Child health

To the Editor: The study by Robson and colleagues1 predictably produced alarming media headlines. However, we feel the study contains potential inaccuracies that seriously undermine the conclusion that the baby toll is lower in private hospitals. Did the authors ascertain the true impact of fetal abnormality or conditions requiring transfer to tertiary care? Women with threatened preterm labour often transfer to the public system and subsequently remain under the care of public high-risk teams. Babies with a known congenital anomaly detected antenatally by private obstetricians may be similarly transferred. This highest level of care is only available in public hospitals, usually those with dedicated subspecialist services in maternal–fetal medicine, neonatology or neonatal surgery. When babies who have been transferred from private hospitals to the public neonatal intensive care system subsequently die within 28 days of birth, this may be recorded as a public hospital death. The authors stated that the “major adverse outcome associated with social disadvantage is low birthweight” but that assessment of the effect of social disadvantage was beyond the scope of their study. Not accounting for the effect of low birthweight is unacceptable. The National Perinatal Data Collection records birthweight accurately and is easily used to remove the bias of low birthweight. An internationally accepted indicator of optimal perineal outcome is the rate of intact perineum. This is known to be lower in private hospitals but was curiously not reported. Further, a prospective data audit in a tertiary hospital revealed that where episiotomy extends to third- or fourth-degree tear, this is only reported as episiotomy.2 Thus, with twice the rate of episiotomy in private hospitals,3 and its association with severe perineal trauma, this outcome could be seriously under-reported in Robson et al’s study. The authors identify the significantly higher rate of caesarean sections in private hospitals as one of the measurable benefits of this model of care and dismiss any concerns as “orthodoxy”. They have overlooked the significant morbidity and mortality among term neonates associated with the rise in caesarean rates, both elective and following labour. Research using detailed Australian and New Zealand Neonatal Network data to ascertain admission rates of babies of ‘‘low-risk’’ women to neonatal intensive care units and special care nurseries not only found higher rates of admission across each gestational age group after elective caesarean section but also reported the death of two infants.4 Such morbidity and mortality is arguably the most important differential of care experienced by women who give birth in private or public hospitals.

Sally K Tracy · Alec W Welsh · Hannah G Dahlen · Mark B Tracy

To the Editor: A previous report from our institutions identified a steady increase in the prevalence of paediatric treadmill friction burn injuries, from three in 2001 to 17 in 2006.1 We sought to determine whether there was any change in this trend during the past 2 years. Children younger than 16 years with treadmill-related injuries were identified from prospectively collected data from burns and trauma databases maintained by the trauma research nurses at two paediatric tertiary trauma centres in Sydney (the Children’s Hospital at Westmead and Sydney Children’s Hospital) between January 2007 and December 2008. Sixty-five children sustained treadmill-related injuries (17 in 2007 and 48 in 2008); 43 were boys. The mean age at the time of the injury was 3.7 years (range, 9 months to 14 years). Friction burns ranged from less than 1% to 7% of total body surface area, and most patients sustained a total body surface area burn of 1% or less (58 patients). The most common site of injury was fingers and/or hand (49), followed by forearm or upper arm (6), and torso (5). In most cases, a limb or part of a limb was trapped between the rear roller and the treadmill belt. Fourteen patients required surgery, including 13 who underwent a skin grafting procedure. Most injuries occurred while the treadmill was in use by others, with the children approaching unnoticed from behind (46). In nine cases, the injury happened when the patients themselves, at a mean age of 7.8 years (range, 2–12 years), were using the treadmill. The substantial increase in prevalence of treadmill injuries in children during the past 2 years may be related to increased sales of treadmills as the community becomes more conscious of obesity. The data also reflect other Australian studies that show that children younger than 5 years are at greatest risk, accounting for 90% of paediatric treadmill injuries during the period January 2004 to June 2007.2 Despite the risk of injury, particularly for children, there appears to be no current national regulations governing the supply of treadmills or advice that should be given to customers at the point of sale. The New South Wales Government introduced legislation in June 2009 mandating prominent permanent warning labels to be affixed to all new treadmills — the Fair Trading Amendment (Treadmills) Regulation 2008 (NSW). The NSW Office of Fair Trading, with assistance from the NSW Severe Burn Injury Service and Kidsafe NSW, has developed an alert poster (copies of which may be downloaded or ordered from their website) for display at childcare centres, playgroups and places where domestic treadmills are sold.3 The Australian Competition and Consumer Commission recently published a safety alert brochure on domestic treadmills, which contains a safety checklist.4 Although helpful, the brochure does not include previous recommendations such as caution with headset use (ie, decreased awareness of children near the treadmill), and the use of mirrors or alternative positioning to ensure children approaching the treadmill can be seen.1 As most injuries occur within the first 6 months of purchase of the treadmill,5 educating parents seems to be most important around the time of purchase. Design modifications could also reduce the risk of entrapment of a digit or hand.2 It is likely that, without better application of current injury prevention strategies, the prevalence of these injuries will continue to increase.

Lawrence H Kim · Deborah A Maze · Susan Adams · Sarah Guitonich · Siobhan Connolly · Anne Darton · Andrew J A Holland

To the Editor: Contact burns in children caused by hair-straightening devices are increasingly common. Although the dangers of hair dryers and other similar devices are well known,1 there is less awareness of the risks associated with hair straighteners. The relevant Australian Standard does not mention hair straighteners.2 Four recent studies from the United Kingdom have reported on this problem,3-6 but there is no readily identifiable published information from Australia. Hair straighteners consist of two opposing ceramic plates that are held apart when not in use. The plates are reported to reach average temperatures of 169.5°C within 4 minutes 20 seconds of being switched on. They can cause burns (temperature > 66°C) on short-term contact (10 seconds) for a period of up to 9 minutes 20 seconds after being switched off,3 and can take 30 minutes to cool to below 50°C, at which temperature they can cause superficial burns on prolonged contact. Using data collected by the Stuart Pegg Paediatric Burns Centre at the Royal Children’s Hospital, Brisbane, and the Queensland Injury Surveillance Unit, we identified 22 patients treated for hair-straightener injuries between January 2004 and June 2009. Sixteen of these were treated within the past 2 years. The median age of patients was 43.4 months (range, 9 months to 14 years). A mean of 1% of total body surface area was involved. Injuries were to the forearm and hands (16 patients) (Box), foot and lower leg (five patients), and the back (one patient). The burns were significant, with 19 partial-thickness burns, and three full-thickness burns requiring surgery. Nine of the 22 children (41%) required long-term scar management. We observed two typical patterns of injury. In toddlers (16 patients aged 9–48 months), the main mechanism of injury was grasping or pulling down a hair straightener that was either turned on or cooling, with inadequate supervision a common factor. An early-teen group (three patients) had self-inflicted burns from accidental contact or misuse, including one patient who misguidedly used the device in an attempt to remove leg hair, sustaining full-thickness burns requiring skin grafting. Increased awareness of the potential dangers of hair straighteners might help prevent burns. We suggest four precautions: Hair straighteners should be placed out of reach of children during use and storage; Children should be supervised while the device is warming or cooling; Manufacturers should label the device to warn of potential dangers; and Manufacturers should either redesign the device so that plates are not exposed, or provide a cool-touch cover. Burns to a toddler’s hand caused by contact with a hair-straightening device

