was negative. Stool culture isolated Salmonella enterica serovar Paratyphi B var Java, sensitive to ceftriaxone and ciprofloxacin, with a raised azithromycin minimum inhibitory concentration (MIC) of 64 mg/L by ETEST (bioMérieux); an MIC > 16 mg/L indicates non-wild-type4 and is associated with treatment failures. Owing to his immunocompromised state, the patient received a 14-day course of ciprofloxacin (MIC, 0.016 mg/L). Our review of 2015–2017 data from the Western Australian public pathology provider revealed that two of 31 typhoidal Salmonella isolates (Salmonella Paratyphi A and Salmonella Typhi bacteraemia, each acquired in India) and one of 15 non-typhoidal Salmonella isolates (S. typhimurium, no clinical details provided) had an azithromycin MIC > 16 mg/L. Ceftriaxone resistance was low at 0% (0/117) of typhoidal Salmonella and 0.4% (7/1648) of non-typhoidal Salmonella; ciprofloxacin resistance was higher at 48.0% (47/98) of typhoidal Salmonella and 6.8% (94/1384) of non-typhoidal Salmonella. By comparison, azithromycin MIC > 16 mg/L was found in 16.1% of typhoidal Salmonella from travellers returning to the Netherlands,5 and in 1.3% of non-typhoidal Salmonella in the United States.4 Azithromycin use while travelling probably selected for resistant Salmonella infection in this case. However, our data show that azithromycin susceptibility cannot be assumed in Salmonella infections; testing should therefore occur in serious cases, along with ongoing surveillance for evolving resistance.

Alan J Rogers · Gar-hing A Lee · Peter Boan

To the Editor:Based on the Royal Australian and New Zealand College of Psychiatrists clinical practice guidelines for mood disorders,1 Malhi and colleagues have produced guideline summaries for major depression2 and bipolar disorder.3 The major depression summary is likely to be used as a stand-alone guideline by primary care physicians treating depression.2 Bipolar disorder often presents as recurrent depression.1,3 It is therefore worrying that the major depression summary omits discussion of bipolar disorder. Identifying bipolar disorder is important because the treatment is different from that required for other types of depression.2,3 The bipolar disorder summary looks to the early detection of mania, as bipolar depression cannot be reliably distinguished from major depression.3 However, there are clues to a bipolar diagnosis during the preceding depressions. Bipolar disorder might be suspected in a pervasive depressive episode which does not make sense psychologically.4,5 A family history may also be suggestive.1 Bipolar disorder should be fully integrated into the management of major depression. After diagnosing major depression, ask routinely: “Could this be an episode of bipolar disorder?”. While the question cannot be answered definitively, it most definitely warrants the asking. Suspecting bipolar disorder can provide the patient and family with some explanation and can involve them in decisions about treatment. Suspecting bipolar disorder earlier could lead to a better outcome. It may allow earlier bipolar treatment and avoid exacerbating the condition with antidepressant or psychotherapy monotherapy. At least, we could warn patients of the risk of inducing mania or cycling with antidepressants.1,3 Omitting bipolar disorder from the guidelines for major depression means that such a warning may not be considered. The major depression summary2 recommends lithium, atypical antipsychotics and electroconvulsive therapy for treatment-resistant depression. Some psychiatrists believe that these are only effective in treating melancholic depression. For the more common treatment-resistant non-melancholic depression, stronger psychotherapies such as dialectical behaviour therapy and acceptance and commitment therapy may be more efficacious than stronger biological therapies. A final thought:Depression’s a broad diagnosis and mostly a kind of neurosis. But try to enable the bipolar label and really improve the prognosis.

Norman Zimmerman

In reply

Gin Malhi

To the Editor:The Editorial by Harvey and Diug1 on the value of food fortification as a public health intervention was prompted by demonstration of the effectiveness of mandatory iodine fortification in reducing iodine deficiency.2 Mandatory fortification of wheat flour for bread making was introduced in Australia at the same time to prevent neural tube defects. Harvey and Diug state that the two are conceptually different, as the former addresses a population iodine deficiency, whereas folic acid fortification is to compensate a presumed genetic defect that cannot be individually recognised, thus raising ethical questions about exposing the many for the benefit of the few. However, this is the case in almost all public health interventions. Using an example of Harvey and Diug, we expose the whole population to the mandatory fortification of flour with thiamine to prevent Wernicke–Korsakoff syndrome, a condition largely confined to people with a chronic alcohol problem. The concern they raise about mandatory folic acid fortification1 is exposure to unmetabolised folic acid, proposed as possibly increasing adverse effects, but which have not been clearly or conclusively shown. They refer to an Irish study reporting that seven of the 68 children in the study had detectable levels of unmetabolised folic acid in their blood.3 Ireland does not have mandatory folic acid fortification; the main sources of folic acid were voluntarily fortified breakfast cereals and fortified milk — products that are fortified with relatively high levels of folic acid. In Australia, breakfast cereals and other food products are also permitted to be fortified voluntarily — breakfast cereals often contain around 200–300 μg of added folic acid per 100 g (or about 100 μg per serve). This compares with mandatory fortification of flour of 200–300 μg per 100 g flour, or about 40 μg folic acid per slice of bread. While either source could lead to circulating unmetabolised folic acid, the higher doses in voluntarily fortified products are more likely to do so. With the introduction of mandatory fortification, there was a reduction in neural tube defects.4 Importantly, there has been a 68% reduction in previously higher rates of neural tube defects in Indigenous people.5 Mandatory fortification provides a more equitable, consistent and cheaper source of folic acid to the population than voluntary fortification. Let’s leave mandatory folic acid fortification preventing neural tube defects in our population.

