Letters

To the Editor: Trachoma, caused by the bacterium Chlamydia trachomatis, is the leading cause of infectious blindness worldwide.1 In Australia, the burden of disease falls almost exclusively on the Aboriginal population.2 However, there has been little consistent data collection on the prevalence of trachoma in recent years in Australia.3,4 Furthermore, despite Australian Government recommendations for biennial screening of people aged 40–54 years and annual screening of people aged ≥ 55 years in areas where trachoma is or has been endemic,5 very little screening of older people for trachomatous trichiasis has been conducted.2,4 We report on the first large-scale population study in 30 years of the current prevalence of active and cicatricial trachoma in the Northern Territory Aboriginal population. We conducted a standardised clinical screening study of five Aboriginal communities in the Katherine Region of the NT over a 5-week period in 2007. A representative sampling frame of those believed to be currently living in each community was constructed using the medical clinic patient list, the council housing list and the local knowledge of Aboriginal Health Workers seconded from the clinics to assist with the project. All people in each community were invited to undergo a clinical eye examination for trachoma. The parameters of the World Health Organization simplified grading scheme6 were used to determine prevalence of the five signs of trachoma: tarsal conjunctival follicles, intense inflammation, tarsal scarring, trichiasis and corneal opacity. A total of 1316 people (85.2% of the total estimated population), including 415 children aged under 10 years, were screened for trachoma. Across the five communities, active trachoma (assessed as the presence of either follicles or inflammation in one or both eyes) was at an endemic level (> 10%). The prevalences of active trachoma, scarring and trichiasis in different age groups are summarised in the Box. The overall rate of active trachoma in children under 10 years of age was 19.8% (95% CI, 16.0%–23.9%) (n = 82), and two communities had hyperendemic prevalence of trachoma (> 20%) in this age group. The youngest child observed with active trachoma was just over 1 year old. The prevalence of scarring in people aged 20 years and over was 32% (95% CI, 28.3%–35.9%) (n = 193). The youngest person identified with scarring was 7 years old. Six people (2.3% of all people aged 40 years and over) were identified with trichiasis requiring urgent ophthalmological attention. Across the population, this placed the prevalence of unoperated trichiasis at more than four times the acceptable threshold set by the WHO. A seventh person had had trichiasis surgery. That trachoma is still hyperendemic in Aboriginal communities more than 30 years after the National Trachoma and Eye Health Program first identified the extent of trachoma is unconscionable. Urgent and sustained public health and clinical interventions are required, with greater commitment from politicians and health policymakers, if Australia is to join the ranks of other developed nations in eradicating endemic trachoma. The guidelines for trachoma control developed by the Communicable Diseases Network Australia5 need to be resourced appropriately and implemented. Prevalence of active trachoma, scarring and trichiasis in five Aboriginal communities in the Northern Territory in 2007, by age group* TFI = active trachoma (follicles [TF] and/or inflammation [TI]). TS = trachomatous scarring. TT = trachomatous trichiasis. * Vertical bars indicate 95% CIs.

Katrina Roper · Claude-Edouard C Michel · Paul M Kelly · Hugh R Taylor

To the Editor: The oculocardiac reflex is a potentially life-threatening phenomenon requiring prompt recognition and management. It is defined as a 20% or greater reduction in heart rate and/or the presence of arrhythmias during stimulation of the orbital contents.1 It is most commonly encountered in the context of paediatric squint surgery. We report its occurrence in a young healthy adult man after a traumatic facial injury. While being transported to hospital by ambulance, he had intermittent bradycardia, with a heart rate as low as 38 beats/min, and was administered a 1 g dose of intravenous atropine. His medical and ocular histories were unremarkable, and he had no history of unexplained syncope. In the emergency department, his heart rate remained low (40 beats/min) and his blood pressure was 122/52 mmHg. There was diffuse periorbital lid swelling and bony tenderness along the inferolateral orbital margin. He had restricted upgaze of his left eye; during this manoeuvre, his heart rate dropped to 20 beats/min and he developed hypotension, with a blood pressure of 92/48 mmHg. He was given three intravenous 500 μg boluses of atropine to improve his haemodynamic condition. An electrocardiogram showed sinus bradycardia, and subsequent recordings showed intermittent Mobitz II second-degree atrioventricular block. A computed tomography scan of the left orbit showed a moderately displaced fracture of the orbital floor involving the maxillary bone, with entrapment of orbital fat and the inferior rectus muscle (Box). Given the presence of the oculocardiac reflex with haemodynamic compromise, the fracture was immediately repaired surgically. Postoperatively, the patient’s blood pressure was 134/90 mmHg and his heart rate was 86 beats/min, with normal sinus rhythm. He recovered full eye movement, and no further oculocardiac reflex was recorded. He remained well 1 year after discharge. The oculocardiac reflex was first described by Aschner as a slowing of the radial pulse when pressure was applied to the eye.2 It is a rare but recognised occurrence among young healthy adults with orbital fractures. Clinical manifestations of the reflex may include bradycardia, hypotension, nausea, vomiting and syncope.3 The reflex is acknowledged as an important indication for immediate surgical repair of the orbit.4 In addition to reducing morbidity from the reflex, urgent repair is beneficial as it releases incarcerated soft tissue, leading to a more favourable outcome with less likelihood of squint.5 Cardiac decompensation due to traumatic facial injuries should alert clinicians to the possibility of the oculocardiac reflex and the need for urgent surgical intervention. Computed tomography scans of the patient’s left orbit Sagittal (A) and coronal (B) computed tomography scans showing left orbital floor fracture with entrapment of the inferior rectus muscle (arrows).