Zoe M Poiner · Michael D Kerr · Belinda A Wallis · Roy M Kimble

Clinical record A 4-month-old girl was referred to an ophthalmology clinic in May 2008 for assessment of a left convergent squint (esotropia). First noticed 3 weeks previously, the squint had become increasingly prominent. The child’s parents had also noted increased watering of the eyes, ascribed, by the child’s paediatrician, to congenital nasolacrimal duct obstruction. The infant was born preterm (at 36 weeks’ gestation), and had a history of congenital hypothyroidism and a perimembranous ventricular septal defect. There was no family history of glaucoma, and no history of intrauterine infection or birth trauma. Examination confirmed left esotropia. The infant’s eye movements were full, implying a concomitant squint. Her pupils were reactive to light, and with no afferent defects. She was photophobic when her pupillary light reflexes were tested. Aversion to light prevented assessment of visual function. There was tearing (epiphora) in both eyes. The corneas were mildly cloudy and appeared enlarged (buphthalmos); the horizontal corneal diameter measured 13.0 mm in the right eye and 12.5 mm in the left (Figure). A more detailed examination was performed under general anaesthesia. Intraocular pressure (IOP) was elevated at 27 mmHg in the right eye and 28 mmHg in the left (IOP reference range [RR] for an infant under general anaesthesia, 5–14 mmHg).1 The angles were open, and the optic nerve cup-to-disc ratio was increased bilaterally (0.6; RR for infants, < 0.4). Bilateral primary congenital glaucoma was diagnosed. Treatment began immediately with topical ocular antihypertensives and oral acetazolamide, and bilateral trabeculotomy was performed in a staged manner over the next month. At follow-up 13 months after diagnosis, ocular antihypertensive agents had been discontinued, and IOP was acceptable (16 mmHg bilaterally). Horizontal breaks in the basement membrane of the corneal endothelium (Haab striae) were present. Although visual outcome could not be assessed until the child was older, acuity (measured using Teller Acuity Cards) was subnormal bilaterally and worse in the right eye (20/380) than in the left (20/190). To treat amblyopia, the left eye is currently being patched for 2 hours a day. The patient will be reviewed at regular intervals to assess visual function and measure IOP. This case of primary congenital glaucoma (PCG) illustrates the typical clinical features of this condition, which, if untreated, results in blindness. In this case, the infant was referred to our ophthalmology service by a general paediatrician, who was reviewing her for thyroid and cardiac disease; neither of these conditions has a known association with congenital glaucoma. The difficulty in recognising PCG lies partly in its rarity; PCG has a reported incidence of 1 in 30 000 live births in Australia.2 Congenital glaucoma can also be mistaken for a number of common, benign conditions: conjunctivitis, corneal injury, in-turning eyelashes from associated conditions such as epiblepharon (a congenital anomaly in which a fold of skin lies across the lower lid margin), or, as in this case, congenital nasolacrimal duct obstruction. The significance of our patient’s squint is uncertain, although most likely it was a result of her deteriorating visual function. The pathophysiology of PCG appears to be dysgenesis of the trabeculum or its surrounding structures, which results in impaired aqueous outflow and increased intraocular pressure (IOP).3 The conventional outflow path for aqueous humour is shown in the Box. Elevated IOP results in breakdown of corneal endothelial function and an influx of aqueous humour into the normally anhydrous corneal stroma. Prolonged elevation of IOP results in excavation and undermining of the neural and connective tissue of the optic disc, and the development of optic neuropathy. The first clinical signs of PCG include the triad of blepharospasm, photophobia and excessive tearing. Progressively, the corneas become oedematous, lose clarity, and, if untreated, may become opaque. Elevated IOP in an immature eye also results in progressive enlargement of the cornea and sclera, known as buphthalmos (“ox eye”). Potential for corneal enlargement generally ceases when the child reaches 3 years of age, although scleral enlargement can increase beyond this age.3,4 The horizontal corneal diameter in full-term newborn infants averages 9.8 mm; a corneal diameter greater than 11 mm is enlarged.5 A horizontal corneal diameter greater than 12 mm in a 12-month-old child suggests abnormality.6 Progressive enlargement of the cornea may also result in horizontal breaks in the basement membrane of the corneal endothelium (Descemet membrane), known as Haab striae.3 Lessons from practice Congenital glaucoma is a sight-threatening differential diagnosis in an infant who presents with watering eyes. Key clinical features of congenital glaucoma are a cloudy cornea, excessive tearing, blepharospasm, photophobia and an enlarged globe. In infants, corneal size is a surrogate marker of intraocular pressure. Enlargement and asymmetry in corneal diameter requires further investigation. Patients with suspected congenital glaucoma require urgent referral to an ophthalmologist. The mean age of diagnosis is 4.4 months.2 Severe disease is occasionally observed in neonates, although in its early stages PCG tends to have few signs. An urgent referral to an ophthalmologist is required if tearing is associated with photophobia or blepharospasm; the cornea is hazy; or the eye or cornea is enlarged or asymmetrical. It is important to distinguish PCG from congenital nasolacrimal duct obstruction: infants with the latter also have excessive tearing, but, in contrast to PCG, the cornea remains clear, there is no enlargement of the globe and no photophobia or blepharospasm. Nasolacrimal duct obstruction is common, typically innocuous, and frequently resolves spontaneously within the first 12 months of life. It can be safely assessed and managed by the primary-care physician. Diagnosis of PCG relies on IOP measurement. The patient is usually assessed under general anaesthesia, not only to aid IOP measurement, but to permit accurate measurement of corneal diameter and thickness, detection of refractive errors, viewing of the angle structure and a detailed examination of the optic disc. Surgery is the first-line treatment for PCG. The two most common procedures are goniotomy and trabeculotomy, both of which involve microsurgical dissection of the trabecular meshwork, with the aim of increasing aqueous outflow. Ocular antihypertensive agents are an important adjunct to surgery, and are often used as a temporising measure. Screening for amblyopia and correction of asymmetrical refractive errors are undertaken until the child’s vision is developmentally mature to ensure the best visual outcome achievable for the child. Lifelong follow-up is often required. With modern treatment, a visual outcome of better than 6/15 is achieved in up to 79% of cases of PCG; whereas, if untreated, this condition carries an exceedingly poor visual prognosis.3,7 Normal production and outflow of aqueous humour Aqueous humour is produced by the ciliary body and passes from the posterior chamber through the pupil into the anterior chamber. Its outflow path includes the trabecular meshwork, Schlemm canal and the episcleral venous system. The proposed pathophysiology of primary congenital glaucoma is dysgenesis of the trabecular meshwork.

Adam K Rudkin BM BS, BJuris, BA(Hons) · Jwu J Khong MB BS(Hons), MMed · Theresa M Casey MB BS, FRANZCO

To the Editor: Wiseman and colleagues reported the 9-month virological follow-up of babies born to pregnant women attending urban antenatal clinics who tested positive for hepatitis B surface antigen (HBsAg).1 Evaluation of outcomes is vital to determine implementation and effectiveness of current policy. The authors state that hepatitis B immunoglobulin (HBIG) and hepatitis B virus (HBV) vaccine were delivered within 12 hours of birth to all infants of HBsAg-positive mothers. Nine months after birth, transmission was documented in only four infants, all of whom were born to mothers who were positive for hepatitis B “e” antigen (HBeAg) and had very high HBV DNA levels (> 108 copies/mL). Yet one of the four infected infants had inadvertently not received the “routinely offered” HBIG. Whether any other babies (even if not infected) also failed to receive timely active and passive immunisation was not explicitly reported. The other three infected infants completed HBIG injection and HBV vaccination according to the “recommended schedule”. Given that the Australian immunisation handbook states that [t]he first dose of monovalent hepatitis B vaccine should be given at the same time as HBIG ... as soon as possible — preferably within 24 hours of birth, and definitely within 7 days,2 the exact time is unclear. Potentially, a delay of many hours to many days could occur. Yet, for all infectious diseases for which post-exposure prophylaxis is given, administration as soon as possible after exposure is universally recommended to prevent transmission.3 For babies born to known HBeAg-positive mothers, particular effort is warranted to ensure that they receive HBIG and HBV vaccine immediately after delivery, and certainly within hours of birth. There are many difficulties in achieving high rates of follow-up in this group, and only 66% of babies in the study by Wiseman and colleagues had virological follow-up results available. Unfortunately, the authors did not make the important distinction between babies lost to follow-up and those who were not yet 9 months old at the time of follow-up. This is in spite of the fact that the study included many South-East Asian women, who have markers of high HBV replication and whose follow-up is suboptimal.4 Evaluation of HBV vaccination policy requires that studies report fully on outcomes, including loss to follow-up. Also, given that delay in administration of HBIG and HBV vaccine after delivery may be a critical source of variation in outcome, future studies should specifically report this information separately for all births to HBsAg- and HBeAg-positive mothers, and for any cases in which transmission does occur.

Sandra C Thompson

In reply: We thank Thompson for her comments. We endeavoured to contact women by phone, by letter, or through their local doctor (if known). With respect to the 69 infants lost to follow-up, five of the mothers declined assessment, four had moved interstate or overseas with their families, five had infants who had not reached 9 months of age, and the remaining mothers were uncontactable. Follow-up of a cohort of this kind is difficult, for reasons that include language barriers and high rates of mobility. Furthermore, at the time of the study, testing the babies was not standard practice and not enthusiastically received by all mothers. We are not a public health unit and are not resourced to pursue follow-up beyond the measures described. Nevertheless, through strong engagement with the mothers, who were referred on the basis of their hepatitis B virus (HBV) infection, we achieved follow-up for a large number of babies. The data stand as valuable but not perfect. As mentioned in our article,1 vaccination practice for babies born to infected mothers is for hepatitis B immunoglobulin and the first HBV vaccine dose to be given (in opposite thighs) within 12 hours of birth. The babies’ vaccination records were checked by consulting the “blue book”, a standardised medical record for infants, and, for those infected, by cross-checking with the hospital medication chart.

Miriam T Levy · Elke Wiseman

Australian autism handbook. The essential resource guide for autism spectrum disorders. Benison O’Reilly, Seana Smith. Sydney: Jane Curry Publishing, 2008 (xv + 399 pp). ISBN 978 0 9804758 1 4. Autism is not as rare as we once thought. Recent Australian research indicates autism occurs in one child in 160, and half a million Australians are living in a family that has a child or adult with autism. The annual cost of autism spectrum disorders (ASDs) to the community is estimated at between $4.5 and $7 billion. It is an expensive disability for both the government and for families. For example, the cost of intensive applied behavioural analysis for a family is around $40 000 per annum, with a program in the preschool years lasting 2 to 4 years. While most of the literature on autism, especially for parents, is published in the United States or the United Kingdom and refers to American or British services, we now at last have an Australian guidebook for families. The authors are parents of children with ASD, and the book is primarily written for families of a newly diagnosed child. However, the Australian autism handbook will be invaluable for clinicians as a resource when talking to families and providing advice on services and resources. The text often refers to Australian research, and we need to recognise the degree and depth of Australian expertise and research on ASD. This book provides current information on services in each state or territory, the latest Medicare initiatives, and research areas of Australian specialists and academics. Clinicians will be interested in the perspectives and experiences of families (such as the susceptibility of parents of a child with autism to develop signs of depression), and to learn more about the latest treatments that parents have heard about and may request for their son or daughter with autism.

