Volume 212 Issue 1

Understanding how to interpret diagnostic test accuracy studies is a key skill that health practitioners need to develop in order to undertake evidence- based practice

Katy JL Bell · Petra Macaskill · Clement Loy

Erratum Kim J, Ussher JG. Orbital rhabdomyosarcoma: a rare ophthalmic condition. Med J Aust 2019; 211: 398‐399. https://doi.org/10.5694/mja2.50365 In this Lessons from practice article, the fifth sentence in the second paragraph on page 398 should read: “A suspicion for orbital rhabdomyosarcoma was raised and an urgent magnetic resonance imaging scan was performed”. In Box 3 on page 399, the title should read: “Coronal view of magnetic resonance imaging scan of the orbits. The rhabdomyosarcoma tumour is located in the superonasal aspect of the right orbit”.

Warrillow S, Raper R. The evolving role of intensive care in health care and society. Med J Aust 2019; 211: 294‐297. https://doi.org/10.5694/mja2.50340 In this Perspective article, in Box 3 on page 295, the number of ICU beds in Western Australia should read: “162 ICU beds”.

Estimates adjusted for competing risks of mortality can be more meaningful, but make some comparisons more difficult

Elizabeth Buckley · David M Roder

Child protection services in Australia require fundamental workforce and organisational reform

Steve Kisely · Jake Najman

The current method for calculating lifetime risks overestimates these risks, especially for men

Anthea C Bach · Kelvin SE Lo · Thanya Pathirana · Paul P Glasziou · Alexandra L Barratt · Mark A Jones · Katy JL Bell

Mental disorders in children known to child protection services during early childhood

Melissa J. Green · Gabrielle Hindmarsh · Maina Kariuki · Kristin R. Laurens · Amanda L Neil · Ilan Katz · Marilyn Chilvers · Felicity Harris · Vaughan J Carr

Rates of non-reconstructive, non-reparative arthroscopic procedures in people over 50 years have declined over the past 10 years

So Mang (Simon) Lee · Wasim Awal · Christopher Vertullo

The clinical significance of asymptomatic infection is uncertain, and routine testing is not recommended

James D Stewart · Brooke Webb · Michelle Francis · Maryza Graham · Tony M Korman

Migraine affects over a billion people worldwide in any year and is the second most common cause of years lost due to disability

Michael Eller · Peter J Goadsby

Infants with GORD should first be distinguished from those with physiological GOR and then be managed in a step-wise fashion, using non-pharmacological measures where possible and pharmacological measures where necessary

Robert N Lopez · Daniel A Lemberg

To the Editor: In July 2019, sarcopenia — a progressive and generalised skeletal muscle condition involving loss of skeletal muscle mass and function1 — was awarded a code in the International Classification of Diseases, tenth revision, Australian modification (ICD‐10‐AM). This recognition has arrived 30 years after Irwin Rosenberg first described the condition in 1989.2 Sarcopenia is independently associated with poor quality of life, falls, fractures, institutionalisation and mortality.1 About 13–19% of community‐dwelling older adults may have this condition, and prevalence is highest among those living in residential care.1 All individuals experience declines in muscle mass and function during ageing, but only those who meet the criteria described in the Box are considered to have sarcopenia. The definition currently promoted by the Australian and New Zealand Society for Sarcopenia and Frailty Research is the initial European Working Group on Sarcopenia in Older People definition,3 which was adopted after a Delphi consensus.5 Measures of muscle strength and physical performance such as grip strength, chair stands and gait speed are cost‐effective and easy to perform in clinical practice. Obtaining measures of muscle and lean mass may be challenging outside of the research setting. Therefore, in individuals with low muscle strength or physical performance, in the absence of other potential causes (eg, osteoarthritis), sarcopenia should be suspected and safe and effective interventions can be offered. Patients with, or at risk of, sarcopenia should be recommended exercise therapy, in particular, progressive resistance training.1 This type of training prescribed by treating clinicians can be implemented by allied health professionals, including exercise physiologists and physiotherapists. Protein supplementation can prevent loss of muscle, but this is most beneficial when combined with progressive resistance training.1 A number of randomised controlled trials are underway examining different therapeutics for the treatment of sarcopenia.1 With the advent of the ICD‐10‐AM code, primary care clinicians, allied health staff, and members of the public will begin observing sarcopenia diagnoses on medical correspondence. Hospital funding models may adjust in line with the ICD‐10‐AM code and in recognition of the increased complexity and risk of complications that comes with caring for patients with sarcopenia. An understanding of this condition, its implications and treatment is key in providing evidence‐based care to patients living with sarcopenia. Box – Diagnostic tools and measurements to diagnose sarcopenia* using the initial European Working Group on Sarcopenia in Older People (EWGSOP) definition†3 Component Thresholds and equipment Low muscle strength Hand grip strength using dynamometer: Men: < 30 kg Women: < 20 kg Low physical performance Men and women over 4 m course: Gait speed: ≤ 0.8 m/s Low lean mass ALM using whole‐body DXA (adjusted for height, m2): Men: < 7.26 kg/m2 Women: < 5.50 kg/m2 ALM = appendicular lean mass; DXA = dual x‐ray absorptiometry. * Diagnosis of sarcopenia is based on low lean mass and low physical performance or muscle strength. † The EWGSOP have developed a revised definition for sarcopenia (known as EWGSOP2);4 however, this has not yet been recommended for use in Australia.