Vivek B Pandya · R Max Conway · Richard Conway

To the Editor: Microbial keratitis associated with soft contact lens wear is a well recognised, not uncommon, clinical entity and a preventable cause of ocular morbidity.1,2 A 31-year-old woman who occasionally wore soft contact lenses presented to a general practitioner with a 2-day history of bilateral red eye associated with ocular discomfort, photophobia and purulent discharge. She was diagnosed with bilateral conjunctivitis, commenced on chloramphenicol drops and told to return in 5 days. Her symptoms initially improved, but then worsened. Seven days after symptom onset, she presented to hospital for assessment. History revealed that she had worn soft monthly disposable contact lenses twice in the previous month to correct her mild myopia. On examination, the patient’s visual acuity was equivalent to being legally “blind”, being hand movement in the right eye and light perception in the left. On inspection, both eyes appeared grossly abnormal. The right eye had a large central corneal abscess and the left eye had a complete corneal abscess with 360° peripheral corneal thinning (Box, A) — a significant risk for globe perforation. The conjunctiva was markedly injected bilaterally. Corneal scrapes, the contact lenses and the case containing turbid solution were sent for urgent gram stains and microbiological culture. The patient was admitted to hospital and received intensive topical treatment with gentamicin 0.9%, cephalothin 5% and tobramycin ointment. The corneal scrapes revealed Pseudomonas aeruginosa as the causative organism. The patient showed slow improvement with antibiotic therapy. Although the infection cleared, the residual corneal scarring resulted in permanent loss of corneal clarity and hence vision. Four months after treatment was commenced, the patient’s visual acuity had improved to 6/24 in the right eye and 6/36 in the left (Box, B). An Australian review of outcomes after keratitis found that 52% of patients had a final visual acuity of worse than 6/12, the legal visual acuity for driving.3 In this patient, despite saving both eyes and the improvement in her vision, she still has significant functional impairment, being unable to work as a teacher or drive. Corneal transplantation is now her only option for potentially regaining the loss in her functional vision, with a minimum expected recovery time of 2 years. GPs have a difficult job distinguishing between red eye requiring immediate referral and red eye that is not vision-threatening. All contact lens wearers who present with red eye need to be examined for yellow/white corneal infiltrates and, if present, or if the patient cannot be assessed adequately, immediate referral is mandatory. P. aeruginosa is the most common pathogen and one of the most aggressive organisms isolated in contact lens-related microbial keratitis.4 As it is invariably resistant to the bacteriostatic chloramphenicol, the appropriate empirical treatment is either fluoroquinolones or cephalosporins, which ideally should be commenced after corneal scrapes have been performed.5 Left eye at presentation and after 4 months of treatment A: At presentation, there was marked conjunctival injection, 100% epithelial defect (stained with fluorescein [green]) and severe circumferential peripheral corneal thinning (arrow). B: Four months after presentation, there was dense central scarring and peripheral corneal neovascularisation (arrow). Vivek B Pandya, Ophthalmology Resident1Alessandra Martins, Ophthalmology Registrar1,2Shanel Sharma, Ophthalmologist1,21 Department of Ophthalmology, Sydney Eye Hospital, Sydney, NSW. 2 Department of Ophthalmology, Royal Prince Alfred Hospital, Sydney. shanelATunsw.edu.au Green M, Apel A, Stapleton F. A longitudinal study of trends in keratitis in Australia. Cornea 2008; 27: 33-39. <PubMed> Keay L, Edwards K, Naduvilath T, et al. Microbial keratitis predisposing factors and morbidity. Ophthalmology 2006; 113: 109-116. <PubMed> Green MD, Apel AJ, Naduvilath T, Stapleton FJ. Clinical outcomes of keratitis. Clin Experiment Ophthalmol 2007; 35: 421-426. <PubMed> Stapleton F, Keay L, Sanfilippo PG, et al. Relationship between climate, disease severity, and causative organism for contact lens-associated microbial keratitis in Australia. Am J Ophthalmol 2007; 144: 690-698. <PubMed> Constantinou M, Daniell M, Snibson GR, et al. Clinical efficacy of moxifloxacin in the treatment of bacterial keratitis: a randomized clinical trial. Ophthalmology 2007; 114: 1622-1629. <PubMed> (Received 17 Mar 2008, accepted 28 Jul 2008) ©The Medical Journal of Australia 2008 www.mja.com.au PRINT ISSN: 0025-729X ONLINE ISSN: 1326-5377

Vivek B Pandya · Alessandra Martins · Shanel Sharma

To the Editor: A 37-year-old man infected with HIV through exposure to men who have sex with men (MSM) presented with a 6-week history of intermittent fevers, patchy alopecia and a widespread brown/grey macular rash involving his face, trunk, abdomen and all limbs, with scaling of the face, palms and soles. He had no symptoms of meningism or visual disturbance, and had a chronic mild intermittent headache with no recent change in frequency or intensity. His most recent CD4 cell count was 70 cells/μL and his HIV viral load was > 100 000 copies/mL. On admission, a serological test for syphilis was reactive and showed a rapid plasma reagin (RPR) titre of 1 : 64 and a positive enzyme immunoassay for antibody (EIA-Ab), whereas at the onset of the rash 6 weeks previously, a serological test for syphilis was negative. A punch biopsy of the skin lesions showed a perivascular infiltrate with lichenoid inflammation consistent with secondary syphilis. An ophthalmological review showed a bilateral anterior uveitis. Examination of cerebrospinal fluid (CSF) showed a white cell count of 1 × 106/L (100% lymphocytes), a normal glucose level, a mildly elevated protein level of 0.45 g/L and a weakly positive result for a fluorescent treponemal antibody absorbed (FTA-ABS) test. CSF RPR, EIA-Ab and Treponema pallidum particle agglutination (TPPA) test results were all non-reactive. The patient was diagnosed with asymptomatic ocular and neurosyphilis, and treated with intravenous benzylpenicillin (1.8 g 4-hourly for 15 days) and prednisolone eye drops (four times daily for 14 days). The rash faded and the anterior uveitis subsided in the first week of treatment. There is currently a syphilis epidemic among MSM in Victoria, with the number of syphilis notifications increasing 25-fold between 2000 and 2006.1 A strong association between HIV infection and infectious syphilis has been demonstrated in recent years, including in Victoria.2 HIV-infected MSM with early syphilis have a 1.7% risk of having symptomatic early neurosyphilis3 and a 13% risk of having symptomatic ocular syphilis regardless of CD4 cell count.4 There is no pathognomonic finding in ocular syphilis, and the disease may manifest as uveitis, retinitis, optic neuritis, perineuritis, retinal detachment and papillitis. It is recommended that all patients with ocular syphilis undergo CSF examination and be managed as if they had neurosyphilis.5 Current guidelines also recommend CSF examination in HIV-infected patients who have late-latent syphilis, syphilis of unknown duration, any neurological signs or symptoms, or suspected treatment failure.6 The finding of asymptomatic ocular syphilis in our patient suggests there should be a low threshold for eye examination in HIV-infected people with early syphilis, even in the absence of any ocular symptoms, as the diagnosis of ocular syphilis dramatically alters the management of these patients.