Tony Attwood

To the Editor: We report a case of a 13-year-old girl with cystic fibrosis (CF) and chronic Pseudomonas aeruginosa lung infection who developed an unusual infection that was challenging to manage. At a regular review, and with no obvious change in clinical respiratory status, the patient’s forced expiratory volume in 1 second (FEV1) was 70% of the predicted value — a drop from her usual 90%. A subsequent 3-week admission, including treatment with standard antipseudomonal antibiotics, physiotherapy and addition of nebulised dornase alfa, did not significantly improve her lung function. She was discharged home on a trial of azithromycin. One month later, she had a non-productive cough, and a bronchoalveolar lavage specimen showed no growth on culture. Four months later, the patient presented with increased non-productive cough and sudden further deterioration in FEV1 to 52% of the predicted value. She was admitted and given standard intravenous antipseudomonal antibiotics. Culture of a repeat bronchoalveolar lavage specimen grew Mycobacterium abscessus, sensitive to clarithromycin, imipenem and amikacin; hence, the patient was given intravenous imipenem and amikacin for 3 weeks. During this period, high-resolution computed tomography (CT) of the patient’s chest showed mucus plugging, marked diffuse parenchymal involvement with typical “tree-in-bud” appearance and, surprisingly, given her poor lung function, only moderate bronchiectasis (Box). Two years earlier, results of a chest CT scan were normal. The patient was discharged home on long-term nebulised amikacin, oral ciprofloxacin and oral clarithromycin. Her lung function gradually improved after discharge and, 6 months later, her FEV1 was 69% of the predicted value and a sputum culture produced no growth. CF is a risk factor for non-tuberculous mycobacterial (NTM) lung disease, which is notoriously difficult to eradicate. A recent multicentre prospective study in the United States estimated that, in patients with CF who are older than 10 years, the prevalence of non-tuberculous mycobacterium was around 13%. The most common species were M. avium complex (72%) and M. abscessus (16%).1 Another study suggested that M. abscessus was more common in paediatric patients.2 Clinical signs and symptoms of NTM infections are usually difficult to distinguish from those of chronic respiratory infections that occur during the advanced stages of CF. High-resolution CT often reveals features of parenchymal involvement, as demonstrated in our patient. No guidelines exist for treating NTM infections in the CF population. However, for M. abscessus infection, oral clarithromycin in combination with intravenous amikacin and either cefoxitin or imipenem for 2–4 months has been recommended, with sputum surveillance for at least 12 months after a negative culture result.3 Suppressive maintenance therapy with clarithromycin, intermittent intravenous antibiotics and aerosolised amikacin have all been reported, but not confirmed by controlled studies. Surgical resection may be curative in localised disease. As the life expectancy of patients with CF improves, the prevalence of NTM infections is likely to increase. The American Thoracic Society recommends that all patients with CF who are on macrolide therapy should be screened annually for atypical mycobacteria.3 Atypical mycobacteria should always be borne in mind when treating patients with CF and an unexplained decline in lung function. Computed tomography scan showing diffuse parenchymal involvement, mucus plugging and moderate bronchiectasis in a girl with cystic fibrosis and non-tuberculous mycobacterial lung disease

Abdullah A Yousef · Adam Jaffé

Australia is in a unique position to assess the impact of two different rotavirus vaccines In 1973, Ruth Bishop and her colleagues in Melbourne were the first to identify rotavirus gastroenteritis in infants. Rotavirus has since been recognised as the most frequent cause of severe childhood gastroenteritis worldwide. In temperate climates, infection occurs predominantly in winter and spring. The spectrum of disease ranges from severe gastroenteritis to mild or clinically inapparent infection. Reinfection is common. In Australia, the peak age of hospitalisation for rotavirus infection is 6–24 months; however, in Indigenous children, infection occurs earlier and is more severe.1 About half of the 20 000 annual hospitalisations for acute gastroenteritis in Australian children under 5 years of age are attributed to rotavirus.2 The first rotavirus vaccine licensed in the United States (RotaShield [Wyeth, Madison, NJ, USA]) was withdrawn from use in 1999, after barely 9 months, due to an increased occurrence of intussusception after vaccination (attributable risk, one case per 10 000 vaccine recipients). Two other live attenuated oral vaccines (RotaTeq [Merck, Whitehouse Station, NJ, USA], a pentavalent human–bovine reassortant vaccine; and Rotarix [GlaxoSmithKline, Rixensart, Belgium], a human monovalent vaccine) have recently been approved for use in many countries after extensive clinical trials showed them to be effective against the most common circulating strains, and found no evidence of an association with intussusception.3,4 The RotaTeq vaccine was introduced into the US vaccination schedule in February 2006. A report from a national network of sentinel laboratories, published in June 20085 and updated in October 2008,6,7 shows that the 2007–2008 US rotavirus season was significantly delayed, shortened and diminished compared with the 2000–2006 seasons. Only 4% of children aged under 3 years who were hospitalised with acute gastroenteritis had rotavirus-positive stools in 2008 compared with 56% in 2006, and only 9% of emergency room patients with acute gastroenteritis tested positive for rotavirus compared with 58% in 2006. Reductions in hospitalisation of up to 85% for rotavirus gastroenteritis and 56% for all-cause diarrhoea in young children were also reported, suggesting very large savings in hospital costs.6 Although these findings need confirmation over future seasons, this rapid vaccine impact is particularly striking given that, at the time, the estimated vaccine coverage was just 56% for one dose in infants aged 3 months and 34% for three doses by age 13 months.5 Reassuringly, preliminary data from surveillance in the US over the first 19 months of its rotavirus program, when over 9 million doses of vaccine were distributed, do not indicate any association of RotaTeq with intussusception or other serious adverse events.8 In Australia, rotavirus vaccination commenced in the Northern Territory in October 2006 and in the remaining jurisdictions in July 2007. Rotarix is used in the NT, New South Wales, Tasmania and the Australian Capital Territory, and was used in Western Australia until May 2009. RotaTeq is used in Victoria, South Australia and Queensland. This geographical split results in about half of the birth cohort receiving Rotarix (two-dose schedule) and half receiving RotaTeq (three-dose schedule). Program implementation has been faster in Australia than in the US, with an estimated coverage, by December 2008, of 87% for at least one dose of vaccine received by 4 months of age, and 84% for a full vaccine course (either two or three doses) received by 13 months of age (Mr Brynley Hull, Epidemiologist, National Centre for Immunisation Research and Surveillance, personal communication). Australia is in a unique position to assess the impact of the two vaccines because of the geographical split. However, it is important to recognise that the prevailing strains of rotavirus vary by region and change unpredictably from year to year.9 As the composition of the two licensed vaccines differs, effectiveness against certain strains, such as those not contained in the vaccines, may vary. An early study during a rotavirus outbreak in the NT showed that Rotarix was effective against the lately emerged G9 strain.10 Although Australia has an established national strain surveillance system,9 it needs to be enhanced, as samples for strain typing have not always been representative of all geographical areas or accompanied by clinical data. National disease notification using laboratory-confirmed cases needs to be implemented, and further studies of field effectiveness should be undertaken. Adverse events following vaccination in Australia are reported and reviewed nationally. The vaccines have not been associated with an excess of serious adverse events during the first 6 months of the program.11 Additionally, all cases of any-cause intussusception are reported by paediatricians to the Australian Paediatric Surveillance Unit, with enhanced active surveillance for intussusception being undertaken in a pilot program. Although efficacy of both vaccines persisted in clinical trials for 2 years,12,13 the full extent and duration of vaccine effectiveness, the degree of herd immunity, and whether a shift in disease incidence to older age groups has occurred, are yet to be determined. Identifying the emergence of new strains of rotavirus, either spontaneously or under vaccine pressure, will also be essential. Successful implementation of rotavirus vaccination in developing countries — where more than 95% of the world’s annual rotavirus deaths occur — is also much anticipated, possibly using new, less costly vaccines.7 In this issue of the Journal, Lambert and colleagues14 report on rotavirus notifications and laboratory tests performed in Queensland before and after the introduction of an infant rotavirus vaccination program. This is the first published evidence of a substantial population-based decline in rotavirus disease activity in Australia since introduction of the vaccine. Furthermore, laboratory-confirmed rotavirus infection appears to have declined not only in the cohort eligible for vaccination (infants aged under 2 years), but also in older children and in adults, suggesting a herd immunity effect, as has been observed in preliminary data from the US.7 Much points to the potential for Australia’s rotavirus vaccine program to have a substantial impact on acute childhood gastroenteritis, both in terms of health care utilisation and broader social and economic effects. It is important to document this with well targeted research and surveillance.

