Child health

Australia does not do well in the early detection of congenital hearing impairment. Only about 25% of infants born with hearing impairment are diagnosed by the age of 12 months, and for many children deafness remains a disability leading to severe and lasting language impairment.1 The technology for newborn hearing screening has now been in regular use in many parts of the world for much of the past decade, and there is at last some persuasive evidence that very early detection helps these children achieve normal language skills.2,3 This evidence is far from perfect: 4 only one randomised controlled trial of detection rates with and without newborn screening has been reported, and no randomised controlled trial has yet examined outcomes of hearing screening. Nonetheless, universal newborn hearing screening has become not only possible but expected in the United States and Canada, the United Kingdom and many European countries. However, it has not yet been widely implemented in Australia. As a result, the excellent diagnostic and rehabilitative services available to all Australian children once the diagnosis of hearing impairment has been made contrasts strongly with our patchy and very incomplete ascertainment of hearing impairment in the first year of life. The Western Australian Newborn Hearing Screening Programme is therefore an important step, as is the recent announcement that a program will commence throughout New South Wales by the end of 2002. In a report of the WA program in this issue of the Journal, Bailey et al (page 180)5 demonstrate that a high-quality, sustainable universal newborn hearing screening program can operate in Australian birthing hospitals. It appears to be a model program, with exceptionally high coverage, high acceptability, low referral rates, and low rates of babies lost to follow-up. It exceeds most benchmarks set in 2000 by the US Joint Committee on Infant Hearing,6 and is in line with the Australian National Consensus Statement on Newborn Hearing Screening.7 Nonetheless, it raises a number of difficult issues. Bailey and colleagues report that the hearing screening program has achieved more than 96% coverage in the five participating metropolitan hospitals. However, together these screened infants represent only about half Western Australia's annual births — unfortunately, the "easy" half. The program operating throughout the US State of Colorado,8 one of the few approaching a true population coverage, has demonstrated that hospitals with fewer than 400 births annually do worse on average than large hospitals in terms of coverage (substantially lower) and referral rates (substantially higher). Australia is characterised by vast distances and a very large number of small hospitals. For instance, the State of Victoria has a similar birthrate to Colorado, but nearly twice as many birthing hospitals (about 110, compared with 60), most of which are small. Statewide or national newborn hearing screening therefore poses considerable logistic and economic obstacles in Australia, and these are not necessarily surmountable. But what are the consequences of limiting ourselves to larger hospitals? Let us assume that 50% of a State's population receives a very high quality hearing screening program which achieves 95% coverage, 90% sensitivity, 95% follow-up, and 80% compliance with early fitting of hearing aids and intervention (as some parents choose neither). This equates to less than a third of that State's hearing-impaired children benefiting from the program. If any one of these parameters is lower, then the number of children potentially benefiting falls even further. Despite individual gain, median age at diagnosis and overall outcomes for the State would improve little. If universal screening is to lead to population benefits, then universal it needs to be — despite the challenges. A poor alternative is to screen only babies with a risk factor for deafness. Asking about the presence of a risk factor becomes the universal "screen", followed by a targeted screening test of hearing itself. At face value, this may seem cheaper, but it is not easier and certainly detects fewer children. While almost all children with hearing loss detected in the Western Australian series so far have had a risk factor, in larger series this applies to only about 50% of babies.8,9 Neonatal intensive care and special care nurseries typically contain about 30%–40% of all infants found to have moderate or greater hearing loss in newborn screening programs9,10 and are relatively easily targeted, as are babies with obvious head and neck abnormalities. Other risk factors, such as family history of early hearing impairment, pose greater problems. Accurate elicitation requires skilled enquiry and mothers may not recall, or even know, that a risk factor is present until after the diagnosis is made, thus reducing sensitivity. The Victorian Infant Hearing Screening Program has recently highlighted the very low positive predictive value of family history and some other risk factors, with close to 200 babies needing to be referred to diagnose one child with hearing loss.11 Low sensitivity combined with poor positive predictive values equates to spending a lot of money to miss many children. Finally, risk-factor screening raises issues of equity, as the many children with hearing impairment, but without a discernible risk factor, would be denied access to hearing screens in such a program. A final issue is that of program sensitivity. At 0.7 per 1000, Western Australia's detection rate for children with bilateral congenital hearing impairment of more than 35 dB HL (hearing level) is lower than the usual rate of 0.9–1.0 per 1000 detected (with hearing impairment of more than 40 dB HL in the better ear).8,9 Most likely, this is a chance finding reflecting the small size of the series — it "just happened" that relatively few babies with hearing impairment were born during this time period. Alternative explanations include equipment problems or program insensitivity. The Western Australian program is unusual in that a baby is not referred until screening has shown three "fail" responses. This lowers the false positive rate and increases program specificity — both of which are desirable. But in screening programs rises in specificity are typically accompanied by falls in sensitivity. It may be that, in this case, the pendulum has swung too far towards specificity at the expense of sensitivity, and that, after years of worrying about excessive referral rates, they are — at last — too low. Currently, we are not serving well the hundreds of children born each year with moderate or greater hearing impairment in Australia. Universal newborn hearing screening seems one way of improving this situation. It is not reasonable to defer implementing a program until the evidence is stronger, since stronger evidence is unlikely to be available soon. Rather than stopping us from implementing programs, this should spur us to acquire such evidence. Because Australia has not yet widely introduced newborn hearing screening, we have an unusual capacity to study these questions prospectively. National benchmarks and a minimum dataset should be established, and we should start carefully and systematically examining outcomes for hearing-impaired babies born now against which to compare gains over the coming years. We should also keep an open mind. In 10 years' time, Australia should be able either to guarantee continuation of an effective program, or to move resources rapidly from a program that, despite best efforts, has proved ineffective.

Melissa A Wake MD, FRACP, MB ChB

Otitis media — definitions Acute otitis media without perforation: Presence of middle-ear fluid with symptoms or signs of suppurative infection. Bulging of the tympanic membrane is the most reliable sign in Aboriginal children. Acute otitis media with perforation: Acute suppurative infection with recent discharge from the middle ear (within the last 7 days). Otitis media with effusion: Presence of middle-ear fluid without symptoms or signs of suppurative infection. Chronic suppurative otitis media: Persistent discharge from the middle ear through a tympanic membrane perforation for more than 6 weeks. Chronic suppurative otitis media (CSOM) (see Box) is very uncommon in First World countries and is best regarded as a disease of poverty. The World Health Organization has indicated that a prevalence rate of CSOM greater than 4% in a defined population of children is indicative of a massive public health problem requiring urgent attention.1 That CSOM affects up to ten times this proportion of children in many Aboriginal communities is an indictment of the poor living conditions in these communities.2 The associated hearing loss has a life-long impact, as it occurs during speech and language development and the early school years. Why is chronic suppurative otitis media so recalcitrant?Many factors contribute to poor health outcomes. In biological terms, the greatest risk factor for the early onset and persistence of otitis media is nasopharyngeal colonisation by multiple bacterial species and subtypes.3 In Aboriginal communities with overcrowded households, infants are frequently exposed to siblings whose nasopharyngeal carriage rates are almost 100% for each of the major otitis media bacterial pathogens.3 In non-Aboriginal children, the host response to a low-dose infection usually eradicates pathogens, which, in turn, down-regulates inflammation and limits tissue damage. In contrast, we believe that early exposure of very young Aboriginal infants to a large bacterial inoculum (or frequent exposures to immunologically distinct pathogens)4 provides constant stimulation of the inflammatory cascade, which damages mucosal tissue yet fails to eradicate pathogens.5 This begins a vicious cycle that may persist throughout childhood: early exposure, persistent bacterial colonisation, and chronic mucosal disease. Furthermore, such infants themselves become chronic carriers and pose a risk to other, younger infants. This cycle is facilitated by overcrowded and poor living conditions, lack of appropriate washing facilities,6 and limited access to appropriate healthcare services. Bulging of the tympanic membrane is the best diagnostic predictor of perforation.7 Other signs and symptoms of acute otitis media (such as pain, fever, irritability or redness of the tympanic membrane) are frequently absent in this population. The implications of this lack of signs or symptoms are clear — parents do not see their child as unwell and thus children remain untreated. Together, this biological model and clinical pattern help us to understand the intractable nature of otitis media in Aboriginal children. Currently, failure to apply existing knowledge is a more important problem than lack of knowledge. Aboriginal children have poorer access to therapy, hearing aids, special teachers, classroom soundfield systems and other rehabilitative programs.2 Furthermore, there is inequitable distribution of funds from the Commonwealth Hearing Health Services Program, with evidence that the hearing health needs of Aboriginal children are not being met.8 What strategies have worked?A systematic review of existing evidence and primary care guidelines for the management of otitis media in Aboriginal and Torres Strait Islander people2 identified effective primary prevention strategies: improving nutrition and the home environment, increasing breastfeeding, and reducing passive smoking. A small but important role was noted for vaccines (the polysaccharide, polyvalent pneumococcal vaccine and the new pneumococcal conjugate vaccine). Controversies remain regarding the effectiveness of antibiotics in primary prevention and the impact of maternal pneumococcal vaccination on infant disease.2 High doses and prolonged courses of antibiotics are often required for the treatment of acute otitis media and CSOM,7 but the optimal use of topical ear preparations remains uncertain.2 Where appropriate primary healthcare interventions have failed, timely referral to otolaryngologists for assessment and surgical interventions can improve hearing outcomes.2 However, access to such specialist care for children in remote Aboriginal communities is suboptimal. Audiological rehabilitation is critical, requiring the provision of ongoing education about effective communication strategies and appropriate use of devices to assist hearing. These include standard hearing aids and bone conductors, as well as classroom devices such as soundfield amplification systems (which provide a uniform soundfield throughout the classroom and increase the speech-signal : noise ratio), and FM systems (a form of personal amplification whereby an FM signal from a microphone worn by the teacher is picked up by a receiver worn by a child with hearing loss).9 What needs to happen in the future?Greater community control over improvements to education, employment opportunities, housing infrastructure and primary healthcare services is long overdue. To realise these improvements requires substantially increased resources, linked to community responsibility. In the meantime, initiatives that increase access to primary healthcare for the detection and management of ear disease and facilitate access to other services should continue. An example is the Office for Aboriginal and Torres Strait Islanders Health Hearing Health Program.10 Realistic expectations about the benefits and harms of evidence-based healthcare interventions should be incorporated into updates of currently available clinical guidelines, and the information made accessible to families. The Commonwealth needs to reform the provision of rehabilitative services and coordinate approaches to soundfield amplification in schools. The research priority is to determine the best use of preventive strategies and interventions (including educational, medical, surgical and audiological initiatives). Multidisciplinary research in the areas of diagnosis, new antibiotics, the role of biofilm and vaccines is also appropriate. Bacterial biofilm is a community of interacting bacteria attached to a surface and encased in a protective matrix of exopolysaccharide. Formation of biofilm in the middle-ear mucosa of Aboriginal children with CSOM may explain the recrudescence of bacterial otorrhoea after viral upper respiratory tract infections.11 Pneumococcal conjugate and innovative protein-based vaccines are aimed at inducing a mucosal immune response. Several Australian trials are currently examining the impact of pneumococcal conjugate vaccine on nasopharyngeal carriage rates and perforation of the tympanic membrane. Only with urgent attention to improving housing and access to running water, nutrition and quality of care, and giving communities greater control over these improvements, will this massive public health problem be solved so that Aboriginal children can take their rightful place in this, the century of communication.