Matthew T Kitson · Michelle K Yong · Jennifer F Hoy

To the Editor: Snowboarding is increasing in popularity, but Australian snowboarders have been shown to have 2.4 times as many fractures as skiers, with 35% of upper limb injuries being fractures.1 The most common site of injury is the wrist, accounting for 21.6% of all snowboarding injuries.2 It has been suggested that the use of wrist guards could reduce the risk of injury, particularly as snowboarding injuries tend to be impactive rather than torsional.3,4 However, concern has been raised that use of wrist guards will redistribute the impact of the force to more proximal areas of the arm, causing elbow injuries.5 We conducted a case–control study at the Mount Buller Medical Centre, Victoria, during the 2004 and 2005 ski seasons to assess: the association between wrist guard use and wrist fracture in snowboarders in Australia; and the association between wrist guard use and the severity of wrist and elbow injury. Cases were defined as any snowboarder seen at the clinic with a fractured wrist (n = 119). Controls (n = 375) were snowboarders — identified by their boots — who attended the clinic, either as companions to case participants or other patients, or as patients presenting for a reason other than wrist fracture. Study participants completed a questionnaire about wrist guard use and snow-sport behaviour. The site and severity of fractures were recorded by clinic staff. Logistic regression was used to determine adjusted odds ratios for risk factors against the main outcome measure of wrist fracture and injury in snowboarders with and without wrist guards. Characteristics strongly associated with wrist fracture were being of school age (odds ratio [OR], 2.37; P < 0.001) and being a novice at snowboarding (OR, 3.41; P < 0.001) (Box). After adjustment for all significant variables — sex, age, days of snowboarding and snowboarder ability — the odds of having worn wrist guards were lower in snowboarders with a wrist fracture (cases) than in those without such a fracture, but the difference did not reach significance (adjusted OR, 0.58; 95% CI, 0.32–1.04; P = 0.07). Full analysis of all factors considered is available from the authors. Among the sample of 494 snowboarders, 15 had elbow injuries, comprising: five with soft tissue injuries (4/86 wearing wrist guards v 1/391 not wearing wrist guards; adjusted OR, 17.6; 95% CI, 1.93–160.2; P = 0.01); and 10 with elbow fractures or dislocations (3/86 wearing wrist guards v 77/391 not wearing wrist guards; adjusted OR, 1.84; 95% CI, 0.46–7.30; P = 0.39). The association between wrist guard use and increased soft tissue elbow injuries, but not elbow fractures and dislocations, supports the value of wearing wrist guards to reduce overall injury severity. Despite a lack of overall statistical significance, the clinical context and consistency in direction of the findings suggest that snowboarders who wear wrist guards in Australian snow conditions could benefit from a reduction in wrist fracture injury of approximately 42%. This is consistent with reports from other countries that show a protective effect of wrist guards of 52% to 87%, with the greatest benefit in novice snowboarders.4 We suggest that wrist guard use should be strongly recommended for novices, and should be mandatory for school-aged snowboarders. Local schools in the Mansfield district, near Mt Buller, have adopted a policy of “no wrist guard = no snowboard”, and we hope that other schools visiting Mt Buller, and indeed other ski resorts in Australia, will follow this lead. Characteristics associated with wrist fracture among snowboarders Characteristic Cases (n = 119) Controls (n = 375) Odds ratio (95% CI) P for difference Wearing wrist guards today No 100 (84%) 299 (80%) 1.00* Yes 18 (15%) 75 (20%) 0.72 (0.41–1.26) 0.25 Missing data 1 (0.8%) 1 (0.3%) Age (years) 0–19 72 (61%) 149 (40%) 2.37 (1.55–3.63) < 0.001 > 19 46 (39%) 226 (60%) 1.00* Missing data 1 (0.8%) Ability of snowboarder Novice 60 (50%) 112 (30%) 3.41 (1.79–6.49) < 0.001 Intermediate 43 (36%) 173 (46%) 1.58 (0.82–3.04) 0.17 Advanced 14 (12%) 89 (24%) 1.00* Missing data 2 (2%) 1 (0.3%) * Reference category.

Graham M Slaney · Judith C Finn · Angus Cook · Philip Weinstein

To the Editor: Streptococcus suis is an emerging zoonosis in humans and a common pathogen in Australian pigs.1 However, only two cases of human infection have previously been reported in Australia.2,3 We recently treated two Australian piggery workers, from the same town in New South Wales, for S. suis endocarditis. The first patient, a previously healthy 46-year-old woman, presented in October 2006 with a 3-month history of fatigue, anorexia, night sweats and weight loss of 20 kg. Her job involved hands-on work at a piggery. She was afebrile, with blood pressure of 145/50 mmHg, bilateral clubbing, splenomegaly, and a long diastolic murmur without evidence of heart failure. Transthoracic echocardiography confirmed severe aortic regurgitation associated with a vegetation. Blood cultures grew S. suis. The patient was treated with benzylpenicillin (1.8 g, 4-hourly for 6 weeks) and gentamicin (60 mg, 8-hourly for 2 weeks). Severity of aortic regurgitation necessitated aortic valve replacement. The second patient, a 58-year-old man, presented in January 2008 with headache, fever (38.7°C), neck stiffness and confusion. He had been unwell for 1 month with fevers, sweating, fatigue and weight loss of 6 kg. His job involved transporting pigs from local piggeries, including the one at which the first patient worked, to an abattoir, and involved direct contact with pigs. On admission, he was treated with ceftriaxone (2 g) and benzylpenicillin (2.4 g). Cerebrospinal fluid (CSF) examination showed leukocytosis (10 300 × 106/L; reference range, < 5 × 106/L) with 95% polymorphs. Scanty gram-positive cocci were visible, but there was no growth on culture of the CSF. Blood cultures grew S. suis. Transthoracic echocardiography revealed an aortic valve vegetation with trivial regurgitation. The patient was then treated with benzylpenicillin (1.8 g, 4-hourly for 4 weeks) and gentamicin (80 mg, 8-hourly for 2 weeks), and made a full recovery. Both cases were investigated by the NSW Department of Health, including assessment of workplace practices, staff education and rates of porcine infection at the piggeries and abattoir at which the patients had worked, but no significant factors for infection were identified. Since the first reported human infection with S. suis in Denmark in 1968,4 more than 400 cases have been reported, including an outbreak in China in 2005 that affected 215 people.5 The most common manifestations are meningitis (affecting 72.5% of patients) and bacteraemia (24.2%); endocarditis is relatively uncommon (1.1%).5 In a series of 16 cases of S. suis endocarditis, the mean period between onset of symptoms and diagnosis was 23 days, and seven patients required valve replacement.6 Similarly, our patients had subacute presentations: severe aortic regurgitation and secondary meningitis. In Australia, it is likely that there have been other S. suis infections in humans that have gone unrecognised because of mild presentations, difficulties with laboratory diagnosis, and empirical treatment of unrecognised infection. While it is unlikely that S. suis is a common zoonosis in Australia, these cases show that it is an occupational hazard in Australian piggeries, with potential public health, animal health and medicolegal implications.