Jesse Zanker · David Scott · Sharon L Brennan‐Olsen · Gustavo Duque

To the Editor: As reported by Rowe and colleagues1 in their retrospective analysis of maternal immunisation, uptake of influenza and acellular pertussis vaccines among pregnant women remains unacceptably low. One contributing factor may be inconsistent messaging. Historically, vaccine manufacturers have included precautions about the lack of data on use in pregnancy in their product information sheets. Such precautions have been shown to lead to vaccination hesitancy and refusal among pregnant women.2,3 In contrast, the current edition of the Australian Immunisation Handbook states: “Pregnant women are routinely recommended to receive influenza vaccine … and pertussis‐containing vaccine”.4 In 2018, the Therapeutic Goods Administration asked its Advisory Committee on Vaccines to provide independent expert advice on the available safety data on influenza vaccination in pregnancy with regards to the pregnancy category of influenza vaccines. The Advisory Committee on Vaccines advised that “adoption of Australian Pregnancy Category A should be considered by sponsors for certain inactivated influenza vaccines”.5 Pregnancy Category A signals to doctors and the public that the vaccine has been used by large numbers of expectant mothers with no evidence of harm to their babies. This is in line with the Australian Immunisation Handbook: “Clinical trial data and observational studies show no increased risk of congenital defects or adverse effects in the fetuses of women who received influenza vaccine during pregnancy”.4 Following the publication of the Advisory Committee on Vaccines statement, two of the four adult influenza vaccines and one of the two acellular pertussis vaccines used to vaccinate pregnant women in Australia have changed their pregnancy category to Category A. These changes show that the Australian regulator is receptive to feedback from the medical community on how to improve immunisation rates. Hopefully, the reclassification of the pregnancy category of these vaccines will translate into increased maternal uptake and better outcomes for Australian mothers and babies.

Heidi Shukralla · Michael Coory

To the Editor: Reperfusion therapies in acute ischaemic stroke have become well recognised in recent years. The article by Campbell1 summarises current practice and addresses the benefits and challenges of several reperfusion therapies, but it misses one key prevention strategy. Carotid stenosis is a significant cause of ischaemic stroke — it is present in about 20% of patients with stroke2 — and can lead to the formation of thromboembolism or haemodynamic failure from hypoperfusion.3 Multidisciplinary care is vital to the management of acute stroke, and carotid endarterectomy is a safe and effective procedure that significantly reduces the risk of stroke and improves perfusion to the brain.4 Carotid endarterectomy plays an important role as reperfusion therapy in acute ischaemic stroke and is integral clinical practice in the management of stroke.5

Suk Cheng · Toby Richards

In reply

Bruce CV Campbell

To the Editor: A 64‐year‐old woman presented to our emergency department with progressively reduced consciousness over 3 days. This was preceded by 2 days of vomiting and diarrhoea. She had been systemically well before this, with no acute medical issues. She had type 2 diabetes and had been commenced on combination 10 mg empagliflozin and 5 mg linagliptin a year ago after having experienced diarrhoea with metformin. Her most recent glycated haemoglobin level was 58 mmol/mol (reference interval [RI], 20–42 mmol/mol). She had also been trialling the Atkins diet for about 2 months before presentation. Her initial blood tests demonstrated high anion gap metabolic acidosis, an initial blood sugar level of 10.3 mmol/L (RI, 3.2–5.4 mmol/L] and a serum ketone level of 4.7 mmol/L (RI, < 0.6 mmol/L). She was diagnosed as having euglycaemic ketoacidosis secondary to using a sodium–glucose cotransporter type 2 (SGLT2) inhibitor (empagliflozin) and precipitated by her diarrhoeal illness and her Atkins diet. After a dextrose and insulin infusion, the anion gap normalised within 4 hours of presentation. She became progressively more alert within 24 hours of presentation. She was discharged 2 days after presentation with directions never to recommence empagliflozin. This case highlights the risks of combining ketogenic diets such as the Atkins diet with SGLT2 inhibitors, as outlined by Grammatiki and colleagues.1 SGLT2 inhibitors have a diuretic effect as they block the reabsorption of sodium as well as glucose.2 Hypovolaemia stimulates release of counter‐regulatory hormones such as glucagon, cortisol and adrenaline, which further increase insulin resistance, lipolysis and ketogenesis. Our patient's diarrhoeal illness preceding presentation likely exacerbated this hypovolaemia and therefore ketogenesis. High protein, low carbohydrate ketogenic diets such as Atkins in isolation usually only result in a mild, temporary ketosis.3 In the setting of an SGLT2 inhibitor and infective illness, however, it increased our patient's susceptibility to ketosis.

Shampa Sinha · Daniel Gavaghan · Steven Yew