Kristine K Macartney MB BS, MD, FRACP · Margaret A Burgess MD, FRACP, FAFPHM

Objective: To assess the impact of introducing a publicly funded infant rotavirus vaccination program on disease notifications and on laboratory testing and results.Design and setting: Retrospective analysis of routinely collected data (rotavirus notifications [2006–2008] and laboratory rotavirus testing data from Queensland Health laboratories [2000–2008]) to monitor rotavirus trends before and after the introduction of a publicly funded infant rotavirus vaccination program in Queensland in July 2007.Main outcome measures: Age group-specific rotavirus notification trends; number of rotavirus tests performed and the proportion positive.Results: In the less than 2 years age group, rotavirus notifications declined by 53% (2007) and 65% (2008); the number of laboratory tests performed declined by 3% (2007) and 15% (2008); and the proportion of tests positive declined by 45% (2007) and 43% (2008) compared with data collected before introduction of the vaccination program. An indirect effect of infant vaccination was seen: notifications and the proportion of tests positive for rotavirus declined in older age groups as well.Conclusions: The publicly funded rotavirus vaccination program in Queensland is having an early impact, direct and indirect, on rotavirus disease as assessed using routinely collected data. Further observational studies are required to assess vaccine effectiveness. Parents and immunisation providers should ensure that all Australian children receive the recommended rotavirus vaccine doses in the required timeframe.

Stephen B Lambert MB BS, MAppEpid, FAFPHM · Cassandra E Faux MSc(ClinMicro) · Lisa Hall BTech(BiomedSc)(Hons), PhD · Frances A Birrell MPH, MAppEpid, GCSc(Stats) · Karen V Peterson DipT, BEd, MHlthSc · Christine E Selvey MB BS, MSc · Theo P Sloots BSc, GradCertMgt, PhD · Michael D Nissen BMedSc, FRACP, FRCPA · Keith Grimwood MD, FRACP

Extracorporeal membrane oxygenation (ECMO) is a technique that involves oxygenation of blood outside the body, and provides support to selected patients with severe respiratory or cardiac failure. The two major ECMO modalities are venoarterial and venovenous. Data from several randomised trials support the use of ECMO in neonatal respiratory failure, and a recent randomised controlled trial of ECMO in adults has produced encouraging results. The evidence base for ECMO use in cardiac disease is developing, but progress has been slowed by considerations of clinical equipoise and evolving indications for ECMO. Advancing ECMO technology and increasing experience with ECMO techniques have improved patient outcomes, reduced complications and expanded the potential applications of ECMO. Awareness of the indications and implications of ECMO among doctors managing patients with severe but potentially reversible respiratory or cardiac failure may help facilitate better communication between health care teams and improve patient recovery.

Steven J Lindstrom MB BS(Hons), BMedSc(Hons) · Vincent A Pellegrino MB BS, FRACP, FJFICM · W Warwick Butt MB BS, FRACP, FJFICM

Could a technique using fetal DNA from the maternal circulation mean the end of invasive prenatal testing? Since the first application of ultrasound to it 50 years ago, the “black box” that is the pregnant uterus has gradually yielded to efforts to gain increasingly precise information about the condition of the fetus. Technological advances in ultrasound and, more recently, magnetic resonance imaging have seen the production of high-resolution displays of fetal anatomy and physiology. Specific information about the fetal genome, however, has until now only been available through the application of invasive techniques. Amniocentesis and chorionic villus sampling have been used to diagnose fetal aneuploidy (such as Down syndrome) and an ever-increasing range of genetic conditions. But these invasive procedures come at a cost — an associated 1% risk of pregnancy loss1 limits their application and causes significant stress for women thinking of undertaking such testing. Screening tests such as ultrasound and maternal serum screening to assess aneuploidy risk have been developed to allow more judicious application of invasive procedures, but of themselves cannot accurately diagnose the fetal condition, and false negatives and positives both occur. Now, the era of non-invasive prenatal diagnosis beckons — offering the ability to obtain specific and accurate genetic information from the fetus without the need for an invasive procedure and its associated risks. The article by Hyland and colleagues in this issue of the Journal reports on the first potential clinical application of non-invasive prenatal diagnosis in an Australian population — the determination of fetal RHD status in Rhesus (Rh) D-negative women.2 About 17% of Australian women are RhD-negative.3 These women are at risk of isoimmunisation, caused by the passage of RhD-positive fetal red blood cells across the placenta during pregnancy and childbirth. The resultant antibodies produced by the mother can cross the placenta and cause fetal anaemia due to haemolysis of fetal red blood cells. Women who are isoimmunised require intensive fetal surveillance, and are at risk for fetal death and neonatal brain injury if timely intervention is not performed. The incidence of isoimmunisation has been dramatically reduced since the introduction of preventive strategies, but these rely on administration of plasma-derived RhD immunoglobulin to all RhD-negative women. The technique employed by Hyland et al involves detecting cell-free fetal DNA (ffDNA) in maternal plasma by real-time polymerase chain reaction (PCR).2 ffDNA constitutes about 4%–6% of all cell-free DNA in the maternal circulation and can be reliably detected as early as 7 weeks after conception.4 The use of ffDNA to detect the RHD gene in RhD-negative pregnant women was first described by Lo and colleagues in 1998.5 Others have since applied the technique, and a recent meta-analysis demonstrated 96.1% sensitivity and 96.5% specificity for correctly determining fetal RHD status.6 To minimise false-negative results, internal controls are used to confirm the presence of fetal DNA. The SRY gene was initially used for this purpose, but as this only detects male fetuses, Hyland and colleagues have also utilised the RASSF1A gene to confirm the presence of fetal DNA from female fetuses.2 Where they were able to determine the fetal RHD status, their predictions showed 100% accuracy when compared with the infants’ serotype determined from cord blood after delivery. In a small number of cases, determination of fetal status could not be achieved. This technique requires further evaluation in larger studies to clarify the true performance characteristics of the test, and to allow algorithms to be developed for dealing with indeterminate results and the RHD gene variants seen in some ethnic groups. However, if these issues can be satisfactorily addressed, the potential applications are significant. In the small group of women with isoimmunised pregnancies, it will allow the determination of fetal RHD status without resorting to invasive tests. In addition to the risk of pregnancy loss, invasive procedures also have the potential to cause further sensitisation and worsen the natural history of the condition. More broadly, this testing has the potential to reduce unnecessary exposure of pregnant women to RhD immunoglobulin. Currently, RhD immunoglobulin is administered for antenatal prophylaxis, potential sensitising events, and postnatally for RhD-positive infants. This regime has been very effective, reducing the incidence of sensitisation during pregnancy by more than 90%.7 However, up to 40% of RhD-negative women receive treatment unnecessarily, as they will be carrying an RhD-negative fetus from a heterozygous partner.8 Routine introduction of non-invasive fetal DNA testing would therefore be likely to have cost implications for delivery of this preventive treatment. Non-invasive detection of fetal RHD status is already being incorporated into clinical practice in Europe, and the feasibility of using this approach to make decisions about prophylaxis has been demonstrated.9 The use of ffDNA can also be applied more broadly than determination of fetal RHD status. Already, reports exist of the non-invasive prenatal diagnosis of Huntington disease,10 cystic fibrosis11 and other conditions. Detection of the SRY gene allows determination of fetal sex in women at risk of carrying a fetus with an X-linked condition.12 The non-invasive diagnosis of Down syndrome and other aneuploidies remains challenging, but newer techniques such as methylation-dependent PCR and digital PCR hold promise.13 As with many technological advances involving reproductive choices, there are ethical concerns associated with this test. Sex determination for social rather than health reasons, for example, could result from unregulated use of such technologies. There is a pressing need for vigorous discussion of these issues. Non-invasive diagnosis of specific fetal gene status using fetal DNA from the maternal circulation without any risk to the pregnancy may be the “holy grail” of prenatal diagnosis. The determination of fetal RHD status is nearing availability as a clinical tool, and is likely to be the first of many applications of non-invasive prenatal testing over the coming decade. Is a future without amniocentesis and chorionic villus sampling dawning? Not quite yet, but at least there is some light on the horizon.