Karina J Kennedy · Assad A Jadeer · Chong W Ong · Sanjaya N Senanayake · Peter J Collignon

To the Editor: The study by Nichols and colleagues1 and the associated editorial by Hughes2 struck a chord of familiarity for me, as patient safety issues are currently high on the political agenda in the United Kingdom. An estimated 850 000 incidents of harm or near harm affect National Health Service (NHS) hospital patients in the UK each year.3 In April 2004, the Health Foundation (an independent charity that aims to improve the quality of UK health care), together with the Institute for Healthcare Improvement, launched the Safer Patients Initiative (SPI). The four hospitals initially chosen to participate conducted hospital-wide programs to radically improve patient safety, with the aim of reducing adverse events by 50% by October 2006. In November 2006, Phase 2 was launched, adding 20 more sites.3 These hospitals meet regularly to report on progress and exchange ideas. Discrete projects focus on medicines reconciliation, ward-based care, critical care, and perioperative care. The overall aim of the SPI is to improve the patient safety culture within each organisation. Specific targets for all participating hospitals include a 15% reduction in mortality of in-hospital patients; 300 days between central line bloodstream infections in critical care units; 80% of blood sugar levels in diabetic patients falling within their target treatment range; a 30% reduction in cardiac arrest calls; and 50% reductions in methicillin-resistant Staphylococcus aureus bloodstream infections, harm from anticoagulation, and surgical site infections. In my intensive care unit, hand hygiene compliance among medical staff has been regularly audited and has improved from a range of 20%–90% per day to 60%–100%. This compares favourably with a recent Australian hand hygiene initiative.4 When practice improvements are shown in one location, the project team takes on the responsibility of spreading these across the hospital. Initial scepticism from senior clinicians and nurses in my hospital has generally been replaced by cooperation and, in many cases, ideas for other ways to improve delivery of safer clinical care. Large multisite evidence-based trials in intensive care units in the United States showed that, with focused effort on sterile technique and catheter care and by rectifying lapses in standard procedures, a reduction of 66% in catheter-related bloodstream infections was possible.5 The SPI is trying to replicate results such as these within a relatively short period. My intensive care unit has now gone 190 days without a line-related bacteraemia; previously, we had infections almost every month. The SPI Phase 2 completion date is November 2008, with full national reporting due at that time. It is intended that practice improvements will then be spread across the NHS. The experience in my hospital has been that sharing experiences both within the hospital and externally has led to tangible progress in this area.

Peter J Shirley

To the Editor: The recent article on the review of the University of Sydney Medical Program (USydMP)1 by Goulston and Oates included a lengthy list of “changes made or planned in accordance with key recommendations”.2 Regrettably, and to the despair of many, the most needed change will not take place. It is reported in the review that the average age of future USydMP graduates will be 29–30 years, as it has been for the past decade.1 From 2008, those who aspire to be surgeons will competitively enter the new Surgical Education and Training (SET) program of the Royal Australasian College of Surgeons (RACS) after completing “at least their second postgraduate year”.3 The SET program is for 5–6 years, depending on the specialty. Most trainees subsequently take a subspecialty fellowship for 1–2 years, either in Australia or overseas, by which time our hapless graduates will be 40 years old. A woman may have to have leave of absence for a pregnancy. A postgraduate degree is now a prerequisite for an academic career and this involves an additional 2–3 years of full-time research. Finally, it takes in the order of 5 years to establish a referral specialist practice in most branches of medicine. In the review document, Goulston and Oates nihilistically state “There is no opportunity for streaming within the USydMP”.1 There is no mention of undergraduate education in Australia, let alone the streaming of such education, in the article from the RACS outlining the SET program.4 However, strangely enough, it is noted therein: “North American students must make their long-term career choice in the final year of their medical school and are streamed accordingly”. One wonders if there is any purposeful communication between the RACS and our universities. There certainly should be. It is imperative in this day and age that undergraduate and postgraduate medical education be considered as a continuum so that we can begin to rid ourselves of the absurdly long and manifestly inefficient process outlined above. The historian and journalist Paul Johnson put his astute finger on the problem in writing a column about universities generally: “. . . a visitor from another planet, unfamiliar with the history of the institution, would think it odd that our ablest boys and girls, at a time when their mental and physical powers are at their highest, are withdrawn from the service of society and kept in comparative idleness . . .”5 One can but conclude that, at least for future surgeons, the wrong people are at the helm at the RACS and at the University of Sydney’s Faculty of Medicine.

Thomas K F Taylor

In reply: Taylor raises several issues that the Royal Australasian College of Surgeons (RACS) has carefully considered. The new Surgical Education and Training (SET) program commenced this year.1 The acronym SET could equally mean Shorter Efficient Training. In the previous program, 2–5 years of basic surgical training was followed by 4–6 years of advanced training, resulting in surgeons entering specialist practice an average of 10 years after graduating with their medical degrees. We responded to societal and regulatory factors, including the older age of medical (compared with other) graduates, sex, work–life balance, safe-hours requirements, workforce pressures and competition from other specialties. Our new system aims to streamline training by early selection directly into one of nine surgical specialties and completion of training by Postgraduate Year 7 or 8 in most cases. It is not only shorter, but more comprehensive than previously. It is much more than an apprenticeship, where training occurs by random clinical exposure. We are covering defined curriculum objectives for every trainee by offering training in metropolitan and regional hospitals, synthetic laboratories and the private sector. We are moving away from reliance on the number of years of training and numbers of operations as measures of experience. We are focusing on the development of a range of surgical competencies encompassing professionalism, communication, collaboration, clinical decision making, scholarship, leadership and health advocacy, as well as essential medical and technical expertise. These competencies are regularly monitored by performance assessment throughout training. At the completion of training and the RACS fellowship examination, a surgeon is competent to commence practice as a specialist. Additional formal training experience is optional. Of course, the RACS promotes the concept of lifelong learning. The RACS and universities are communicating. Common concerns are the compromised state of basic science education and the limited exposure of medical students to a range of surgical specialties. The College has had discussions with many universities and health authorities about the possibility of “streaming” in the later years of medical school and in Postgraduate Years 1 and 2. It is worth noting that the University of Sydney has plans for the final 2 years of its course to be integrated, with increased emphasis on critical care and surgery.2

Ian R Gough

In reply: We are in sympathy with Taylor’s concerns about the length of medical training and point out that a more careful reading of our review of the University of Sydney Medical Program1 contained the following comments (on page 203): Discussion with the Royal Australasian College of Physicians canvassed the possibility that students might master some educational modules during their medical degree which would be credited by the College. This could well apply to other Colleges. Such a process would be more easily achieved if the Colleges moved to an overall “point system” i.e. students (especially in nonclinical areas such as Ethics, Quality and Safety etc) could study postgraduate modules pari passu with the USydMP, gaining some points towards their chosen college specialty qualification. This is followed by three recommendations on page 204: Students with an early interest in a specialty could gain some speciality experience or credit towards their specialty by either working towards an MPhil and by making use of the electives, options and Honours research project. The future situation with regard to medical training in some of the specialties is fluid eg, the Royal Australasian College of Surgeons is introducing a method of streaming for surgical training (SET) and IMET [Institute of Medical Education and Training] is looking at criteria for competency in the residency years. In view of this the Dean should explore further opportunities for streaming when the options for future specialty training become clearer. Early streaming should be re-examined by Faculty when the curriculum and educational changes being considered by some of the Colleges become clearer.