Harvey L Coates MS, FRACS · Peter S Morris PhD, FRACP · Amanda J Leach PhD · Sophie Couzos FRACGP, FACREM, FAFPHM

Aim: To report the preliminary findings of a pilot program to screen newborn babies for congenital bilateral permanent hearing loss.Setting: The five largest maternity hospitals in Perth, Western Australia. Screening was gradually introduced over seven months from February to August 2000.Participants: All babies born at these hospitals after the introduction of hearing screening until 30 June 2001.Methods: One or both of two automated screening devices were used: one measuring transient evoked otoacoustic emissions (TEOAE) and the other automated auditory brainstem responses (AABR). If a "pass" was not obtained in both ears, screening was repeated. All babies who did not obtain a pass in either ear at follow-up were referred for audiological assessment.Main outcome measures: Prevalence of permanent bilateral hearing loss.Results: Of 13 214 eligible babies, 12 708 (96.2%) received screening. The main reason for missing screening was early hospital discharge (309; 2.3%). Of the screened babies, 99% had a pass response in both ears at either the initial or follow-up screen. Twenty-three babies were referred for audiological assessment, and nine were diagnosed with bilateral permanent hearing loss (0.68/1000; 95% CI, 0.31–1.28).Conclusions: Despite our program meeting process quality indicators, our detection rate was low. Before extending the program to smaller hospitals, we need to validate our screening instruments and put in place a system to monitor false negative results.

Helen D Bailey BHealthSci(Nurs)Hons, MPH · Carol Bower MB BS, PhD · Jay Krishnaswamy MSc · Harvey L Coates MS, FRACS

Chronic lead poisoning may manifest clinically as abdominal pain, constipation, proteinuria, haematuria, peripheral neuropathy and muscle weakness.1 With more significant lead poisoning, encephalopathy may occur.2 Sustained blood lead levels of over 0.5 μmol/L in early childhood are likely to be associated with intellectual underperformance.3 However, congenital lead poisoning and its subsequent management has rarely been reported in preterm infants. Treatment is with chelating agents, which reduce lead concentrations in the blood and tissues by forming water-soluble complexes that are cleared by the kidneys.4 We report a case in which the neonatal blood lead level was the highest recorded for a surviving infant. Clinical recordA 24-year-old pregnant woman, who had recently emigrated from India, was found to have a haemoglobin level of 70 g/L at 24 weeks' gestation. At that time it was noted that she was a vegan and had a normal blood film and iron studies. At 30 weeks' gestation, she presented with abdominal pain and a progressive confusional state culminating in seizures. The blood film now showed basophilic stippling, a typical sign of lead poisoning (Box 1), and subsequent testing showed she had a blood lead concentration of 5.2 μmol/L (the National Health and Medical Research Council's public health goal is a level of ≤ 0.48 μmol/L).3 Chelating therapy was initiated with intramuscular dimercaprol and intravenous calcium disodium edetate (CaNa2EDTA).5 Thirty-six hours later the woman had an antepartum haemorrhage, and, after induction of labour, she gave birth to a 1.6 kg (75th percentile) female baby by vaginal delivery. Apgar scores were 4 and 6. The infant was flaccid and areflexic and did not move in response to noxious stimuli, although spontaneous ocular movements were present. As she had emerging alveolar hypoventilation and no gag reflex, she was intubated and ventilated. The clinical suspicion of bilateral diaphragmatic palsy was later confirmed by fluoroscopy. Basophilic stippling was not seen on the infant's blood films, although Heinz bodies were present. Lead concentration in the cord blood was 7.6 μmol/L (12 hours before birth, maternal blood lead concentration had been 2.3 μmol/L). The concentration of erythrocyte porphyrins was 20.3 μmol/L (normal range, 0.4–1.7 μmol/L), and radiographs of the long bones showed an increase in the bone density adjacent to the metaphyses (both signs of lead poisoning). Within 24 hours of birth, the infant was commenced on chelation therapy (intramuscular dimercaprol 4 mg/kg/dose every four hours and intravenous CaNa2EDTA 50 mg/kg/day, given after the second dose of dimercaprol). The blood lead concentration initially rose to 11.8 μmol/L within the first 48 hours of therapy, then fell rapidly over the next few days. The high urinary lead concentration of 52 μmol/L on Day 3 was an indicator that lead was being excreted. The time course of blood and urinary lead concentrations for the first 14 weeks post partum is shown in Box 2. On Day 7, it was judged appropriate to cease intravenous chelating therapy. Succimer (an oral chelating agent) 30 mg/kg/day5 was commenced three days later. At that time, the urinary lead concentration had fallen to 4.2 μmol/L. Over the three-week course of succimer, urinary lead concentrations fell further, while blood lead concentrations remained relatively constant. As the succimer appeared to be having little effect, it was discontinued on Day 31, and intravenous CaNa2EDTA was recommenced 48 hours later. A rise in urinary lead excretion was observed after this course and subsequent courses of parenteral therapy. By Day 42, facial, bulbar, proximal-limb and diaphragmatic muscle activity had improved sufficiently to allow successful extubation. By Day 53, the blood lead concentration appeared to have fallen to a satisfactory level, and an attempt at maintenance therapy using oral succimer at the higher dose of 60 mg/kg/day was commenced.6,7 However, the blood lead concentration increased during the second course of succimer, with a corresponding decrease in the urinary lead concentration. Intravenous CaNa2EDTA was recommenced. When chelation therapy was subsequently discontinued for two weeks, the blood lead concentration again rose, and a fifth course of CaNa2EDTA was initiated. Progress of infant after first 14 weeks. By three months' corrected age (ie, about 5 months after birth) the infant was able to fully feed by sucking, although there was significant gastroesophageal reflux. Her peripheral weakness had almost resolved, but bilateral wrist drop and poor head control persisted. Blood lead concentration had fallen to 1.8 μmol/L. It was decided to reintroduce oral succimer at 60 mg/kg/day. This appeared to be effective, as the lead levels not only fell in the blood but increased in the urine. A brainstem auditory response at four months' corrected age showed right sensorineural deafness. (A magnetic resonance image of the brain at three weeks of age had been normal.) Throughout the hospital stay her serum calcium, zinc, iron, renal and liver function tests were normal. The infant was discharged home, on succimer, at five months' corrected age with a blood lead concentration of 0.95 μmol/L. A neurodevelopmental examination at the time revealed a two-month delay. Her two siblings, aged two and four years, were found to have blood lead concentrations of 0.6 and 0.3 μmol/L, respectively. Lead source identification. An environmental audit of the home and the local Sikh community kitchen revealed no obvious source of lead. Interviews conducted with the mother established that she had been taking several tablets, prescribed by an Ayurvedic doctor in India for treatment of a gastrointestinal complaint, periodically over the course of the past nine years. Analytical results for the various tablets are presented in Box 3, the most notable being the high lead content of two of the tablet types (4.5%–8.9% lead). The mother's tablet use in the nine months before the child's birth represented a lead intake of at least 50 times the average weekly lead intake of Western populations.2,8 Correspondence with the Ayurvedic doctor in India, who prescribed the brown ("HSY-15") tablets in this case, has not yet provided any clues as to the origin of the lead in these tablets. DiscussionClinical considerationsThe diagnosis of intrauterine lead intoxication was made on the basis of a maternal encephalopathy with a high blood lead concentration, maternal anaemia with basophilic stippling, and a high cord-blood lead concentration. Infant blood lead levels of a third to a half the peak level reported here are usually associated with severe cerebral oedema and death.2 In this instance, the infant was encephalopathic and profoundly weak and had diaphragmatic palsy at birth. The limb weakness clinically appeared to be predominantly neuropathic. Several electrophysiological attempts to clarify the presence of either a neuropathy or a myopathy failed owing to technical and interpretive difficulties. Although lead-induced peripheral neuropathy is well described,9 diaphragmatic palsy is unreported. There was no evidence of renal involvement or proteinuria, possibly due to the infant's renal immaturity. There was no basophilic stippling in any neonatal blood film. This relative paradox — the absence of basophilic stippling despite lead intoxication — has been noted previously.10 The unilateral sensorineural deafness is likely to be due to lead toxicity.11 Previous reports of congenital lead intoxication indicate that maternal and cord blood lead levels correlate.12 The marked discrepancy in this case (2.3 μmol/L [mother] v 7.6 μmol/L [cord]) could be due to the possibility that at high maternal blood lead concentrations the lead-binding capacity of the erythrocytes becomes saturated13 and more lead is available for transfer to the fetus. Alternatively, the discrepancy could be due to in-utero mobilisation of lead from fetal tissues without adequate maternal clearance. This latter consideration indicates a potential detrimental effect on the fetus of chelation therapy in pregnancy. As chelating agents bind lead into complexes that are cleared by the kidneys, an increase in urinary lead concentration was expected after administration of each of the chelating agents. This phenomenon was consistently observed after courses of dimercaprol and CaNa2EDTA. However, variable doses of oral succimer during the preterm period did not lead to corresponding increases in urinary lead concentration, despite raising the dose to a level higher than those recommended in the literature.5-7 Only when oral succimer was recommenced at three months' corrected age did the predicted response occur. This apparent early ineffectiveness of succimer could be due to absorptive failure from the infant's immature gut. Furthermore, succimer is a prodrug that requires cysteine for activation.2 It is unclear whether or not this enzymatic activation process is mature in the premature infant. Public health considerationsWhile lead was the principal concern in this case, mercury was also detected in some of the tablets (Box 3). Weekly ingestion of one of the tablets containing 400 μg would exceed the Australian average weekly mercury intake by at least fourfold.8 Mercury poisoning was of secondary concern in the current circumstance, and chelation therapy was expected to remove the mercury along with the lead. This does, however, illustrate that herbal medicines may contain more than one potentially toxic component. In many countries, including Australia, it is legal to import herbal remedies for personal use, although some restrictions apply.14 In addition, testing programs for contaminants in herbal remedies are virtually non-existent. Acute lead poisoning has been reported from traditional and herbal medicines and cosmetics obtained from India,15-17 the Middle East,18-19 Mexico20 and Asia.20-21 This should be a matter of grave concern to patients who take such remedies, and to health professionals and health authorities in these countries and in Australia. 1: Mother's blood film just before parturition, showing basophilic stippling of red cells 2: Infant blood and urinary lead concentrations from birth to 14 weeks of age* *Horizontal lines across top of graph indicate periods of parenteral therapy with calcium disodium edetate and oral succimer. Dotted horizontal line shows National Health and Medical Research Council public health goal for maximum lead concentration in blood (0.48 μmol/L). 3: Metal analysis of tablets used by the patient* Tablet colour Lead per tablet (mg) (%) Mercury per tablet (μg) (%) Brown ("HSY-15") 45 (8.9%) 15 (0.003%) Red 23 (4.5%) NA Pink 1 (0.2%) 400 (0.08%) Green 2 (0.003%) 10 (0.002%) *Analysis by IMVS Laboratories, Adelaide. NA = not analysed.