Carol Bower · Fiona J Stanley · Mike Daube

To the Editor:Tick-borne infectious diseases, including rickettsial infections, acquired in Australia or after international travel remain a diagnostic challenge.1 A 68-year-old man presented with umbilical pain 10 days after returning from a 2-month camping trip through the south-west of the United States (ie, Texas, New Mexico, Arizona, Colorado and Utah). On examination, a live tick was detected and removed from the patient’s umbilicus (Box). The umbilical pain resolved after tick removal. There was no development of fevers, constitutional symptoms, or rash to suggest a tick-borne illness. Laboratory investigations were unremarkable. He was educated about the signs and symptoms of tick-borne illnesses and prescribed a single dose of doxycycline 200 mg for prophylaxis due to his high risk exposure. The tick was identified as Dermacentor andersoni (Rocky Mountain wood tick), which is endemic to North America and not known to occur in Australia.2 D. andersoni adult ticks are principal vectors of Rickettsia rickettsii (the cause of Rocky Mountain spotted fever), and are associated with transmission of other pathogens to humans, including Colorado tick fever virus and Francisella tularensis (the cause of tularemia).2,3 Although isolated from D. andersoni ticks, transmission of Coxiella burnetii (the cause of Q fever) is uncommon. D. andersoni is not known to transmit Lyme disease.2 Analysis of the tick for rickettsial DNA was positive. No Borrelia DNA was detected. Rickettsia was isolated in cell culture and identified as Rickettsia peacockii based on sequencing of the 17kDa, OmpB, gltA and Sca4 genes. R. peacockii is a member of the spotted fever group of rickettsiae.3,4 The presence of R. peacockii in ticks is correlated with reduced prevalence of R. rickettsii.2,3 R. peacockii is closely related to R. rickettsii, and deletion or mutation of genes, possibly resulting in loss of virulence in R. peacockii, have been identified.3 R. peacockii is not known to be a pathogen of humans or other animals.3,4 Rickettsial serology 10 weeks after the tick bite showed detectable antibodies (titre, 1/256), predominantly to the spotted fever group of Rickettsia, compatible with exposure to R. peacockii identified in the tick. Unfortunately, definitive seroconversion or a rising antibody titre was not able to be demonstrated as no earlier sera were available for parallel testing. Pre-existing antibodies from a distant rickettsial exposure from his tick-prone lifestyle (history of extensive international camping trips) cannot be excluded. The patient remains asymptomatic 9 months later and is still an avid traveller. Tick-borne rickettsial infections in Australia include Queensland tick typhus (Rickettsia australis), Flinders Island spotted fever and Australian spotted fever (Rickettsia honei) and Q fever transmitted by ticks including Ixodes spp., Amblyomma triguttatum and Bothriocroton hydrosauri.1 With increasing international travel, recognition of tick-borne rickettsial diseases is becoming more important. Dermacentor ticks have been detected on livestock exported from North America into Europe.5 This case shows the ability of human ectoparasites, and their potentially pathogenic bacteria, to bypass stringent Australian quarantine controls. Further studies of Australian and imported tick-borne infections are required to increase understanding of these emerging infectious diseases. Box – Dermacentor andersoni removed from the patient’s umbilicus

Sadid F Khan · Mythili Tadepalli · John Stenos · Stephen R Graves · Tony M Korman

To the Editor:We congratulate Cheney and colleagues1 for throwing light on the contributions of overweight and obesity on adverse birth outcomes by analysing data from a teaching hospital in central Sydney.1 Around 16% of the women presenting between 2010 and 2014 were overweight, while 7% were obese. Furthermore, despite obesity being an important risk factor for adverse pregnancy outcomes, their study showed a lack of recording of body mass index (BMI) in patients’ records. Adverse pregnancy outcomes are more common among Indigenous Australian women than non-Indigenous women;2 obesity levels are high in pre-conception and in pregnancy, and the subsequent adverse impact on increased metabolic health in offspring is likely contributing to early onset of diabetes and chronic disease in Indigenous Australians. Hence, we want to extend the debate to report on what is happening in primary health care (PHC) settings for Indigenous women. We have analysed continuous quality improvement data from audits of adherence to evidence-based guidelines for maternal care in 65 Indigenous PHC centres (1091 patient records) across Australia during 2012–2014.3 The majority of women at most PHC centres had the first trimester weight recorded (mean, 90%; range, 60–100%), but there was wide variation in recording of BMI (mean, ∼ 60%; range, 0–100%) (Box). This indicates that most barriers to BMI recording are more to do with clinicians’ understanding of the value of and ability to calculate BMI than around women’s willingness to be weighed. For women with an abnormal BMI (mean, ∼ 30%; range, 0–100%), there was wide variation in documented BMI management plans (mean, ∼ 40%; range, 0–100%). Dealing with these generally low levels of recording and wide variation in recording between PHC centres is a vital early step in limiting the contribution of obesity to adverse pregnancy outcomes and improving long term health outcomes for the mother and baby. Women attending PHCs that had participated in continuous quality improvement activities were more likely to receive recommended pregnancy care related to screening and brief interventions for modifiable lifestyle-related risk factors, such as obesity.4,5 These findings support the incorporation of continuous quality improvement activities into the delivery of maternal care. Box – Record of scheduled maternal care services received by Indigenous women at Indigenous primary health care centres, 2012–2014* BMI = body mass index. * More information on how to interpret box plots is available in Gibson-Helm et al,3 page 21.

Jodie Bailie · Jacqueline A Boyle · Ross S Bailie