Kerry J Goulston · R Kim Oates

To the Editor: During the recent international cricket series between Australia and India, we were alarmed by the sight of our Australian cricketers prominently badged with the logo of the fast food giant KFC. Australia is experiencing an epidemic of overweight and obesity, a problem that is especially affecting children, adolescents and young adults.1 This epidemic is worsening as a direct result of unhealthy eating habits and low levels of physical activity. Obesity is associated with chronic and costly diseases that lead to premature death and ill health. These include diabetes, cardiovascular disease, respiratory problems, sleep apnoea, certain cancers, mental illness and osteoarthritis, which can begin in adolescence.1 Cricket in Australia enjoys considerable popularity and a strong national following. Our cricketers are national sporting heroes who enjoy widespread support and respect throughout the community, particularly among younger members of the community, who aspire to emulate them. Against this background, we are increasingly concerned and disappointed that Cricket Australia has a sponsorship agreement with, and consequently promotes, KFC — going as far as publicly declaring the company the “official fast food restaurant of Cricket Australia”.2 This advertising uses the standing of cricket and its players to endorse and promote unhealthy eating habits, one of the major root causes of obesity in Australia. KFC products have caloric and fat contents well above the national dietary guidelines, which recommend < 30% energy from total fat and < 10% energy from saturated fat.3 For example, a standard serve of original-recipe chicken contains about 58% total fat and 24% saturated fat.3 Furthermore, we have shown that even one common KFC meal per week can adversely affect recommended healthy diets.4 It is ironic and regrettable that Cricket Australia, while having done so much for the sport, encourages the promotion of unhealthy, high-fat, high-calorie KFC products that negate the benefit of increased physical activity associated with playing cricket. With the explosion of obesity-related illness, we need champions to encourage health-promoting behaviours, particularly healthy eating and increased physical activity. The enthusiastic encouragement of unhealthy and undesirable eating habits should have no place in sporting sponsorship. Not so long ago, similar sentiments were being expressed about tobacco sponsorship of sport, which fortunately has been eradicated. Cricket Australia should consider its responsibilities to Australia’s children and youth and review its sponsorship by KFC. This would benefit the health of the community and demonstrate leadership and social responsibility by Cricket Australia and Australia’s elite cricketers.

Stephen Colagiuri · Ian D Caterson

In reply: Cricket Australia (CA) actively supports physical activity, healthy eating and healthy lifestyles and continues to invest considerable effort in encouraging Australians to play cricket, in everything from formal, organised competitions to social games in the backyard, in parks and schoolyards and at the beach. In a time of declining community physical activity, we are heartened to see that active participation in cricket is growing strongly, and note that female cricket is the fastest growing female sport in Australia. As a community-based, not-for-profit organisation, we are heavily dependent on the support of all of our sponsors, including KFC, to be able to implement the activities we undertake. These range from community-based programs that get kids running around outside to programs in schools, clubs and Indigenous communities, and further activity needed to develop and put elite international cricketers onto the field. In relation to KFC, we believe in a little of everything and everything in moderation. Setting aside the truly elite athletes, the formula that is going to work best for most cricketers and cricket fans is reasonable, not extreme, training and physical activity, together with a balanced diet, not one that features total abstinence from high-energy foods. Our view on alcohol is the same. Our CA advertising featuring Merv Hughes encourages fans to enjoy a beer, but not at the rate of one per over. The overall issue is about balance. Consumer research — commercially confidential, so it can’t be referenced here — shows that KFC consumption in Australia is an occasional treat, not a dietary staple. More broadly, CA is comfortable that Australian cricket’s collective activity has a net positive impact in encouraging healthy and active lifestyles.

Peter Young

To the Editor: Growing revenue from the sale of products for nicotine-replacement therapy (NRT), such as nicotine patches, has fuelled media interest in the likelihood that “reformed smokers” are “getting hooked on nicotine replacement”.1 While there may be anecdotal evidence of long-term use, there are no current population-based data to indicate whether this is the case in Australia. Overseas data suggest long-term use of NRT is low.2,3 For example, a United States study found the median duration of patch use decreased from 30 days to 21 days following over-the-counter NRT availability.2 Another study found that more than 75% of NRT purchases were for 1 month, while only 5% of smokers purchased NRT for more than 3 consecutive months and less than 1% of purchases continued to 24 months.3 An Australian survey conducted in 2000 suggested that most NRT use (61%) was short-term, lasting less than 2 weeks.4 More recently, our 2004 telephone survey of smoking-related perceptions and practices included an item on length of NRT use. The survey involved households selected at random from the New South Wales electronic white pages, with quotas applied to the sample based on NSW census proportions. The study was approved by the University of Newcastle Human Research Ethics Committee. Of the 3503 participants (response rate, 43%), all 539 current smokers and 1013 former smokers were asked about NRT use. Those who had made their most recent quit attempt in the previous 2 years reported on their NRT use during that quit attempt. Of the 138 who had used NRT on their most recent quit attempt, only three (2%) used an NRT product for 12 weeks (the recommended length of use). Only four NRT users (3%) reported using the product for more than 3 months, and none reported using NRT for more than 6 months. It appears that fears of widespread addiction to NRT products are probably unfounded. In fact, lack of compliance with use recommendations, resulting in inappropriately short episodes of use, is probably a bigger problem, and one that may help explain the disappointing effectiveness of NRT under “real world” over-the-counter conditions.5 Data on frequent repeated short-term use of NRT products would be useful to round out the picture on NRT use in the over-the-counter environment.