Paul A Tait BPharm · Amish Vora MB BS · Simon James FRACP · D James Fitzgerald PhD · Beverly A Pester BA MA

The rates of bronchiectasis for Indigenous children from remote Australian communities are unacceptably high, with one study showing 14.7/1000 Aboriginal children. Children with bronchiectasis need to be identified early for optimisation of medical treatment. Under-reporting of cough is common. Bronchiectasis should be suspected in children with recurrent bronchitis or pneumonia, and when, despite appropriate therapy, pulmonary infiltrates or atelectasis persist 12 weeks beyond the index illness. During acute infective episodes, oral antibiotics and chest physiotherapy to clear the airways should produce prompt resolution; otherwise, hospitalisation is necessary. Management follows the cystic fibrosis model of regular review, encouragement of physical activity, optimising nutrition, maintenance of immunisation and avoidance of environmental toxicants, including passive smoke exposure. Successful management and prevention of bronchiectasis will require improvements in housing, nutrition, and education, as well as access to comprehensive healthcare services, with coordination between primary and hospital-based healthcare providers.

for the Working Group on Indigenous Paediatric Respiratory Health

With our high standards of sanitation and healthcare, how important is breastfeeding? Any breastfeeding advocate can rattle off a list of the advantages of breastfeeding to infants, their mothers and society. The list of benefits ranges from better emotional attachment to a lower risk of childhood leukaemia or dental malocclusion. However, claims of benefit have been contentious, with many studies failing to demonstrate a clear advantage and some even showing increased risk of a negative health outcome with breastfeeding. The constituents of human milk suggest that it has evolved to promote infant health and human growth, particularly to protect children from infections and to support the rapid growth of the human brain. Despite advances in science and manufacturing, infant formula will always be a poor copy of human milk. It is improbable that a substitute will ever reproduce the full spectrum of human milk proteins, milk sugars (numbering over 100), live white cells and antibodies programmed by infections in the infant's environment, together with constant variations in milk content to meet the needs of the growing infant. But does this matter in a developed country such as Australia? Is there justification in the argument that women are being pushed too hard to breastfeed, or is there more to infant nutrition than the provision of clean water and biologically safe artificial feeds? Many studies reporting the effects of breastfeeding, both positive and negative, have major methodological flaws. Indeed, robust studies are difficult to carry out. Random allocation of study participants to either a "breastfeeding" or an "artificial feeding" group is unethical, especially if we accept the belief that "the epidemiologic evidence is now overwhelming that, even in developed countries, breastfeeding protects against gastrointestinal and (to a lesser extent) respiratory infection, and that the protective effect is enhanced with greater duration and exclusivity of breastfeeding".1 So evidence for the effects of breastfeeding must rely largely on observational cohort and case–control studies. Blinding to the intervention group is difficult, except at the analysis level. Moreover, mothers who elect to breastfeed differ from those who don't — the former group are generally better-educated women of higher socioeconomic status, who are more likely to have partners and less likely to smoke. All of these factors are likely to be independently associated with positive health outcomes, so failure to adequately adjust for these confounders generally favours positive breastfeeding outcomes. On the other hand, apparently poorer outcomes may result if mothers preferentially breastfeed more vulnerable infants. Difficulties with defining terms such as "breastfeeding" and "exclusively breastfed", and with defining endpoints such as "atopic disease", also make comparisons between studies difficult. So, have the roughly 2000 papers on breastfeeding and human milk listed in Medline since the year 2000 helped answer the question of whether or not it matters if a term infant born in a country like Australia is breastfed? I will confine my comments to the three most common health problems in Australian children: infection, obesity, and asthma. In Australia, there are almost 20 000 hospital admissions a year for acute gastroenteritis in children under five years old. Rotavirus accounts for about half of these episodes and is also one of the most important nosocomial infections in paediatrics. A Belarussian study2 (involving 17 000 healthy mother–infant pairs intending to breastfeed) showed that, in centres randomly assigned to deliver support for breastfeeding (as outlined by the Baby Friendly Hospital Initiative3), there were increases in exclusive and continued breastfeeding and reductions in episodes of gastrointestinal infection. In an Italian study4 of infants aged 1–18 months admitted to an infant ward, fewer breastfed infants contracted rotavirus infection (10.6% v 32.4%), and none of these became symptomatic. It has been shown that human milk lactadherin prevents symptoms in breastfed infants infected with rotavirus by binding to the virus and inhibiting its replication.5 Obesity is the commonest chronic health problem in Australian children. This has health implications both in and beyond childhood, as about half of obese children become obese adults. The effect of breastfeeding on later overweight/obesity remains contentious. A 2001 review of 18 studies6 concluded that most studies examining the effects of breastfeeding on later obesity had found an insignificant effect, although two of the studies actually found a positive association between breastfeeding and later body fatness. Since that review, four large studies7-10 (involving between 2000 and 14 000 children) have shown a lower prevalence of overweight in previously breastfed children, with several showing decreasing risk with longer duration of breastfeeding. The three studies of older children (aged 5–14 years)8-10 also found a negative association between breastfeeding and obesity (with adjusted odds ratios [ORs] ranging from 0.66 to 0.8). Similar results in these three studies, despite differences in method, suggest that the finding may be robust. The second most common chronic health problem in Australian children is asthma. A large Western Australian study showed a substantial reduction in risk of childhood asthma, as assessed at six years of age, if exclusive breastfeeding is continued for at least the first four months of life.11 This was included in a systematic review with meta-analysis of 12 prospective studies,12 which gave a summary OR of 0.70 (95% CI, 0.60–0.81) for asthma among children who had been breastfed, with a greater effect in children from families with a history of atopy (OR, 0.52; 95% CI, 0.35–0.79). The studies were mainly of younger children but included children up to 8.4 years. Another prospective study of more than 330 000 children followed to age 24 months supported these findings: breastfeeding of less than nine months' duration was associated with an increased risk of asthma or wheezing, and a dose–response effect was observed with breastfeeding duration.13 However, a recent report has suggested that atopic children with asthmatic mothers are more likely to develop asthma in later childhood if they have been exclusively breastfed.14 There may be interesting possibilities for intervening to further reduce atopy in at-risk families. Mothers of infants who develop atopic sensitisation have a higher intake of saturated fat,15 and their breast milk is much lower in some long-chain unsaturated fatty acids (which may have antiallergenic properties16). Perhaps improving maternal diets and the use of probiotics17 may reduce the prevalence of atopic disease in their children. I have selected three childhood conditions for which small changes in prevalence or disease severity would have a major impact on the health of the nation. The US Department of Agriculture, Food and Nutrition chose otitis media, gastroenteritis and necrotising enterocolitis, and estimated that the United States would save a minimum of US$3.6 billion dollars a year if breastfeeding rates increased by 10% at initiation and by 20% at the age of six months.18 While we should be careful not to convey to mothers that breastfeeding will make their child a trim, non-atopic, infection-free genius, the balance of the evidence is that breastfeeding is of benefit in many ways. Every healthcare professional in contact with young children and parents should be familiar with their responsibilities under the World Health Organization Code19 to encourage and promote breastfeeding — for the health of the nation.