Stephen A Cole MB BS, FRANZCOG, CMFM · Helen F Savoia MB BS, FRCPA

A 6-week old infant who had been conceived through in-vitro fertilisation (IVF) presented with a skin lesion and enlarged lymph nodes, and developed severe respiratory distress. Mycobacterium tuberculosis was identified; his mother was the only potential source identified. To our knowledge, this is the first case of congenital tuberculosis after IVF reported in Australia and the second worldwide. It highlights the importance of adequate screening during investigation of infertility and the difficulties in diagnosing congenital tuberculosis. Clinical recordsA 29-year-old Bosnian woman, who had migrated to Australia 8 years earlier, conceived through in-vitro fertilisation (IVF). Her baby, a boy, was born at 28 weeks’ gestation by emergency caesarean section for fetal distress in labour. His mother made an uneventful recovery after the delivery. The baby’s birthweight was 1154 g (50th percentile), and neonatal assessment was consistent with gestational age. He developed mild respiratory distress syndrome and required a short period of endotracheal intubation and artificial ventilation, from which he was successfully weaned. He had several significant problems during the early neonatal period, including prolonged neonatal jaundice (which required repeated episodes of phototherapy), hypothyroidism (serum thyroid-stimulating hormone, 9.2 mU/L; reference range, 0.30–5.00 mU/L) and right-sided Erb palsy. At 6 weeks of age, while still in hospital, the infant developed a 1 cm brown–pink macular lesion on the left side of the neck, and was noted to have an enlarged (1.5 cm) left axillary lymph node. Empirical antistaphylococcal therapy was introduced without any apparent effect. Biopsy of the lymph node was planned, but before this could be performed, the lymph node became acutely more enlarged, and the infant’s condition deteriorated rapidly. He developed severe respiratory distress and required re-intubation. A large mediastinal lymph node mass was noted on chest x-ray and magnetic resonance imaging (Box 1), and bronchoscopy showed extrinsic compression of the trachea and bronchi at the level of the carina. Excision biopsy of the axillary lymph node showed necrotising granulomatous inflammation, and acid-fast bacilli were identified on Ziehl–Neelsen and auramine–rhodamine staining. Mycobacterium tuberculosis was identified in lymph node tissue and endotracheal aspirates by polymerase chain reaction (PCR) and culture. M. tuberculosis was not identified in cerebrospinal fluid, blood or gastric aspirate by PCR or culture. Empirical treatment with isoniazid, rifampicin, ethambutol and pyrazinamide was commenced, along with prednisolone, and the infant’s condition stabilised, then improved. Abdominal ultrasound examination did not show features of a primary complex in the liver. The M. tuberculosis isolate was sensitive to all first- and second-line agents. The baby developed moderate neutropenia after 4 weeks of therapy, which resolved after discontinuation of ethambutol; pyrazinamide was ceased after 12 weeks of therapy. After 4 months of therapy, further left axillary and cervical adenopathy was noted. The largest node was about 1 cm in diameter and fluctuant. The nodes settled spontaneously without excision or treatment change. The infant experienced two episodes of wheezing associated with clinical features of viral upper respiratory tract infection (at 8 and 10 months into the course of antituberculous therapy, respectively). Chest x-rays on each occasion did not show evidence of mediastinal node enlargement. His recovery was otherwise uncomplicated, and he completed a planned 12 months of therapy. The child’s mother had no significant medical history apart from infertility. Infertility investigations had included ultrasound, hysteroscopy and diagnostic laparoscopy. A uterine curettage (as part of the work-up for infertility) 5 years before the pregnancy had shown “granulomas” in the endometrium (Box 2), but stains for acid-fast bacilli were negative. Culture for M. tuberculosis had not been performed at the time. Following the diagnosis of tuberculosis (TB) in her child, an interferon-gamma release assay (IGRA [QuantiFERON-TB Gold, Cellestis, Melbourne, Vic]) was performed, and gave a positive result. Chest x-ray revealed old fibrotic changes in the right upper lung, but no evidence of active tuberculous disease. She was prescribed antituberculous medication. Extensive contact tracing was performed. The father and all close contacts of the baby during his stay in the neonatal unit (including 118 health care workers, 20 neonates and 32 relatives) were screened with an IGRA or tuberculin skin test, and positive results were followed up with chest x-ray. No other cases of active TB were found, suggesting that the index patient did not acquire TB postnatally, but had congenital tuberculosis. DiscussionThis is the first case of congenital TB after IVF reported in Australia, and to our knowledge only the second case reported in the literature.1 This case suggests two valuable lessons: the importance of considering congenital TB in babies who develop a suggestive clinical illness in the first weeks of life, and the need for accurate assessment for and exclusion of TB in women proceeding to IVF. Congenital TB is a rare condition, with around 350 cases reported in the literature.2-10 The fetus can be infected by direct spread through the umbilical cord, by aspiration or swallowing of infected amniotic fluid, or by direct contact with maternal genital lesions during delivery.11 TB can be difficult to recognise in infants as symptoms may be non-specific and easily mistaken for more common neonatal illnesses, such as bacterial sepsis or congenital viral infections.12 Symptoms usually present 2–3 weeks after birth, and the disease can quickly progress to dissemination and death if not promptly treated. In 1994, criteria for diagnosis of congenital TB were revised.3 They comprise documentation of tuberculous lesions in the infant and one or more of the following: lesions in the first weeks of life; a primary hepatic complex or caseating granuloma; documented tuberculous infection of the endometrium or placenta; or exclusion of the possibility of postnatal transmission by investigation of close contacts. Our patient met the criteria for congenital TB: he had tuberculous lesions in early life; his mother had documented granulomas of the endometrium; and extensive contact tracing found no evidence of transmission to the child from other close contacts. Confirmation of endometrial TB in the mother, by repeat endometrial biopsy with PCR and culture for TB, would have been ideal, but would not have altered management in either the mother or the neonate. Thus, it was elected to treat the mother on the basis of the neonate’s culture results, rather than subject her to another procedure. Globally, there has been a slow decline in the incidence of TB; but this is more than offset by population growth, with the number of new cases worldwide increasing between 2005 and 2006 from 9.1 to 9.2 million (an increase of 0.6%). Increases occurred in the African, Eastern Mediterranean, European and South-East Asian regions.13 In Australia, the total number of TB cases reported in 2006 was 1201 (5.8 cases per 100 000 population). The incidence varies dramatically between populations in Australia, with 0.9 cases per 100 000 population in the non-Indigenous population, climbing to 20.1 per 100 000 population in those born overseas.14 Within the group born overseas, incidence ranges from 2.0 per 100 000 population for those born in the United Kingdom to 405 per 100 000 population for those born in Somalia.14 Genital TB is a major cause of infertility in women belonging to high-risk groups, causing up to 17% of cases of infertility.15 Its incidence is increasing in Western continents. Twenty-nine cases of genitourinary TB were reported in Australia in 2006 (2.5% of all reported cases of TB).14 In Australia, it is estimated that one in every 60 babies is conceived through IVF .16 As IVF is a useful treatment for infertility caused by TB, it can be expected that in the future more women with TB as a cause of their infertility will present for IVF. It is therefore imperative that women from high-risk groups undergo evaluation for and exclusion of TB. Investigations should include an IGRA or tuberculin skin test. If either gives a positive result, expert opinion should be sought to determine the need for more invasive investigations, such as endometrial biopsy. If an endometrial biopsy reveals granuloma, it is imperative that the specimen be sent for PCR and culture for TB, even in the absence of acid-fast bacilli. Consultation with an infectious diseases physician or clinical microbiologist is then warranted. In summary, this case highlights the fact that TB should be considered and excluded in high-risk women undergoing IVF, and that TB should be considered in ill neonates who have a poor response to conventional antibiotic therapy. 1 Magnetic resonance imaging scan of a 6-week old infant A scan showing multiple enlarged lymph nodes in the mediastinum measuring up to 13 mm (right paratracheal, subcarinal and right hilum) and in the axillae (largest on the left) and cervical area. 2 Section of endometrium from the infant’s mother A section of endometrium sampled 5 years before the infant’s birth showing a granuloma. (Image courtesy of Dr John Rees, Southern Health Pathology Department, Melbourne, Vic.)

Rhonda L Stuart MB BS, FRACP, PhD · Anthony Lewis MB BCh, MMed(Microbiology), FRACP · C Andrew Ramsden FRCP, FRCPCH, FRACP · Richard R Doherty MB BS, FRACP

To the Editor: We concur wholeheartedly with Gill and colleagues1 in support of recognising obesity as a public health issue, and we dispute claims that the current problem of obesity is being exaggerated. Gill and colleagues point out that obesity trends have climbed over decades, and state that 6%–8% of Australian school children are affected.1 While this is a substantial burden of over a quarter of a million children, we also consider that restricting definitions of obese to arbitrary cutoff points may underestimate the problem, given that the entire distribution of childhood weight is increasing, not just the extreme group classified as obese. Adiposity is related to cardiovascular outcomes such as myocardial infarction and stroke in a (curvi)linear fashion. Defining obesity by arbitrary cutoff points is vulnerable to differences between sexes, ethnicity and age, and limits our understanding of obesity-related diseases. It is well known that cardiovascular risk factors cluster, particularly the adiposity-driven components of the so-called metabolic syndrome. In the Western Australian Pregnancy Cohort (Raine) Study, we have used cluster analysis to identify a group of children at risk of future cardiovascular disease with features of the metabolic syndrome.2 The differences in characteristics are shown in the Box. The “high risk” and “low risk” cluster groups differ widely in terms of not only body mass index, the most widely used measure of obesity, but also waist circumference (a measure of central adiposity), insulin resistance, blood pressure, and levels of triglycerides, high-density lipoprotein cholesterol, total cholesterol (data not shown) and low-density lipoprotein cholesterol (data not shown). Not only the conventionally used 95% confidence intervals, but also the 99% confidence intervals do not overlap for any of these intermediate cardiovascular risk factors. We found that 29% of children were in the high-risk cluster at the age of 14 years2 and a similar analysis suggested that even at age 8 years, 25% of children were at increased risk of future obesity, cardiovascular disease and diabetes.3 C-reactive protein (CRP) level is known to be associated with future cardiovascular diseases in adults,4 and with an adverse metabolic profile in children.5 The “high risk” children had significantly higher CRP levels at the age of 14 years than their low-risk counterparts. Certainly, the magnitude of this problem, affecting up to a third of our youth, needs to be addressed by government and health-planning bodies. We suggest our approach of cluster analysis will help identify earlier those children at substantially increased risk of cardiovascular and other adiposity-related disorders in Australia. Features of the cluster groups with respect to components of the metabolic syndrome, showing 99% CIs* BMI = body mass index. HOMA = homeostatic model assessment (for quantifying insulin resistance). SBP = systolic blood pressure. HDL = high-density lipoprotein cholesterol. * From Huang et al.2 Reprinted with permission from the American Diabetes Association.