Christine L Paul · Flora Tzelepis · Raoul A Walsh · Billie Bonevski

To the Editor: In the 4 February issue of the Journal, Playford and colleagues highlighted that clinical schools are encouraging interns and postgraduate year 2 (PGY2) trainees to complete some training in rural locations,1 a good strategy considering the link between living in a rural area and working there later.2 Prevocational training in New South Wales and the Australian Capital Territory is undertaken in 15 training networks administered by the NSW Institute of Medical Education and Training (IMET). Networks typically include a city tertiary referral hospital, a metropolitan district hospital and a rural hospital. Until now, all trainees were allocated to a network by an “optimised-preference” algorithm that maximises trainees’ preference for a particular network but does not guarantee their first choice. Intern and PGY2 rotations occur in the hospitals throughout the network, including rural sites. Over the past few years, IMET has received requests to expand the number of rural sites accredited to provide trainees with all or most of their prevocational training in a rural site because: graduates with an interest in rural medicine want more opportunities for rural-based training; rural hospitals associated with a rural clinical school want to “retain” their rural students after graduation; and investment in rural clinical schools and the expanding service roles of rural hospitals has increased the attractiveness and viability of rural postgraduate training. In 2006, as part of its review into the delivery of prevocational training in NSW, IMET piloted the Rural Preferential Recruitment (RPR) process: Accredited rural hospitals advertise positions under RPR. Interested trainees apply directly to these hospitals while applying for network optimised-preference allocation. These hospitals run a merit-based selection process before the main allocation process. Trainees who receive and accept an offer from a rural hospital are removed from the main allocation list. Trainees who do not gain a position from the RPR process remain in the main allocation process. In 2006, four rural hospitals were involved in RPR and recruited 15 interns for the 2007 clinical year. In 2007, 11 rural hospitals attracted 122 applications from 58 applicants, and 35 doctors began a rural internship in January 2008. IMET recently evaluated the RPR scheme, and there is clear demand for quality prevocational training in rural areas, particularly when applicants can choose their hospitals. We hope this increase in rural exposure during the prevocational years will result in more doctors spending all or part of their careers in rural practice.

Louise Rice · Marie-Louise Stokes · Mark A Brown · Kirsten A Campbell · Cassandra Smith

To the Editor: Cunningham and colleagues discussed the rationale for using a live attenuated vaccine against varicella zoster virus (VZV) in preventing herpes zoster (HZ) in an older population.1 They also noted the difficulties in using a live vaccine in immunocompromised adults. Although generally considered less immunogenic than its live counterpart, an inactivated VZV vaccine would be ideal for vaccinating immunocompromised hosts. There is little information in the medical literature on inactivated VZV vaccines. However, the studies that do exist tested inactive vaccine on adult populations and showed favourable performance when compared with a live vaccine.2,3 Despite these promising results, the inactivated vaccine seems to have gone out of favour. Furthermore, if an inactivated VZV vaccine was used in the childhood vaccination programs against varicella, then it would simultaneously solve two problems caused by the vaccine strain of the virus, namely the development of infectious varicella and the reactivation of the vaccine strain as HZ.4 Cunningham and colleagues discussed the benefits of vaccinating an older population with VZV vaccine,1 but did not raise the intriguing possibility that the vaccination program might reduce rates of listeriosis in older people.4 A recent study examined the T-cell response in mice to latent herpesvirus infection, and found that it led to activation of macrophages that, surprisingly, protected the host against subsequent infection with other pathogens such as Listeria monocytogenes.5 Given that protection from HZ through vaccination is achieved by stimulating T-cell numbers above a critical threshold for HZ,6 it could be hypothesised that VZV vaccinees may be protected against listeriosis, an infection to which older people are more susceptible. The basis of this hypothesis is that macrophage activity would be stimulated by the T-cell response to the VZV vaccine, thereby providing cross-protection against L. monocytogenes. Prospective follow-up of vaccinees in Australia over time could refute or confirm this hypothesis.

Sanjaya N Senanayake

To the Editor: Spriggs and Gillam1 recently evaluated the updated guidance on ethical conduct in human research from the National Health and Medical Research Council (NHMRC),2 with particular reference to paediatric consent. The introduction in 2007 of the National Ethics Application Form (NEAF; http://www.neaf.gov.au) represented an attempt to streamline the process of obtaining ethics approval from multiple human research ethics committees (HRECs) for multicentre research. In 2007, just prior to mandatory introduction of the NEAF, we submitted identical NEAFs to 13 HRECs, covering all Australian states and territories, for an epidemiological study into childhood empyema. All but one HREC accepted the NEAF, but, despite use of the same form by the majority, we identified a variety of inconsistencies. With regard to child consent or assent, 11 HRECs required a single child information sheet and consent form; one required two separate age-appropriate forms; and one questioned the planned involvement of children in the consent/assent process and did not require a child’s consent. This latter response arguably contravenes the United Nations Convention on the Rights of the Child, which provides for a child’s right to information in a form they can comprehend, whether or not they have the ability to make decisions.3 Other inconsistencies included the time taken to obtain approval, which ranged from 1 day to 197 days (median, 31 days). One HREC defined a child as being aged less than 18 years; the others used a cut-off of 16 years. One HREC responded that the application did not specifically address local Aboriginal and Torres Strait Islander peoples’ issues, which suggests that the NEAF may not be sufficient to cover such site-specific requirements. One HREC required plain-language translation of consent and information sheets, and another required Aboriginal translation. Also of concern, the NEAF requires justification for the inclusion of Aboriginal or Torres Strait Islander children and other groups where ethical considerations may be different, such as children with intellectual impairment or mental illness. This approach places the wrong emphasis on the desired outcome, which is to give due consideration to cultural, social, health, psychological and local issues that may introduce ethical concerns that are not the same for all children, and it risks exclusion of some children from research that is relevant to them. We suggest the NEAF should instead include a justification for exclusion of any children as a result of cultural or religious background or social or psychological problems. This would provide an alternative way of gathering information about ethically relevant issues, to ensure best practice in ethical conduct or research. Clearly, there is a lack of consistency across Australia in engaging children in research, including the consent/assent process. We believe that use of the NEAF alone is insufficient to rectify these inconsistencies, and now is the time to consider a single national ethics committee for Australia, similar to the National Research Ethics Service recently introduced in the United Kingdom (http://www.nres.npsa.nhs.uk).