Patricia McVeagh MB ChB FRACP

Objective: To examine the potential of the New South Wales baby-walker regulation to reduce injury.Design: Injury surveillance data were used to reconstruct baby-walker injury incidents, which were examined in conjunction with the 2000 NSW baby-walker regulation, which requires a specified level of stability and a gripping mechanism to stop the walker at the edge of a step.Setting and participants: Injury surveillance data on injuries to 381 babies collected from hospital emergency departments in South Australia and Victoria, 1986–2000.Main outcome measure: Injury events that would still have occurred with the regulation in place.Results: About half (46%; 95% CI, 32.5%–59.8%) of the serious baby-walker injuries (ie, requiring admission to hospital) are caused by the walker enabling babies to reach hazards other than steps and stairs.Conclusion: The New South Wales regulation has the potential to eliminate only about half the baby-walker injuries. Banning baby walkers altogether is preferable.

Peter G Thompson CertMechEng, MPH

Exposure of the thyroid gland to any irradiation requires lifelong follow-up supervision One of the questions most frequently asked by patients about to receive radioactive iodine as therapy for non-malignant conditions is whether it will result in bodily cancer. This question has been satisfactorily answered in the negative,1,2 so strong reassurance can be given. No such reassurance can be given for the malignant effects of therapeutic external beam irradiation on the thyroid gland. In childhood, the sensitive thyroid gland can be exposed to therapeutic irradiation directly, as in the treatment of localised neck tumours such as lymphoma or sarcoma and in total-body irradiation before bone marrow transplantation. Where the thyroid gland is not directly the target of therapy, it can be affected by scatter irradiation, as occurs during prophylactic cranial irradiation of the central nervous system in haematological malignancies. Thus far, no measures have been found to protect the thyroid gland from external irradiation in these settings. In this issue of the Journal (page 584), Somerville and her colleagues report the first Australian experience in a study encompassing a large number of children recruited to the Late Effects Oncology Clinic of the Children's Hospital at Westmead.3 The period of study covers 10 years. The sample population was divided into a group who received direct irradiation and another, designated as "scatter", in which there was exposure to the upper half of the body as external beam irradiation but no direct irradiation of the thyroid gland. The study was designed to emulate the approach that would commonly be used by a clinician seeking evidence of change in the thyroid gland. Palpation was used to delineate size and other characteristics. The customary thyroid function tests were carried out. These findings were supplemented by high-resolution ultrasound examination of the neck, and, if the findings warranted, fine-needle aspiration biopsy was undertaken. Suspicious findings from any of these evaluations led usually to surgery, but an abnormal ultrasound result was the chief indication for surgery. Some surprising and important revelations have come to light: Palpation of the thyroid gland was unreliable and misleading in a significant proportion of patients, with a preponderance of non-discovery. Ultrasound examination was almost always abnormal when the thyroid gland was palpable, and abnormal in more than 50% of patients in which the gland could not be felt. Thyroid function tests gave little warning of malignancy, and the elevation of thyroid-stimulating hormone in inadequately supplemented patients, although noted, gave no pointer to the status of the thyroid gland as a whole or the underlying presence of malignancy. Fine-needle aspiration biopsy was carried out in a few patients, but did not materially influence their management. The authors advocate total thyroidectomy for multiple nodules on ultrasound examination or where new nodules appear after partial thyroidectomy. Twenty-five patients from the direct-irradiation group had abnormal ultrasound results and underwent surgery, whether or not the thyroid gland was palpable; six of them harboured malignancy. On the other hand, in the scatter group, of 24 patients with similarly abnormal ultrasound results 12 were affected. Not only were localised recurrences frequent, but additional cancers in other areas of the body were noted by the authors, so vigilance in this respect is required. When surgery was carried out, the histological appearance of glands exposed to both types of irradiation indicated widespread damage and evidence of increased endothelial activity ranging from scarring through to nuclear atypia. There are important lessons to be learned. Exposure of the thyroid gland to any irradiation requires lifelong supervision and introspection. This should include high-resolution ultrasound. The extent of thyroid exposure to radiation may be arcane and not recalled when the highlight of the history is focused on areas away from the gland. Most radiation oncology units in Australia have follow-up facilities, but the duration of follow-up is not uniform. Moreover, patients travel and disperse, so their supervision will be most likely carried out by doctors with less experience of such patients. In this regard the American Thyroid Association publishes an excellent information sheet for patients.4 The article concludes with a series of pertinent recommendations which emanate from the study. Although false positive results can occur, the risks demonstrated in this study indicate that the management regimen recommended by Somerville et al far outweighs a sanguine approach to the problem. Implicit in this is the importance of providing patients with information about the potential risks and the need for regular assessment. Somerville et al observe that the Australian experience has disclosed a greater incidence of thyroid abnormality than seen in some other countries. This may derive from differing methods in the extent and depth of the studies, together with the sophistication of the ultrasound. The magnitude of the dose in the reported series did not seem to influence the emergence of malignancy. Only time from the administration of the radiation therapy was important. It will be interesting to learn of the further evolving experience. In this regard, results of fluorodeoxyglucose positron emission tomography, in association with rising thyroglobulin levels, seem to give a clearer delineation of recurrent malignancy than can be obtained by other methods.5 There may come a time when it will be possible to protect patients from scatter irradiation involving the head, neck or upper-body region in the treatment of more generalised cancer such as leukaemia. However, such protection does not appear to be imminent and, even if attained, there will still be a group of potential thyroid cancer subjects as a legacy of the current therapeutic era.

Alex K Cohen AO, MD, FRACP · Agatha A van der Schaaf FRACP

Objectives: To describe a cohort of survivors of childhood malignancy at risk of developing thyroid abnormality, and propose guidelines for management of such patients.Design: Retrospective case series.Setting: Late-effects oncology clinic at a large children's hospital in Sydney.Subjects: 142 patients who had received irradiation to the thyroid from the 1970s onwards, who attended the late-effects clinic from May 1989 to December 1998.Interventions: Thyroid palpation by an endocrinologist or surgeon, serum thyroid-stimulating hormone assay and thyroid ultrasound examination were performed on all subjects and, depending on findings, some subjects proceeded to fine-needle biopsy or surgery (total thyroidectomy). A few patients required adjuvant 131I administration.Outcome measures: Radiation dose received; results of thyroid palpation; thyroid function tests; ultrasound findings; diagnosis of the abnormalities; and outcomes of surgical interventions.Results: 49 subjects (24 of 65 patients who received scatter irradiation to the thyroid and 25 of 78 patients who received direct irradiation) had thyroid surgery. Of these, 12 in the scatter and six in the direct irradiation group were found to have thyroid malignancy. Fifty subjects with abnormal ultrasound results remain under surveillance. Having a palpable thyroid was predictive of malignancy, but age at original diagnosis, sex, current age, time since irradiation, radiation dose, nodule type and nodal involvement were not.Conclusion: There is a significant risk of cancer in thyroid glands exposed to radiation as part of therapy for childhood cancer. This risk is greater for patients who received scatter (versus direct) irradiation. Nodular change is usually not apparent for many years, so lifelong surveillance is necessary. Palpation alone is not sufficient to detect thyroid cancer and thyroid ultrasound examination is recommended.