Rae-Chi Huang · Fiona J Stanley · Lawrence J Beilin

To the Editor: There is a substantial volume of evidence from a range of national and state-based surveys illustrating increases in the rates of obesity and overweight among Australian children over the past two decades,1 concurring with trends observed in most developed countries.2 The recent article by Gill and colleagues highlighted questions that have been raised publicly regarding the extent and impact of levels of obesity and overweight among Australian children, including whether trends have been exaggerated.1 To examine these issues using the latest data available, we present data from the three most recent national surveys in which weight and height of Australian children were measured: the Australian Health and Fitness Survey (1985),3 the National Nutrition Survey (1995),4 and the Australian National Children’s Nutrition and Physical Activity Survey (2007).5 We examined overweight and obesity levels among young Australians from comparable age groups at three time points over more than 20 years, using the same internationally accepted definitions of childhood overweight and obesity. For 1985 and 1995 data, we used the figures reported by Magarey et al in 2001,6 which compared results from the 1985 and 1995 surveys using new standard international definitions to classify overweight and obesity among Australian children and adolescents.7 We calculated body mass index for the 2007 Australian National Children’s Nutrition and Physical Activity Survey using the raw data file obtained through the Australian Social Science Data Archive,8 categorising children as overweight or obese based on the same international definitions used by Magarey et al.6 We based our calculations on the age group common to each of the three surveys: 7–15-year-olds. As shown in the Box, the prevalence of overweight and obesity in boys aged 7–15 years has risen from 11.0% (95% CI, 10.99%–11.01%) in 1985 to 20.0% (95% CI, 19.97%–20.03%) in 1995 and 23.7% (95% CI, 23.68%–23.72%) in 2007. In 7–15-year-old girls, the prevalence of overweight and obesity has increased from 12.2% (95% CI, 12.19%–12.21%) in 1985 to 21.5% (95% CI, 21.47%–21.53%) in 1995 and 25.8% (95% CI, 25.78%–25.82%) in 2007. While data from additional time points are required to map national trends more comprehensively, our analysis clearly indicates an upward trend in overweight and obesity levels in both boys and girls aged 7–15 years between 1985, 1995 and 2007. This trend is cause for alarm, given the widely recognised body of evidence on the significant short-term and long-term consequences of childhood obesity.9 Prevalence of overweight and obesity in Australian children aged 7–15 years, 1985–2007 * Data weighted for age, sex and region with the weighting variable in the raw data file obtained from the Australian Social Science Data Archive.8

Lyn M Roberts · Tessa R Letcher · Alexandra A Gason · Tim Lobstein

To the Editor: We read with interest the article by Alexander and colleagues on child protection issues in severe childhood obesity.1 With one quarter of Australian youth either overweight or obese, individual families (or the health care system) will not benefit from widespread involvement of child protection services in obesity. The authors are clear on this, and describe their case as “sufficiently extreme”. The difficulty lies in defining what is “extreme” and, as health professionals, we have a duty to the community to emphasise that these kinds of cases rarely occur. The illustrative case in the article by Alexander and colleagues required an amalgamation of details from several patients (for confidentiality purposes), and we believe it would be very unusual for a 40 kg 4-year-old girl to exhibit the degree of obesity-related comorbidity described.2,3 Such a degree of “medical urgency” is usually absent when managing young obese children and, in our experience, is thankfully very extreme and markedly different from the more usual scenario of discussions around potential long-term health problems. Also, there are currently no fail-safe mechanisms in place to be 100% certain that there is not an underlying genetic, hormonal or metabolic reason for continuing weight gain in a young child. With the childhood obesity pandemic, it is impossible to routinely investigate all obese youth and, even if it were, research teams are continually finding new causes for why some children continue to gain weight irrespective of lifestyle change. Indeed, the more severe the obesity, the more likely for there to be an organic cause.4 It is not in anyone’s interests for child protection services to be automatically involved because of standard recommendations when, at a later date, an underlying medical cause is discovered. Alexander and colleagues should be congratulated on re-igniting a public discussion on this highly emotive and difficult area of health care. We agree that parenting styles may influence weight regulation in young children5 but, for the above reasons, we would urge extreme caution when considering that parents may be “neglectful”. Within our obesogenic environment, perhaps (deliberate or intentional) non-compliance is an indication that society is neglecting parents, rather than that parents are medically neglecting their children? We are concerned that the development of child protection guidelines will alienate parents and families, leading to a decline in the uptake of programs aimed at preventing and/or treating overweight and obesity. We would recommend that each case be taken on its individual merit and that primum non nocere is as important as Aristotle’s phrase of “practical wisdom”.

Matthew A Sabin · Zoe McCallum · Kay Gibbons · George A Werther · Joseph Proietto

In reply: Primum non nocere means both “first, do no harm” and “above all, do no harm”. We acknowledge there may be both potential harms (the most significant being removal of the child from the family) as well as hoped-for benefits in involving child protection services in cases of severe childhood obesity. Though we strenuously oppose notification of child protection authorities as a general policy, we raised the idea that, in exceptional circumstances, health care professionals may nonetheless have a professional and legal obligation at least to consider notifying such authorities. We did so cautiously because we fear an exception becoming a rule, particularly in services such as ours where we frequently care for children very like the “child” we describe. We agree that the development of obesity usually has multifactorial causes which will include a genetic element. We also agree on the need for public health approaches to the prevention of childhood (and adult) obesity. But whatever the underlying cause of severe obesity in a particular case, and especially in circumstances where parents seem unable to attend to the physical needs of their child, health professionals have an obligation to consider all reasonable means to limiting excess weight gain.

Shirley M Alexander · Louise A Baur · Roger Magnusson · Bernadette Tobin

Objective: To collect nationally representative epidemiological data on early-onset eating disorders (EOEDs) in children.Design: Prospective, active surveillance using the Australian Paediatric Surveillance Unit with key informant design.Setting: Child health specialists in Australia (July 2002 to June 2005).Patients: Incident cases of EOEDs in children aged 5–13 years.Main outcome measures: Disease rates, demographic characteristics, clinical features and complications, hospitalisation, psychological comorbidity, and concordance of clinical features with Diagnostic and statistical manual of mental disorders, fourth edition (DSM-IV) criteria.Results: We identified 101 children aged 5–13 years with EOEDs (median age, 12.2 years; range, 5.5–13.9 years), of whom one in four were boys. Most were hospitalised (78%), and the mean duration of hospitalisation was 24.7 days (range, 1–75 days). More than 70% of inpatients were admitted to specialised eating disorder units in paediatric teaching hospitals. Among inpatients, 37% met DSM-IV diagnostic criteria for anorexia nervosa; although 61% had life-threatening complications of malnutrition, only 51% met weight criteria. Psychological symptoms were similar to those in adults with anorexia nervosa: 67% of inpatients met both psychological diagnostic criteria for anorexia nervosa (fear of weight gain/fatness and misperception of body shape). Of 19 postmenarchal girls, 18 had secondary amenorrhoea. Nasogastric feeding was used in 58% of inpatients, and 34% received psychotropic medications.Conclusions: This is the first prospective national study of EOEDs. It demonstrates the limitations of applying DSM-IV diagnostic criteria for anorexia nervosa to young children; the high proportion of boys affected by EOEDs; and the significant psychological comorbidity and high frequency of hospitalisation associated with EOEDs. Potentially life-threatening medical complications are common at presentation, suggesting possible missed diagnoses and a need for education of health professionals. The study underlines the severity of EOEDs and the need for joint medical and psychiatric specialist management.