Adam Jaffe · Roxanne E Strachan · Katrina J Williams

To the Editor: I read with interest the letter by Lim and colleagues on anorexia nervosa and senna misuse.1 I have seen abnormal whole body bone scans in patients with severe eating disorders of exactly the same pattern (except for the avid bilateral apical lung and gastric uptake) as the case described. However, I disagree with the interpretation of the bone scan. There was increased periarticular tracer uptake involving long bones. The pattern was not that of hypertrophic osteoarthropathy (HOA). The pattern in HOA is linear tracer uptake by the periosteum, particularly along the distal ends of long bones.2 The scan in the case reported did not show uptake of this pattern, despite radiological evidence showing periosteal reaction and new bone formation of the tibia and fibula at the ankle. The pattern exhibited in this patient was more consistent with metabolic bone disease (increased tracer uptake by the ends of long bones periarticularly, the axial skeleton, calvaria, mandible, sternum and “beading” of costochondral junctions, with faint, or absent, renal uptake),3 although not all of these features were present in this case. Metastatic calcification of the gastric wall (not mentioned by the authors) and upper lobes of the lung was present in this patient. Metastatic calcification of the lungs can be diffuse4 or localised (most commonly) to the upper lobes, as in this case.5 With regard to the bone mineral density results in this case, the authors state that the lumbar and femoral neck T scores were elevated (1.2 and 1.3, respectively). The normal range of the T scores is ± 1.0 standard deviation of young adult normal values.6 Elevated bone mineral density measurements are generally not of pathological significance and are therefore clinically not relevant. In my experience they are usually decreased, and are often osteoporotic, in patients with severe eating disorders.

Andrew F McLaughlin

To the Editor: We share the sentiments of Murphy’s article in the 7 April issue of the Journal.1 As intensive care physicians, the issue of futile care is an almost daily consideration. We agree with his assertion that “the community looks to the (senior) medical practitioners for the security they need to accept decisions of great moment, such as withholding futile treatment”.1 It is common for a referral to an intensive care unit to be made because “We asked the family, and they want everything done”. This is the least confrontational manner of “sorting out the resuscitation status” with the next of kin. Unfortunately, it shifts end-of-life decision making to others, particularly the family in crisis. This places additional stress on an already stressful situation. It often results in undignified, ultimately futile medical interventions and prolongation of dying. It is also a potential pastoral and mental health disaster for families. It is our duty of care to such patients to minimise the iatrogenic damage to their families by having senior clinicians communicate which therapies are appropriate, and thereby help families accept the likely prognosis. Ethically, we believe doctors should not harm families in crisis. Establishing when treatment is futile is difficult. The decision is often qualitative, with differing thresholds for futility. Personal and religious beliefs and anecdotal experience all affect the ability of a clinician to determine when a therapy is futile. We believe it is the duty of the clinician who performs an intervention, not the referring clinician, to determine its utility. A patient should not be referred to an intensive care unit if the intensivist believes the multitude of life-supporting therapies are not of clear benefit. If initiated, the intensivist should determine when such therapies are no longer of benefit. A framework for debate and review of contentious cases should be established within institutions as a matter of process. Sadly, intensive care units are increasingly seen as locations for palliative care. When a patient dies, it is unreasonable for referring clinicians to claim a clear conscience by saying “we did everything we could”, when the outcome is a prolonged, undignified death in an intensive care unit. Such deaths are not just wasteful of resources, but cause unnecessary distress to patients, their families and staff who care for them. We must not mistake “treating” our patients for “caring” for them. Doctors should be part of the solution, not part of the problem.

Thomas R Solano · James D Fratzia

To the Editor: Congratulations to Murphy1 for raising the important and sensitive issue of when to stop trying. This is an issue that needs to be discussed more widely in the community and in hospitals, and presented sensitively to all health students. We know that a significant proportion of the health dollar is spent on the last 12 months of life,2 but, more importantly (as Murphy points out), a clear decision, discussed openly with patients and their families, can save significant pain — both physical and emotional — to all concerned. Advance treatment orders can aid decision making in these situations, but need to be backed up with support for patients’ families when they are to be followed. This issue is with us now but will become more widespread in the future. Health professionals need to be well schooled in this important area of caring. We have to understand when to cease the desire to keep a patient alive. Modern health care has provided incredible advances but we are still not good at knowing and being “strong” in our beliefs and behaviour about when to stop.

Peter M Brooks

To the Editor: In the 7 April issue of the Journal, Murphy encouraged the medical profession to be more proactive about discussing end-of-life care options with family members (or next of kin) with a view to withholding care that may be considered futile by the clinical team.1 While we agree that it is important to offer advice about what course of action the clinical team recommends in a particular case, it is equally important that this advice be based on good evidence and sound clinical judgement. This can be difficult, even for experienced clinicians. Further, it is unwise to leave the family without any alternative but to accept that advice, because this can lead to distrust and disagreement between the family and the treating team. This is not a matter of acquiescing to a family’s unrealistic expectations — often the prognosis is not clear-cut, and there are times when a planned but limited trial of therapy is warranted. In complex situations, the prognosis often becomes obvious, and families can and do draw comfort from the fact that every effort was made, and are then more willing to accept limitation or withdrawal of therapy. In the case of withholding cardiopulmonary resuscitation, the treating team has sole responsibility for the medical opinion, but the family should be involved in the final decision and not have it enforced unilaterally.

Mathew Piercy · Graeme Duke

To the Editor: We support the conclusions reached by Parker and colleagues in their study on the attitudes of Australian medical practitioners to end-of-life decisions.1 They recommend the inclusion of decision-making theory and practice within medical ethics curricula, and highlight the need “to facilitate more discussion between specialties about medical decisions at the end of life”.1 An investigation commissioned to the Australian Institute for Suicide Research and Prevention by the Australian Government Department of Health and Ageing in 2006 aimed to verify receptivity towards, and possible ways of implementing, suicide prevention education in the medical curricula of Australian universities. This mandate also provided the opportunity to assess potential interest in and feasibility for education on end-of-life decisions.2 Our exploratory investigation included interviews of key academics in curriculum or accreditation committees of 10 out of 15 Australian medical schools, 24 general practitioners from six Australian states, and 373 medical students from the University of Queensland.2 Representatives of the medical schools considered it a “very high priority” to implement adequate education on end-of-life issues, including euthanasia, in medical curricula. Most of the interviewed GPs (21/24) and 80% of medical students agreed with this sentiment. Common themes that emerged from the study were the need for good preparedness in coping with difficult situations, and the desired capacity in competently handling decisions that are perceived to be requested with increasing frequency in clinical scenarios.2 End-of-life issues nearly always involve aspects that go beyond the treatment of somatic conditions. Moral convictions, religious beliefs, and self-identification processes (with the patient) all compound the challenge physicians face in their practice. The very complexity of the challenge should push towards more knowledge, and this should be obtained through modern medical curricula.