Helen M Somerville MB BS, MPaed · Albert H Lam MD, FRACR · Michael M Stevens MB BS, FRACP · Kate S Steinbeck PhD, FRACP · Graham Stevens MD, FRANZCR · Leigh W Delbridge MB BS, FRACS

Notification of abuse should trigger initiatives to prevent further abuse and ameliorate adverse consequences There has been concern recently in Australia about the sexual abuse of children by those in authority. Clearly, we expect such people to behave better. However, child sexual abuse is much more likely to involve the ordinary people comprising a child's family and their friends. In 1990 the World Health Organization Global Burden of Disease project1 identified 10 risk factors that, if averted, would reduce the burden of disease by a third (eg, malnutrition, poor sanitation, unsafe sex). For the next revision of the risk estimates, the WHO Collaborating Centre at St Vincent's Hospital, Sydney, was asked to prepare a report on the prevalence and impact of child sexual abuse on health status around the world.2 Here, we comment on the situation in Australia. Child sexual abuse can be subdivided into three levels of severity. Non-contact abuse includes sexual solicitation or exposure by an older person; contact abuse involves genital touching or fondling; and penetrative abuse includes oral, anal or vaginal intercourse by an older person. Prospective studies of the prevalence of child sexual abuse are ethically and legally difficult. Thus, all data are from retrospective reports of men and women asked about their experience of unwanted sexual activity before the age of 18 years. However, establishing the validity of retrospective reports is not easy — only a minority of children who have experienced child sexual abuse report it to their parents, and only a minority of these parents report the abuse to the authorities. Furthermore, unreliable recall represents a threat to the validity of the results. However, follow-up studies show that a false-negative rather than a false-positive bias is the rule.3 Methodological factors like the type of sample used and the number of questions asked to ascertain abuse may also compromise the validity of results. Accordingly, for the WHO study, such method factors were statistically controlled for. Seven studies of child sexual abuse have been performed in Australia.4-12 The adjusted prevalence estimate in males was 5.1% and in females 27.5%, which corresponds with rates in comparable countries. The rates for contact plus penetrative abuse were two-thirds of these (ie, 3.6% in males and 17.9% in females). The onset of abuse occurs at a mean age of 10 years, with most starting before age 12. The abuser is a family member in about 40% of cases, and is known to the child in 75% of cases. The abuser is usually male, mean age 32 years. Child sexual abuse is more frequent in families beset by other adversity, and it is difficult to determine the cause of any increased rate of mental disorders in the presence of an aggregation of risk factors. Two reports of a twin study11,12 that was able to control for the effect of family environment showed increased rates of anxiety, and depressive and substance-use disorders in the abused twin. Rates of suicide attempts were also increased in the abused twin. Child development studies in other countries, in which the family environment was measured independently of sexual abuse or mental disorder, have generated similar results.13,14 People who report contact or penetrative abuse in childhood have double the normal rates of mental disorders and suicide attempts. Attributable risk calculations suggest that 11% of depression in women and 3% of depression in men could be attributed to contact or penetrative abuse in childhood. Quite apart from increased rates of mental disorders, children who have experienced sexual abuse continue for years to show significantly more distress and disturbed behaviour.8 A minority of children are able to surmount this type of adversity and remain unaffected. For those who do not the sequelae can be serious, with great societal costs. What can be done? Teachers and doctors are required to report sexual abuse that comes to their notice. However, this system has the potential to encourage a "don't ask, don't know" attitude. At the same time, it does serve notice to abusers that they are at risk of discovery. In some States, criminal record checks required of anyone who works with children have removed any suggestion that child sexual abuse will be tolerated or excused. Conviction of offenders is not simple, even in the minority of cases in which there is clear medical evidence, as, apart from the child, there are usually no witnesses. Nevertheless, the change in the judicial attitude to child sexual abuse is expected to result in a reduction in incidence. Notification of abuse should trigger other initiatives to prevent further abuse and ameliorate any adverse consequences. Firstly, help for the mother/carer to keep the child safe from further abuse, whether achieved by health visitor support, family counselling, or physical relocation of the family; and secondly, treatment for the child to ensure that disturbed and dysfunctional behaviours and the increased risk of mental disorders do not occur. A recent review of controlled studies of treatment for sexually abused children has provided preliminary evidence that the sequelae can be minimised in the short term.15 It is clear, however, that not all abused children benefit and more research is needed. The management of such children should be driven by science and not simply by compassion.

Gavin Andrews · Bronwyn Gould · Justine Corry

To avoid confusion, the term "autistic spectrum disorders" should only be used as the collective term for a group of defined disorders Autism is a severe neurodevelopmental disorder associated with considerable personal suffering, parental burden and community cost. In recent reports, the prevalence of autism has varied widely from five to 67 cases per 10 000 children, an increase compared with the 3.5–4.5 cases per 10 000 children reported in the 1970s.1,2 This apparent prevalence increase has raised considerable public concern, particularly as it has been temporally linked to the introduction of the measles–mumps–rubella (MMR) vaccine. However, recent epidemiological investigations found no causal link between autism and the MMR vaccine.3,4 The increase in prevalence might indicate a true increase in incidence, but most of the increase can be accounted for by changes in case-finding methods and diagnostic criteria, and by differences in sample sizes, and the age range and intellectual ability of the populations studied.3 The increase in numbers identified has led to a corresponding increase in demand for services. The predominant international approach to diagnosis used by the ICD-10 classification of mental and behavioural disorders5 and the Diagnostic and statistical manual of mental disorders, 4th edition [DSM-IV],6 groups autistic conditions in the category pervasive developmental disorder (PDD) and specifies criteria for the subtypes autistic disorder, Asperger's disorder and atypical autism (PDD – not otherwise specified [PDD-NOS]) (Box). Recently, some confusion has been introduced, as there is a general move away from the term PDD towards the term autistic spectrum disorder (ASD), which has been used in at least four different ways. 1. To refer to a broader group of conditions sharing a "triad of impairments" in social interaction, verbal and non-verbal communication and imagination. Wing7 introduced the term ASD for this purpose. These conditions include the PDDs, but also disorders of empathy and deficits in attention, motor control and perception.8 The term ASD implies a continuum of disturbance in each of these three domains and has led to empirical studies of the continuum of social reciprocity which has implications for testing the clinical validity of categorical diagnostic subtypes of ASD.9,10 Contemporary genetic studies of autism provide evidence of a broad phenotype of social disability, anxiety, depression and unusual personality traits, and a complex interaction of several genes.11 It is not known whether specific patterns of genetic abnormality or the interaction of other risk factors with a common genetic predisposition operate to produce different developmental outcomes, such as severe language disability. Ultimately, genetic studies will determine the validity of categorical diagnoses. In the meantime, for this broad phenotype construct of ASD to have better research and clinical utility each subtype requires international consensus on the discriminating diagnostic criteria, and reliable methods to measure the continuum of each domain. 2. To describe a continuum of intellectual ability among children with PDD — from normal IQ levels (functioning at a high level) through to severe levels of intellectual disability. Some argue that autism is a single-spectrum condition, with the observed differences resulting from different levels of intellectual ability, and that subtypes (eg, Asperger's disorder) are not empirically justified.12 Other studies have used the criterion of significant delay in language development to differentiate children with autism who function at a high level from those with Asperger's disorder. They have found higher levels of psychopathology in children with Asperger's disorder,13 and significant differences in executive function and motor planning between these two groups.14 3. As a description of symptom severity. For example, the Department of Education and Training in Victoria uses the Childhood Autism Rating Scale15 completed by clinicians to provide a cumulative score on the severity of some autistic symptoms to assist in determining funding for education aides. Applying the concept of severity to a disorder that has multiple diagnostic criteria is problematic. For example, a child with autism might have relatively better developed language skills and only a few untroublesome rituals, but may have severe social withdrawal. Can a concept of overall severity be meaningfully applied to such a child and might it overshadow the recognition of a potentially treatable comorbid condition such as anxiety, depression, or attention deficit hyperactivity symptoms? Children with autism who function at a high level are referred to by some as having mild symptoms,12 even though there is evidence that they are often handicapped by high levels of psychopathology.13 4. As a developmental concept. Autistic spectrum is used to describe how skills, such as language, might improve relatively over time so that some children with autism might move from being less able to being more able.16 Use of the term ASD is likely to persist, but to avoid confusion it should be confined to the collective term for a group of defined disorders. Wing used it to promote access to services otherwise denied to young people with autism functioning at a high level.7 This problem still exists, for example in Victoria. Such children do not meet the criteria for funding for an education aide, even though they have a range of severe social, emotional and behavioural problems. Should the inclusion criteria for services be broadened to include the full range of social, emotional and behavioural needs, or, to contain costs, should they be confined to intellectual ability? Behavioural and educational approaches to treatment have received the best empirical support.17 Therefore, allocation of increased funding to support a flexible range of behavioural, educational and family support programs, based on a comprehensive assessment of the diagnostic and cognitive profile and the emotional and behavioural needs of all young people with a PDD, is likely to prove the most economical use of resources in the long term. Pervasive developmental disorders: broad diagnostic criteria Autistic disorder (DSM-IV) Childhood autism (ICD-10) Asperger's disorder (DSM-IV) Asperger's syndrome (ICD-10) Social interaction disability Social interaction disability (as for autistic disorder) Language delay and communication disability No delay in language Restricted, stereotyped behaviour Restricted stereotyped behaviour (as for autistic disorder) Onset before age 3 No delay in cognitive development (DSM-IV only) Other subtypes: Rett's disorder, childhood disintegrative disorder, atypical autism (PDD-NOS). DSM-IV = Diagnostic and statistical manual of mental disorders, 4th edition.6 ICD-10 = ICD-10 Classification of mental and behavioural disorders.5