Sloane Madden MB BS(Hons), FRANZCP, CAPCert · Anne Morris MB BS, MPH, FRACP · Yvonne A Zurynski BAppSc, MAppSc, PhD · Michael Kohn MB BS, FRACP · Elizabeth J Elliot MD, FRACP, FRCPCH

Fixing sex. Intersex, medical authority, and lived experience. Katrina Karkazis. New York: Duke University Press, 2008 (xiii + 364 pp). ISBN 978 0 8223 4318 9. Currently, there is an intense ethical debate about genital surgery for infants born with ambiguous genitalia. The controversy rose to a new level of intensity in Australia in 2008 with the involvement of the Australian Human Rights Commission and the Victorian Government Department of Justice. Doctors in Europe and North America are facing the same dilemmas. This new book, possibly the best contribution to the debate yet published, is very welcome, not only because it is timely but because it is deeply thoughtful, thoroughly researched and very respectful of all points of view. The author, Katrina Karkazis, PhD, MPH, is a Senior Research Scholar with the Center for Biomedical Ethics at Stanford University in the United States. In addressing the historical basis for current understanding of sex and gender, Karkazis discusses the contribution to the understanding of sex development made by John Money (a psychologist at Johns Hopkins University) in depth, in a way that is refreshingly generous. She traces the development of what became the traditional treatment model, the scepticism that emerged, and the origins of Internet-based patient advocacy groups in the mid 1990s. Her exploration of what is posted on discussion boards is balanced by her careful study of what scientific long-term outcome studies have, and have not, delivered. She has also conducted hundreds of interviews with doctors, parents and adult patients. Her book concludes with the following:

Garry L Warne

To the Editor: Isoniazid is used extensively for the treatment of active and latent tuberculosis (TB). It is generally well tolerated by children, and hypersensitivity reactions resulting in skin rash and requiring cessation of treatment are rarely reported in this age group.1,2 We report a case of isoniazid hypersensitivity in a 21-month-old boy potentially exposed to TB in a childcare setting. He was one of over 80 children screened after contact with a childcare worker who showed a positive smear result. His initial tuberculin skin test (TST) was negative and, in line with New South Wales guidelines,3 he was commenced on isoniazid 150 mg daily (10mg/kg/day) while awaiting a repeat TST. After 3 days of treatment, he developed a small number of round vesicular lesions on his tongue. They were associated with mild discomfort but his appetite was not affected. There were three small maculopapular lesions on his legs and back that reportedly looked like mosquito bites before blistering. The child remained afebrile and was systemically well. The family general practitioner considered that this presentation was possibly an allergic reaction and isoniazid was discontinued. Population health staff were consulted, and the risks and benefits of further isoniazid treatment were discussed with paediatric TB specialists. It was recommended that, after the rash had resolved, isoniazid be reintroduced at half the dosage and with close supervision. Two days after isoniazid 75 mg daily was recommenced, the rash recurred. The child’s mother described lesions appearing as “burns all over his tongue” and reported further sores around his lips and six welt-like lesions on his legs. Isoniazid was immediately discontinued, the skin lesions resolved within 5 days and no further antituberculous therapy was administered. His repeat TST 12 weeks after the initial test was negative and he remains well. No other potential triggers for a hypersensitivity reaction were identified. In particular, no other medications were administered during this period or for the week before commencing isoniazid. According to his mother, the child had experienced a similar reaction within 1 hour of a single dose of ibuprofen when he was 8 months old. Several tongue blisters were accompanied by a generalised fine maculopapular rash lasting several days. We concluded that the child most likely had a hypersensitivity reaction to isoniazid that required discontinuation of treatment. We reported this to the Therapeutic Goods Administration, which advised that it had received seven other reports since 1991 of suspected hypersensitivity, but none were for children under 10 years of age.

Tony D Merritt · Peter D Massey

To the Editor: Accidental asphyxia in very young children is an ongoing problem caused by hazardous sleeping environments and toddlers’ inability to understand dangers or to physically extricate themselves once entrapped. Two common problems involve children becoming wedged between mattresses and cot sides or walls, and hanging from clothing caught on projections inside cots.1 Autopsy in such cases requires careful death scene evaluation to prevent confusion with sudden infant death syndrome and to identify any evidence of inflicted injury, if present. National legislation requiring both new and second-hand cots to meet Australian safety standards has reduced the numbers of unsafe cots on the market. I report a case of another continuing, albeit less common, circumstance that is also resulting in lethal outcomes for toddlers — about one child dies every 1–2 years in Australia in this manner.2 A healthy 13-month-old boy was placed in his cot next to a window with blinds from which a cord was hanging. A loop of the cord measuring about 10 cm was hanging inside the cot. When checked later, the boy was found unresponsive, hanging from the cord. Resuscitation attempts were to no avail. At autopsy, a parchmented ligature mark was present around the neck, with facial and conjunctival petechiae. There were no other injuries or significant illnesses present. Death was therefore attributed to accidental hanging. (Further information on this case is available in the Finding of Inquest.3) Prevention of such tragic fatalities requires ongoing public awareness campaigns, using pamphlets such as the Australian Government’s blind and curtain cords safety alert brochure,2 to advise parents and child carers to keep cots and furniture that can be climbed on away from windows that have curtain or blind cords, to use cleats and cord wind-ups to keep cords at least 1.6 m above the floor, to cut loops, and to keep cords that must be looped under tension with tie-down devices. A safety tassel is also available that clips the two ends of a cord together but that easily separates when put under pressure.4 In addition, national legislation similar to that currently enacted in New South Wales and other states would provide uniform guidelines for managing these devices that would include warning labels and written safety information for parents.4

Roger W Byard

Pediatric respiratory medicine. 2nd ed. Lynn M Taussig, Louis I Landau, editors. Philadelphia: Mosby, 2008 (xxiii + 1118 pp). ISBN 978 0323 04048 8. If you are looking for an up-to-date encyclopaedia of paediatric chest disease, then this is it. As expected, this second edition is a substantial improvement over the first. Most of the 75 chapters are short and user friendly. The text is broken up with numerous coloured diagrams, figures, tables, x-ray images and boxed sections highlighting key points, teaching points, pitfalls and controversies. For those who want teaching resources, all images can be captured with ease directly into Powerpoint presentations via electronic access. This edition is slightly less hefty than the previous edition, largely because the references are not included in the book — however, they are accessible electronically, with direct links to MEDLINE abstracts. Most chapters are very heavily referenced (eg, Chapter 3 has over 300 references) and remarkably up to date for a multi-author textbook, including a few references from as late as 2007. Since the editors are from Western Australia and the United States, it is understandable that the majority of the expert authors are also from WA and the US. Nevertheless, all are clearly national and international authorities on their specific topics. Because there are over 130 separate authors, the style and format vary considerably. It is disappointing to see some very user “unfriendly” chapters. For example, in Chapter 35 (bacterial pneumonia) there are over 30 pages of continuous, dense text with only occasional subheadings, and illustrated with a total of only four small x-ray images. To check both content and ease of access, I tested for several of my pet topics — including “plastic bronchitis” and “genetic surfactant deficiency mimicking interstitial lung disease”. Both were readily found, comprehensively covered, and with key references included. At $190.00, the book represents outstanding value for money, given the quality of the content, the outstanding diagrams and figures, and the huge number of electronic references.

Craig M Mellis

To the Editor: The incidence of type 1 diabetes mellitus (T1DM) is increasing in Australia.1,2 There is also general consensus that the incidence of diabetic ketoacidosis (DKA) is increasing in children, as noted in an Australian study.3 We conducted a retrospective audit of the referral pattern of patients with newly diagnosed T1DM presenting to the Children’s Hospital at Westmead, a tertiary referral centre serving the population of western Sydney. Referral data were available for 191 of 204 patients with newly diagnosed T1DM admitted to the hospital between January 2003 and December 2004. Most patients (150; 79%) had presented to their general practitioner before admission to hospital, and the remainder had initially presented to an emergency department. In the former group, the diagnosis of diabetes was indicated in referral letters or admission notes for 128 patients (85%), while a diagnosis other than diabetes (eg, gastroenteritis, urinary tract infection, sepsis) was made for 22 patients (15%). DKA was less common among patients whose referral letter indicated a diagnosis of diabetes compared with those with an alternative or no diagnosis or without a referral letter (27% v 47%; P < 0.001). Most patients (105; 70%) were referred to an emergency department within 24 hours of presentation to the GP, and their rate of DKA was lower than in those referred after 24 hours (31% v 51%; P = 0.03). These data suggest that better understanding by primary carers of the symptoms of new-onset T1DM and earlier referral are significantly associated with reduced risk of DKA. Most patients who first saw a GP (125; 83%) had initial investigations arranged; bedside urinalysis and/or measurement of fingerprick blood glucose levels were performed in 66%, while 31% were sent for formal blood tests. Patients who had bedside investigations performed had a significantly lower rate of DKA than those who had only formal blood tests or no investigations performed (26% v 52%; P = 0.002). It is noteworthy that, among patients who first saw a GP, 23 (15%) were diagnosed with diabetes but were not referred to an emergency department within 24 hours. The reasons for this are unclear but may be due to the GP waiting for confirmatory blood test results. The Australasian Paediatric Endocrine Group and International Society for Pediatric and Adolescent Diabetes guidelines recommend immediate referral for suspected new-onset T1DM, as DKA is fatal if left untreated.4 A public awareness campaign conducted in Italy in the 1990s was successful in reducing the incidence of DKA in children with newly diagnosed T1DM.5 Australian communities might benefit from a similar campaign to encourage prompt identification of symptoms of diabetes in childhood, prompt bedside investigations, and immediate referral to hospital for definitive care.