Diego De Leo · Jacinta L Hawgood

To the Editor: In their recent “Clinical Update” on adrenal insufficiency, Jung and Inder1 state: In patients with adrenal insufficiency who are fasting before procedures, glucocorticoid therapy must be continued, by parenteral routes if necessary. A recent case report has highlighted the adverse consequences of omitting oral steroid therapy in a patient who was fasting before a surgical procedure. The patient developed hypotension and acute renal failure. The patient described in the case report2 was admitted with septic arthritis. His usual cortisone dose of 12.5 mg had been omitted that evening, and his morning dose of 25 mg was not given the next day until after he had returned from the operating theatre. Over the next 3 days, he became overtly septic, and returned to theatre for another knee washout. Cortisone was not given during this time. When he developed acute renal failure on Day 5, dehydration and gentamicin toxicity were listed as possible causes. The article by Jung and Inder does not make it clear that the case report contains nothing of relevance to the management of patients with adrenal insufficiency who are fasting for routine surgical procedures, as this man’s hypotension and acute renal failure actually developed over 5 days in the context of sepsis, dehydration and possible gentamicin toxicity, in addition to prolonged withholding of cortisone and two operations.

Ian J Woodforth

To the Editor: The recent article by Jung and Inder1 provides sensible advice for the safe management of adults with adrenal insufficiency (AI) during illness and surgery, without risking adrenal crisis or excessive steroid dosing. However, the authors make no reference to paediatric practice and no guidelines have been provided for the body-size-related steroid doses required in paediatric patients with AI, either for routine steroid replacement or during illness and surgery. It is important that doctors be aware that the doses recommended by Jung and Inder are not suitable for children with AI. In keeping with recent studies of daily cortisol production, daily hydrocortisone replacement doses of 6–8 mg/m2/day are now recommended for children with secondary AI (eg, due to adrenocorticotropic hormone deficiency), provided the patient has no hypoglycaemia or symptoms of cortisol deficiency.2 In children with primary AI, higher hydrocortisone doses are often necessary (up to 10–15 mg/m2/day) — for example, to minimise adrenal androgen secretion in children with congenital adrenal hyperplasia.3 During minor illness (as defined in Box 3 of Jung and Inder’s article1), a child’s usual daily oral dose of glucocorticoid should be doubled or tripled until recovery.3,4 However, for children with secondary AI who are on the lower doses of daily hydrocortisone (about 6–8 mg/m2/day), these multiples may not constitute adequate doses during stress. In these patients, per-m2 dosing is more accurate (ie, 30–40 mg/m2/day for minor illnesses). During moderate-to-severe illness, for patients who are vomiting, those who have experienced trauma and those undergoing anaesthesia and surgery, the following doses of intravenous hydrocortisone are recommended: For children aged < 3 years: 25 mg initial dose then 25–30 mg/day; For children aged 3–12 years: 50 mg initial dose then 50–60 mg/day; and For adolescents and adults: 100 mg initial dose then 100 mg/day. These doses are in keeping with national4 and international3 recommendations, and equate to doses of 60–100 mg/m2/day of hydrocortisone. The more accurate per-m2 dosing should be used for children who are not within the normal weight range for their age. These recommendations for children are extrapolated from adult studies and also based on expert consensus. Attention to the specific body-size dose adjustments required in paediatric prescribing can provide safe levels of steroid cover while avoiding exposure to excessive steroid doses.

Ann M Maguire · Maria E Craig · Christopher T Cowell

To the Editor: The excellent article by Jung and Inder1 in a recent issue of the Journal contains a detailed discussion of different regimens proposed for glucocorticoid supplementation in the perioperative period and makes recommendations for the use of hydrocortisone therapy according to the degree of “surgical stress”. It is worth noting that, in many cases, these recommendations and the detailed advice of endocrinologists regarding individual patients are rendered moot by the changes in routine perioperative antiemetic therapy that have occurred in the past decade. The use of intravenous dexamethasone as an antiemetic has been the subject of much clinical research. The IMPACT study2 showed that it has an antiemetic efficacy similar to that of ondansetron or droperidol when given prophylactically. Dexamethasone is less expensive than either of these drugs and is ineffective as rescue therapy in the setting of postoperative nausea and vomiting (PONV), unlike the alternative drugs. As a result, it is used routinely on induction of anaesthesia in many cases of surgery associated with an increased risk of PONV or where PONV would pose a risk of injury or delayed discharge. A range of doses of dexamethasone for antiemetic prophylaxis has been investigated without finding superior efficacy from higher doses (of up to 1.0 mg/kg).3 The dose typically used in clinical anaesthesia practice is 0.05–0.1 mg/kg. This is equivalent in glucocorticoid activity to more than the highest dose of hydrocortisone described in the guidelines of Jung and Inder1 and should provide a self-tapering effect over 2–3 days, consistent with their recommendations for hydrocortisone dosing.

James A Mitchell

In reply: We thank Woodforth for his interest in our article.1 The cited case report2 involved a patient with panhypopituitarism who had septic arthritis following a total knee replacement, requiring knee washout. As stated by Woodforth, the patient was without glucocorticoid replacement for 5 days, during which time he underwent two surgical procedures. Symptoms of cortisol deficiency were described on Days 1 and 2 postoperatively, with overt sepsis not manifesting until Day 3. The absence of adequate glucocorticoid replacement while the patient was under a “nil oral” instruction and suffering sepsis was undoubtedly a contributory factor in his decline, given that his condition improved significantly after he had received 24 hours of intravenous hydrocortisone treatment and other supportive care. It appears that the cortisone acetate was withheld because of concerns about administering it without food, as other medications were in fact given. We stand by our assertion that patients with proven or suspected cortisol deficiency should receive adequate glucocorticoid replacement before and after surgery, according to the likely stress of the procedure. Often, for minor procedures, an oral route of administration will suffice. Doses of oral glucocorticoids given under these circumstances do not need to be taken with food. If there are sound clinical reasons for the patient not to have any medications orally, then parenteral administration is appropriate.1 Maguire and colleagues correctly point out that the glucocorticoid dosage recommendations in our article are suitable only for adults. They have made a significant contribution to the literature on the investigation and management of paediatric adrenal insufficiency and we would like to thank them for providing the appropriate glucocorticoid doses for paediatric patients under stress. We are aware of the use of dexamethasone as a perioperative antiemetic, as outlined by Mitchell, although it is not clear how widespread this practice is. He is correct in stating that in cases in which dexamethasone is used for this purpose, the glucocorticoid dose thereby provided is likely to be more than adequate for adrenal replacement. However, dexamethasone has no mineralocorticoid activity, and this must be taken into account when treating patients with primary adrenal insufficiency. Doses of hydrocortisone greater than 50–75 mg per 24 hours provide adequate mineralocorticoid replacement. If dexamethasone is used for patients with primary adrenal insufficiency undergoing surgery, it is imperative that the patient continue to take oral fludrocortisone throughout the perioperative period to provide mineralocorticoid replacement. This highlights the need for good communication between the patient’s general practitioner, endocrinologist, surgeon and anaesthetist to ensure the best patient outcome.

Caroline Jung · Warrick J Inder