Bruce J Tonge MD, FRANZCP

To the Editor: A number of recently published articles indicate that the prevalence of overweight and obesity in children is increasing at an alarming rate on a national1 and international2 level. Overweight children are more likely to become overweight adults and to experience chronic health problems associated with adult obesity. We report results obtained from a survey of primary schoolchildren on the New South Wales Central Coast which extends the time series from that in the article by Magarey and colleagues (1985 and 1995 data)1 to the year 2000. We undertook a cross-sectional study of children at a Central Coast primary school in November 2000 as part of a community study. This study was approved by the Central Coast Health Ethics Committee. All children in each class were asked to take part. With parental consent, weight and height were measured in children from all class groups (aged 7–11 years) by child health nurses using standardised procedures. Children were classified as overweight or obese using the standard international cutoffs for body mass index.3 They were compared with data obtained during the 1985 Australian Health and Fitness Survey (AHFS85) and the National Nutrition Survey of 1995 (NNS95).1 A total of 268 children (127 girls, 141 boys) were surveyed (average of 25 girls and 28 boys of each age). This represented a 70% response rate. The Table shows that the incidence of overweight and obesity in Australian children has continued to increase, with relative risks for the increase between 1985 and 1995 of 1.37 (95% CI, 1.07–1.75) for boys and 1.82 (95% CI, 1.49–2.22) for girls, and relative risks for the increase between 1995 and 2000 of 1.71 (95% CI, 1.21–1.43) for boys and 1.21 (95% CI, 0.87–1.67) for girls. Our findings indicate a marked increase in proportions for boys in only five years since NNS95. While the increase for girls was not statistically significant, the pattern is consistent. Prevalence of overweight and obesity in children aged 7–11 years for 1985, 1995 and 2000 Sex Year Number Overweight (%) Obese (%) Overweight + obese (%) Boys 19851 2425 9.7 1.5 11.2 19951 457 11.6 3.7 15.3 2000 141 16.3 9.9 26.2 Girls 19851 2443 11.0 1.9 12.9 19951 430 17.2 6.3 23.5 2000 127 21.3 7.1 28.4 Thus, the incidence of overweight and obesity in Australian children is steadily increasing. Importantly, according to the 1996 Census Socio-Economic Indexes for Areas,4 the school we surveyed is situated in an area ranked in the middle quintile for relative socioeconomic disadvantage (state and national average), and is immediately adjacent to one 4th- and several 1st-quintile and 2nd-quintile areas. We believe our findings are representative of the Australian population of children. The challenge to healthcare workers is significant. The National Health and Medical Research Council's Acting on Australia's weight5 identifies goals for preventing further weight gain in adults, and eventually reducing the proportion of the adult population that is overweight or obese, and to ensure the healthy growth of children. Recommended strategies range from national dietary and physical activity guidelines to increasing physical activity through the design of towns, transport systems and public recreational facilities. Effective strategies are urgently needed to alter food intake and physical activity at individual, school, community and population levels.

Susan Goodman · Peter R Lewis MB BS, FAFPHM · Andrew J Dixon · Cheryl A Travers

To the Editor: The South Pacific Underwater Medicine Society (SPUMS) recommends that, before starting scuba-diving activities, all candidates undertake a medical assessment by a doctor trained in diving medicine. SPUMS recommends a minimum age of 14 years for all entry-level scuba activities, as does Australian Standard 4005.1. This recommendation is based on the belief that younger children do not have the emotional maturity and confidence to safely manage underwater emergencies. Such emergencies, which may include running out of air, being separated from your buddy, being caught in a strong current, and equipment malfunction, can all result in panic.2,3 A diver who panics will typically make a rapid ascent to the surface, risking life-threatening pulmonary barotrauma and decompression illness.2 Commercial scuba diving instructor agencies are introducing a number of introductory activities for children as young as eight years. SPUMS urges caution in assessing young children as fit to dive. Medical practitioners making these assessments should clearly understand the nature of the activity to be undertaken, the equipment to be used and the nature of the environment in which the training is to occur. They should also understand the nature of the certification to be awarded. The presence of at least one legal guardian during this assessment is desirable to ensure that the risks are fully understood and to ensure the desire for the child to undertake the activity is not that of the parents alone. An individual may meet the criteria laid down in a standard or understand and accept the risks of an aquatic sport. However, it is not clear that a young child is mature enough to make this informed choice.4 Clearly, some 14-year-olds also lack sufficient maturity, and an experienced diving physician will advise them to delay their open-water certification course until greater maturity is demonstrated. Alternatively, some children younger than 14 years may be completely safe in undertaking a highly structured, one-on-one, supervised scuba experience in a swimming pool. However, it should be understood that trialling scuba equipment in a swimming pool has resulted in significant morbidity. SPUMS continues to recommend a minimum age of 14 years for all entry-level scuba activities involving open-water dives, and recommends caution in assessing younger children for all other scuba experiences.

Robyn M Walker MB BS, DPHM

The widespread application of public iodine supplementation programs, which cover about 3–4 billion people worldwide,1,2 is a response to the paucity of iodine in the natural diet in many regions of the world and the severe public health consequences of iodine deficiency.3 However, in some countries, the tendency to low iodine intake has mostly been corrected by haphazard increases in the iodine content of certain parts of the diet.4 In the United Kingdom, dairy products may contain extra iodine as a result of adding iodine to cow feed to increase the animals' reproductive performance or of using iodine-containing cleansing agents in the dairy industry. As reviewed by Phillips,5 this unplanned increase in iodine intake has eliminated endemic goitre in Britain during the last 30–40 years. In the United States, London and colleagues encountered cases of unexplained very high iodine intakes (1100–1300 µg per day) in 1964. Subsequently, they discovered that bakers used iodine-containing conditioners in bread and that this caused high levels of iodine intake.6 Obviously, such unplanned variation in dietary iodine is a hazardous way of providing a population with an adequate intake of iodine, as mechanisms unrelated to disease prevention can profoundly alter iodine intake. To some extent, Australia may be a country where factors other than disease prevention have modulated the intake of iodine, and iodine intake may now be in an unplanned phase of decrease.7 A report by McElduff et al8 (page 317) in this issue of the Journal seems to support this proposition. McElduff and colleagues looked at the frequency distribution of whole-blood thyroid-stimulating hormone (TSH) concentrations in newborns in the northern Sydney area. TSH is measured as part of screening for congenital hypothyroidism. In 5%–10% of infants around 72 hours after birth, TSH values were above 5 mIU/L. The World Health Organization (WHO) recommends assessment of TSH concentrations in newborns to detect population iodine deficiency, and specifies that less than 3% of newborns should have a whole-blood TSH concentration over 5 mIU/L. In a subsample of neonates, McElduff et al found that, during pregnancy, their mothers had a median urinary iodine concentration of 109 µg/L, indicating borderline mild iodine deficiency. WHO specifies that the median urinary iodine concentration in adults should be over 100 µg/L, and an extra iodine intake of 50 µg/day in pregnant and lactating women.1 Thus, the corresponding median urinary iodine concentration of pregnant women would be around 130 µg/L. McElduff et al warn that Sydney may be an area of iodine deficiency, and suggest that iodine intake and risk of disease should be investigated in more detail. Their concern is well founded. Even if there is no documentation that these borderline iodine values are harmful to a mother and child, the margin of safety is small. Furthermore, in Australia, there is apparently no regular surveillance of population iodine status, or of the variable iodine content of dairy products and other foods. The iodine intake may well be even lower in other sections of the Australian population. Severe iodine deficiency may cause brain damage and other developmental disorders,3 and goitre and its complications may affect a significant proportion of the population at all levels of iodine deficiency.9 Any public healthcare system should evaluate iodine intake and prevent disorders caused by iodine deficiency. Several factors need to be taken into account in such an evaluation and prevention program: The relationship between iodine intake and the risk of thyroid disease is not a simple one. Even if iodine supplementation may decrease the risk of some thyroid disorders, the risk of other disturbances at a younger age, such as hypothyroidism and Graves' disease, may increase.4 Severe iodine deficiency, with a median urinary iodine excretion of less than 25 µg/24 h, is an instance where giving any type of iodine supplementation is better than doing nothing. However, at higher levels of intake, careful planning and surveillance are needed. The methods often used for evaluating iodine intake and the risk of disease are not perfect. Neonatal screening showing more than 3% of TSH values over 5 mIU/L is not, by itself, enough to indicate insufficient maternal iodine intake. Detection of neonatal hypothyroidism requires identification of relatively high TSH levels (20–25 mIU/L), and many TSH assays and screening programs are not designed to identify TSH values around 5 mIU/L with reasonable confidence. Technical aberrations can easily give an increased frequency of elevated blood TSH concentrations. One such aberration occurs with sampling of blood before TSH has fully returned to baseline levels after the early postnatal surge. As discussed by McElduff et al,8 early sampling may have contributed to their findings. Iodine deficiency is not the only pathogenetic mechanism leading to an increase in blood TSH levels in neonates. Iodine has an autoregulatory inhibitory effect on the thyroid gland, with a fall in both thyroid hormone synthesis and secretion. Possibly, this mechanism has been developed to protect against hyperthyroidism induced by a sudden iodine load. In a variety of abnormal states the thyroid gland overreacts, producing hypothyroidism. The thyroid of the fetus and infant is considerably more sensitive to iodine inhibition than the maternal thyroid. Excess iodine intake, rather than iodine deficiency, in mother or infant has been a more common cause of transient neonatal hypothyroidism in countries with a relatively low iodine intake, such as Germany, Italy and Belgium.4 In severe iodine deficiency, iodine supplementation to the mother decreases the abnormally high serum TSH in both the mother and the newborn.10 On the other hand, in pregnant women with urinary iodine concentrations around 50 µg/L, iodine supplementation decreases TSH levels in mothers, but not in cord blood. TSH levels in the newborn may even be higher after iodine supplementation.11 The finding of McElduff et al of a positive correlation between maternal urinary iodine concentrations during pregnancy and whole-blood TSH levels in neonates needs further elaboration,8 but it may be an example of iodine autoregulation of the fetal thyroid. Should pregnant women living in mild and moderately iodine-deficient areas receive iodine supplements, and does supplementation involve any risk? An increase in iodine intake will improve thyroid function in pregnant women, which is important for early brain development in their infants.12 There are still things to be learned about the influence of small amounts of iodine on neonatal thyroid function in mild iodine deficiency, and about pituitary/thyroid feedback regulation in the fetus and small infant. A tendency to a slight increase in neonatal TSH level after iodine supplementation may be of little importance, as, in these infants, the serum concentration of T4 (which may be the major thyroid hormone influencing brain development12) does not show a concomitant reduction.11 Finally, iodine supplementation imposes no risk of worsening of postpartum thyroid dysfunction in the mother.13 In conclusion, pregnant women should not be iodine deficient. To strictly follow WHO guidelines on iodine intake, pregnant women with similar urinary iodine levels to those found by McElduff et al could alter their diet towards more iodine-rich foods, or they could take a small iodine supplement as part of the vitamin and mineral supplements recommended for pregnant women in most countries. However, there is at present no evidence that a supplement will have beneficial effects. Ideally, iodine intake should be evaluated and kept optimal in the entire population, taking into account that unnecessary high iodine intakes may be associated with more hypothyroidism.4 The studies by McElduff et al8 and other researchers7 demonstrate the need for national monitoring and adjustment of iodine intake as part of a program of prevention of thyroid disorders and their complications. Such initiatives normally involve government nutrition or public health agencies in collaboration with experts in thyroid diseases, nutrition and epidemiology and prevention.1,2 It would be an added bonus if the program elucidated some of the unresolved issues in the field of population iodine supplementation in developed countries. This would continue the considerable contribution of Australian scientists to the understanding and correction of iodine-deficiency disorders.3,14