Maria E Craig · Catherine H Wong · Joanna Alexander · Ann M Maguire · Martin Silink

A 5-month-old boy with known congenital varicella syndrome presented to our hospital emergency department with generalised herpes zoster (shingles). The child was born in Australia. His Sri Lankan-born mother had developed chickenpox in the second trimester of pregnancy. Examination and investigation of the child at birth for complications of congenital varicella syndrome had revealed only skin changes on the left thigh (Box, A). A new vesicular rash had evolved over 3 days, initially involving right T8 (Box, B) and L4–5 (Box, C) dermatomes, then progressing to cover the entire body. There was no clinical evidence of visceral involvement. Cicatricial scarring had replaced the congenital skin changes (Box, D). Varicella zoster virus was isolated from vesicular fluid. Oral valaciclovir was prescribed for 7 days because the generalised nature of the rash demonstrated an insufficient immune response to varicella reactivation. The symptoms rapidly resolved, with no new scarring. A maternal chickenpox infection during pregnancy can be severe and life-threatening, and can also cause in-utero infection, which may be fatal or result in congenital abnormalities.1 Important features of congenital varicella syndrome include: dermatomal cicatricial scarring (highlighted by this patient); limb defects; intrauterine growth restriction; ophthalmological defects (chorioretinitis, optic atrophy, cataract); gastrointestinal or genitourinary abnormalities; neurological defects (developmental delay, seizures, deafness, limb paralysis, microcephaly).1 Shingles is caused by reactivation of varicella zoster virus. Childhood shingles is uncommon (incidence, 0.05%/year), rarely indicates primary immunodeficiency,2 and occurs more frequently following congenital infection (4.4%/year)2 or chickenpox infection during infancy (0.4%/year).2 Antiviral treatment of shingles in immunocompetent young children is not usually recommended, as complications (including post-herpetic neuralgia) are rare.3 Chickenpox has been mainly a childhood disease in Australia, but in many tropical countries it predominantly affects adults. Immigrants to Australia from these regions (including the mother of our patient) may remain susceptible to varicella infection.4 At least 5% of Australian women of childbearing age were born in tropical countries.5 Varicella vaccine is highly effective and is listed on the National Immunisation Program Schedule6 for childhood immunisation. Lowering the community prevalence of varicella infection by routine childhood immunisation can help protect non-immune adults and immunocompromised patients.1 Opportunistic, proactive identification and immunisation of non-immune adults, particularly for both prospective parents before pregnancy, could help prevent serious consequences. Cicatricial scarring and shingles in a 5-month-old infant with congenital varicella syndrome

Elizabeth K Nairn · Joshua Wolf · Jim P Buttery

Australia needs to develop its own guidelines based on local data New guidelines for testing and treating lipid abnormalities in children have recently been published by the American Academy of Pediatrics and the American Heart Association (Box).1,2 These recommendations, made partly in response to the high prevalence of obesity in children in the United States, provoke consideration of whether they should also be adopted in Australia. The previous US recommendations,3 which targeted cholesterol testing to children with a family history of premature cardiovascular disease or high cholesterol levels, had focused on a population-based approach to treatment through a fat- and cholesterol-restricted diet. Drug therapy was reserved for children with more persistent and extreme elevations in cholesterol level. In contrast, the recent guidelines recommend that testing be broadened to include all overweight or obese children, with the first cholesterol assessment to be done between the ages of 2 and 10 years. The new guidelines further recommend that initiation of drug therapy be considered at a younger age (from 8 years) and with a lower low-density lipoprotein cholesterol (LDL-C) level target for children with multiple cardiovascular risk factors. Indirect evidence suggests that childhood lipid abnormalities are important in the development of cardiovascular disease in adults. For example, autopsy studies indicate that atherosclerosis begins in the young and that the extent of lesions correlates with traditional cardiovascular risk factors, including lipid levels.4 However, advanced atherosclerosis rarely occurs in children and adolescents. Arterial wall thickness in adults, as assessed by carotid artery ultrasonography, is associated with childhood lipid levels, and children with lipid abnormalities display altered arterial structure and function.5,6 However, direct evidence for an association between childhood lipid levels and adult cardiovascular outcomes, such as myocardial infarction and stroke, is not available. Why, then, test children and adolescents at all? Would it be equally effective to test young adults? One important potential rationale for cholesterol testing in children is that lipoprotein levels tend to track from childhood into adult life.7,8 Detection of lipid abnormalities in young children could prompt changes in diet and physical activity that would be required through the whole of life. It is important to note, however, that both universal and targeted lipid testing in children result in a high false-positive rate for adult dyslipidaemia.8,9 Moreover, the predictive value of childhood lipid levels depends on the threshold values used to define dyslipidaemia. Threshold values derived from populations of US children may not be sensitive to trends in childhood lipid levels and overweight and obesity in Australia. The prevalence of childhood overweight and obesity is high and increasing in both Australia and the US.10,11 Moreover, in both countries, lipid abnormalities are common in overweight and obese children,12,13 with low high-density lipoprotein cholesterol (HDL-C) and high triglyceride levels particularly prevalent. Importantly, targeting overweight and obese children for LDL-C testing does not improve the specificity for detecting elevated LDL-C levels in adults.8 Although most overweight and obese children with low HDL-C levels become adults with low HDL-C levels, targeting overweight and obese children for HDL-C testing will not identify the majority of adults with low HDL-C levels.8 Overweight and obese children, whether or not they have high triglyceride and low HDL-C levels, require weight management through changes in diet and physical activity levels. But it is uncertain, particularly in the case of young children, whether knowledge of their lipid status will lead to greater motivation to implement such changes. Improved diet and increased physical activity are both safe and effective ways of reducing cardiovascular risk factors in children, and should be promoted across the whole paediatric population.14-17 Most overweight and obese children could be encouraged to adopt these lifestyle changes without testing their lipid status. Testing for lipid abnormalities could be reserved for older, obese children (> 10 years of age) in the context of an overall assessment of their risk for future cardiovascular disease. Screening based on family history may be hampered by inaccurate or incomplete information and the need for adult family members to have their cholesterol levels measured. However, obtaining an accurate family history, combined with testing of adults to detect those with significant elevation in LDL-C levels, may help identify children with inherited dyslipidaemias (eg, familial hypercholesterolaemia). Such children have the highest risk of premature cardiovascular disease and may benefit most from drug therapy at a young age. The new US recommendations also raise questions about which children should be considered for drug therapy for lipid abnormalities. A number of randomised clinical trials have demonstrated the short-term safety and efficacy of HMG-CoA reductase inhibitors (statins) in children.18 Statins are currently the first-line drug treatment for elevated cholesterol levels in children. However, there is a lack of evidence for their long-term safety, and animal studies have shown they may be toxic to the developing fetus.19 Although there have been no controlled epidemiological studies relating gestational exposure to statins with adverse human pregnancy outcomes, case reports of structural anomalies and the biological plausibility of a teratogenic effect mean that statins are contraindicated in pregnancy.20 Thus, a case can be made for reserving statin therapy for older children at high risk of future cardiovascular disease. In girls, it may be appropriate to delay statin therapy until an age when discussions about reproduction and contraception can occur. A strong family history of premature cardiovascular disease or a rapid progression in surrogate measures of atherosclerosis (eg, carotid arterial wall thickness, measured by ultrasound) may lower the age threshold for statin therapy. In Australia, we should be taking action to address the increasing prevalence of childhood cardiovascular risk factors. However, guidelines from the US may not be appropriate for Australian children, and it is imperative that we formulate new local recommendations based on recent local data. Guidelines for lipid assessment and management in Australia should also propose strategies for reducing cardiovascular risk factors in childhood more generally. This will require discussion and collaboration between clinicians, researchers, and governmental and non-governmental organisations, such as Diabetes Australia, the National Heart Foundation, the Paediatric Cardiac Council of the Cardiac Society of Australia and New Zealand, and the Royal Australasian College of Physicians. In the interim, a careful assessment of the risk of future cardiovascular disease is required for all paediatric patients. This will be based on ascertainment of an accurate family history of premature cardiovascular disease, information on diet and physical activity, anthropometric and blood pressure measurements made at routine paediatric health checks, and the targeted assessment of blood lipid levels in older children with a family history of premature cardiovascular disease or hyperlipidaemia and/or multiple other cardiovascular risk factors, including obesity. Summary of recent changes to recommendations in the United States for cholesterol testing and treatment in children1,2 Stronger recommendations for cholesterol testing in children who have cardiovascular risk factors other than lipid abnormalities — particularly overweight and obesity, but also hypertension, cigarette smoking or diabetes. A stronger recommendation on the timing of initial cholesterol testing: between the ages of 2 and 10 years. A recommendation to consider commencing drug therapy in children aged over 8 years (rather than 10 years), with a target low-density lipoprotein cholesterol level of < 3.3 mmol/L (rather than < 4.1 mmol/L).

Julian G Ayer BSc(Med), MB BS, FRACP · David R Sullivan MB BS, FRACP, FRCPA · Gary F Sholler MB BS, FRACP