Peter Laurberg MD, DMedSci · Susanne B Nøhr

In 1974, Caffey suggested the label "whiplash shaken infant" to describe infants who had subdural haemorrhages without evidence of external injury.1 Much has been learned about inflicted head injury since that time. In September 2001 a conference was held in Sydney to share this knowledge among people from many disciplines who work with, or are affected by, children thought to have been injured in this manner. It was jointly organised by the US National Center on Shaken Baby Syndrome, the Children's Hospital, Westmead, and the Sydney Children's Hospital, Randwick. Definition and controversiesShaken baby syndrome (SBS) is a form of child abuse that occurs when someone violently shakes an infant, most often an infant younger than six months, resulting in brain, eye and skeletal injuries.2 Subdural haemorrhage on CT scan is frequently used as a marker for SBS. In a 1999 population-based study in the United Kingdom, the incidence of subdural haemorrhage due to child abuse was found to be 21 per 100 000 in children under the age of one year and 12.8 per 100 000 in children under the age of two years.3 There is wide variability in the clinical presentation, ranging from non-specific symptoms, such as vomiting, to coma or death. In its less severe forms the diagnosis is often missed, being confused with viral illness or gastrointestinal upset.4 The long-term prognosis in survivors is very poor, with a high incidence of intellectual impairment, cerebral palsy, epilepsy and cognitive/behavioural problems.5 The mechanism of injury is inferred from a possible triad of signs: severe brain swelling and/or diffuse axonal injury; subdural/subarachnoid haemorrhage; and bleeding in the retina, in the absence of a history of significant accidental injury or other medical conditions sufficient to explain the findings. There may also be other evidence of abuse, such as rib or long-bone fractures.6 SBS is a well established diagnosis in paediatrics and paediatric neurosurgery, yet some doctors and lawyers express doubts about its validity. The important question arises as to whether it is possible to differentiate this abusive form of head injury from accidental head injury or disease. Is this constellation of injuries unique to shaking?Injury to the eye. Retinal haemorrhages are present in at least 80% of cases of SBS.7 The critical importance of the role of injuries within the eye, which distinguish inflicted head injury from accidental injury and disease, was emphasised. The importance of accurate description, in terms of number and types of haemorrhages and their distribution within the retina and other parts of the eye, was noted. Only SBS (not accidental injury or disease) can result in a pattern of multiple haemorrhages distributed throughout the retina to the periphery, especially if these are in the presence of preretinal, vitreous or subhyaloid haemorrhage. Haemorrhages in the eyes may be unilateral or absent, depending on the severity of the injury.7 Bleeding in the optic nerve sheath, retinal folds, retinoschisis and retinal detachment are highly associated with severe rotational forces.7 Examination by an ophthalmologist after pupillary dilatation is critical for diagnosis. Brain injury. The mechanisms of brain injury were reviewed. It was contended that abusive head injury results from severe rotational inertia injuries (due to shearing from acceleration–deceleration forces) and secondary (mainly hypoxic) injuries. The resultant symptoms and signs reflect the severity of these forces. Shearing injuries frequently lead to subdural haemorrhage and apnoea,8 with or without diffuse axonal injury; these disturbances can lead to cessation of breathing and concussion or prolonged traumatic coma.9 In contrast, accidental injuries resulting from common household falls cause mainly contact injuries (due to direct mechanical forces) or translational inertia injuries (due to linear acceleration–deceleration), which are usually not life-threatening.10 Most short falls do not reach the rotational velocity threshold to cause even concussion, let alone more serious injury. Short falls do not cause serious injury or death, except in most unusual circumstances, such as with extradural haemorrhage, mass-effect subdural haemorrhages, secondary effects of injury, or in falls from swings, which have a significant angular velocity component. Impact injuries sufficient to cause immediate serious injury or death are commonly associated with evidence of external injury and are seen with motor vehicle accidents and long falls. Subdural haemorrhage. The most common lesion seen in SBS is subdural haemorrhage (SDH). Trauma is the cause of virtually all SDH. There are conditions in which the brain does not fill the space available within the cranial cavity, and this may cause SDH to occur with lesser degrees of trauma than would normally be expected. Benign enlargement of the CSF spaces, which is physiological, has not been shown to predispose to SDH, whereas pathological conditions that enlarge the subarachnoid or subdural space, such as old SDH, post-traumatic hydrocephalus or atrophy, may predispose to haemorrhage with lesser degrees of trauma.11 Different densities seen within an SDH on x-ray may also cause confusion about timing of injury.12 The rapidity with which symptoms develop, the presence of acute brain injury and the presence of retinal haemorrhages will assist in correct diagnosis. Excluding alternative causes for medical findingsAll known disease states simulating abuse need to be excluded, but these are few. Coagulopathy is an important one. Accidental injury, including obstetric injury, needs to be excluded. Common forms of courtroom defence in cases of alleged SBS include that the constellation of injuries seen is due to (i) reaction to vaccination, or (ii) metabolic disorders secondary to vitamin or other deficiencies. However, large-scale studies have shown that vaccines never reproduce the findings seen in SBS.13 Vitamin C deficiency has been hypothesised as a cause for the signs seen in SBS, on the basis of bench research showing that deficiency may predispose to bleeding. But, even if it did, coagulopathy due to other causes does not reproduce the signs found in SBS.7 There is no disease or condition that fully mimics the complete diagnostic picture of SBS. Is impact required for serious or fatal injury?A single study, based on experiments with biomechanical dolls implanted with accelerometers, has suggested that impact is always necessary for serious brain damage or death to occur, but this is disputed.14 The authors of the study measured impact at the end of shaking. The thresholds used to predict injury were generated from adult primates subjected to single-impulse rotational events. There are no equivalent thresholds for shaking injury in adult or immature laboratory animals. The forces generated during whiplash-shaking are different from those seen in falls or other forms of impact. Evidence from the shaking of adults,15 together with numerous articles in peer-reviewed journals and confessions by perpetrators, refute the suggestion that impact is necessary for severe or fatal injury. PreventionEpidemiological research has shown that preventive efforts should target young men and daycare providers as well as parents, particularly fathers.16 Starling et al found that biological fathers inflict the injuries in 45% of cases, and the mother's boyfriend, with no paternal relationship to the child, inflicted the injuries in 25% of cases. Female babysitters and mothers were each responsible for 15% of cases. Another study found very similar results.17 The need to educate people about positive ways of dealing with crying babies was emphasised. "Dads 101", a program for new and expectant fathers that teaches them about the dangers of shaking babies as well as educating them on how to bond with their child, was presented as an example. ChallengesIt is clear that SBS is a preventable form of abuse and that it has dire consequences for the child, the family, the perpetrator, and society at large. Its recognition is important. The recognised episode is frequently not the first episode of shaking. Training of professionals, particularly doctors, to improve recognition of the milder manifestations of SBS would perhaps prevent later manifestations of severe injury and death. Prevention has been shown to work in pilot studies done in maternity hospitals in the United States. The challenge is to reach those most at risk. There needs to be a concerted education campaign involving all those who have the responsibility of caring for very young children. More research still needs to be done, particularly on prevention of shaking and on long-term management of children who have suffered SBS.

Kieran T Moran FRACP

Objective: To determine whether thyroid-stimulating hormone (TSH) concentrations in a large sample of neonates meet World Health Organization criteria for an iodine-replete population (< 3% of neonates with whole-blood TSH concentrations > 5 mIU/L), and, in a small subset of neonates, to examine the correlation between maternal urinary iodine and neonatal TSH concentrations.Design: Cross-sectional study of neonatal whole-blood TSH values obtained as part of a routine newborn screening program.Setting: Royal North Shore Hospital (RNSH) in northern Sydney.Participants: Two anonymous samples of neonates born at RNSH (1316 infants born between August 1998 and April 1999 and 1457 infants born between 1 March and 31 December 2000); and 84 infants whose mothers had attended RNSH between September 1998 and August 1999 and supplied a urine sample for iodine measurement.Main outcome measures: Iodine status of neonates (proportion with whole-blood TSH values > 5 mIU/L), and urine iodine concentrations of pregnant women.Results: In the two large population samples of neonates, 8.1% (95% CI, 6.6%–9.5%) and 5.4% (95% CI, 4.3%–6.6%), respectively, had whole-blood TSH values > 5 mIU/L (prevalence range for mild thyroid deficiency, 3%–19%). Comparing the TSH values of the 1316 anonymous infants and the 84 identified infants showed no difference between the proportions with TSH values > 5 mIU/L (8.1% v 10.7%, respectively; P = 0.39). Urine iodine concentrations in the 84 pregnant women indicated borderline mild iodine deficiency. TSH values in their 84 infants were positively correlated with maternal urine iodine concentrations.Conclusions: Our results suggest that the population of northern Sydney may have mild iodine deficiency. However, the expected relationship between maternal urine iodine levels and neonatal TSH concentrations was not found.

Aidan McElduff PhD, FRACP · Patrick McElduff BMath, PhD · Jenny E Gunton MB BS, FRACP · Graham Hams MAppSc · Veronica Wiley PhD · Bridget M Wilcken MB ChB, FRACP

To the Editor: While we enjoyed reading Sewell's article summarising advances in paediatrics, there was no mention of developments in general paediatric surgery.1 About a third of all patients admitted to a paediatric hospital have surgical conditions. Viable advances would thus have significant implications for many children and their families. Prevention: Although vaccination against infectious diseases remains vital, the greatest killer of children in Australia is trauma.2 Detailed analysis of patterns of injury morbidity and mortality enable recommendations for prevention to be made. Legislation to reduce the risk of scalding was enacted in 1999 in NSW to regulate the temperature of hot water in new homes. Similar measures, in addition to educating families and their local doctors, have been proposed to prevent driveway and horse-related trauma in children.3,4 Overseas data confirm that such interventions may be effective in helping to reduce Australia's present mortality rate from injury of 9.5 per 100 000 children in 1991–1995 to Sweden's rate of 5.2 per 100 000.5 Diagnosis: Laser Doppler imaging of paediatric burns will enable the surgeon to determine the requirement for operative intervention within 48 hours of the burn, expediting treatment and reducing costs.6 In conjunction with the use of cultured keratinocytes, the risk of subsequent scarring should be minimised.7 Antenatal diagnosis of hydronephrosis and hydroureter has assisted in our understanding of the natural history of urological disease in childhood, helping refine the indications for surgical intervention.8 Intervention: The safety of early surgical intervention in childhood is now well established. Many common conditions such as hypospadias are now optimally treated before the child's first birthday, requiring earlier referral.9 Minimally invasive surgery has now evolved into a useful additional technique in children, in conjunction with the development of appropriate indications, suitable instruments and specialist surgical skills.10 While brevity may be an editorial necessity, paediatric surgery encompasses many areas. Although our selection represents a personal choice, advances require active involvement and consultation with colleagues across all specialties.

Andrew J A Holland · Daniel T Cass · John Pitkin

In reply: The points made by three senior surgeons at The Children's Hospital at Westmead Hospital, emphasising important areas of progress in general paediatric surgery, are valid and point to the wide range of advancing activities in paediatric care. Given the difficulty of covering all areas in a brief article, I am pleased that the Letters to the Editor section of the Journal provides another opportunity to broaden the discussion.

Jillian R Sewell

To the Editor: A previously well 21-month-old boy presented with burns on his right thigh. His mother had been making popcorn in a domestic popcorn machine while holding the baby about a metre from the machine to watch it churning out the popcorn through a chute into a bowl. Soon after the corn started to pop, the baby screamed, pointing to his right thigh. The mother immediately removed his nappy and found an unpopped corn kernel lodged between the nappy and the thigh. General examination revealed two 4 mm burns on the child's right thigh (Figure). Kenacomb cream (Bristol-Myers Squibb) was applied four times daily, and the lesions healed after five days, leaving two depigmented scars. Burns to the right thigh caused by a popcorn maker. Although popcorn machines are gaining increasing popularity there are few reports of injury. One report describes corneal burns in three adults caused by steam from microwave popcorn.1 We believe that this is the first reported case of paediatric injury, highlighting the potential hazards of hot-air popcorn machines. Corn's ability to pop lies in the fact that the kernels contain a small amount of water (14% of weight) stored in a circle of soft starch inside the hard outer casing.2 When heated to about 232ºC,3 the water expands, creating pressure within, until eventually the casing gives way. The kernels explode and pop, allowing the water to escape as steam, turning the kernels inside out. It is likely that the temperature of kernels that do not pop (known to popcorn connoisseurs as "old maids")2 can reach as high as 200ºC. Because of their increased density compared with popped kernels, old maids can, as occurred in our case, be thrown further than popped kernels. It is also worrisome that some popcorn machines are designed so that they can be used by children.4 The information booklet that accompanies the popcorn machine in this case does state "close supervision is necessary when this appliance is being used by or near children", and has a warning that as "some hot unpopped corn may be thrown from the machine during the popping process be sure to place the [machine] facing away from you or do not stand directly in front of the machine whilst it is in operation". The mother of the child in our case did not note the warning in the instruction booklet. She was not standing directly in front of the machine. Further, she was of the impression that the fluffy popped corns are not hot. With the increased use of popcorn machines, consumers must be aware of the potential dangers of injuries, especially to young children. Our case emphasises the importance of keeping children at a safe distance while preparing hot food, including apparently harmless, fluffy popcorn.

T H H Guan Koh MA, MB BChir, FRCPCH, FRACP

Some infections are more serious in pregnant than non-pregnant women because of the potential for vertical transmission to the fetus or infant (eg, varicella, rubella, cytomegalovirus infection, toxoplasmosis and listeriosis). Pre-pregnancy or routine antenatal screening for presence of, or susceptibility to, some of these infections and appropriate management can prevent adverse fetal or perinatal outcomes; screening should include rubella IgG, hepatitis B surface antigen, serological tests for syphilis and HIV antibody. If certain other vertically transmissible infections are suspected because of a positive antenatal test result, confirmatory tests for maternal and, if indicated, fetal infection are essential before intervention is considered (eg, cytomegalovirus infection). For some vertically transmissible infections that are not readily preventable, appropriate management of maternal infection can reduce fetal damage (eg, toxoplasmosis).

Series Editors:

Should Australia follow the US decision to base prophylaxis on results of maternal screening? Ever since group B streptococcus (GBS) emerged as the commonest cause of perinatal sepsis in the late 1970s, there has been controversy about prevention strategies. A few hospitals in Australia were among the first in the world to introduce routine antenatal screening for GBS carriage and intrapartum antibiotic prophylaxis for carriers.1 This approach was later vindicated by randomised controlled trials in selected carriers2 and the demonstration of lower rates of sepsis after intrapartum prophylaxis compared with historical rates.3 However, problems remain. Group B streptococcus is a normal vaginal commensal in healthy women, but colonisation is often intermittent, and rates of colonisation can vary from 18% to 27%, depending on the detection method.4 Moreover, vaginal carriage is a very crude predictor of perinatal sepsis, with fewer than 1% of the infants of carriers affected (1–2/1000 overall) without intervention.1,5 In 1996, the Centers for Disease Control and Prevention (CDC) in the United States published consensus guidelines for selecting women for intrapartum antibiotic prophylaxis using either of two alternative strategies. One strategy was based on maternal GBS carriage, and the other on clinical risk factors — preterm labour (< 37 weeks' gestation), prolonged rupture of membranes (> 18 hours) or intrapartum fever (> 38oC).6 The rationale for the latter strategy was that, before widespread use of intrapartum antibiotics, one or more of these risk factors was found in up to 80% of mothers of infants with GBS sepsis.1,7 Gradual implementation of these consensus guidelines in the US was associated with a fall in the incidence of perinatal GBS sepsis from 1.7/1000 in 1992 to 0.5/1000 in 1999.8 In Australia, there was also a decrease in the incidence of perinatal GBS sepsis, from 1.2/1000 in 1991–1993, when three of nine neonatal units surveyed had prevention strategies in place, to 0.5/1000 in 1995–1997, when all 11 units surveyed had prevention strategies.5 A recent review concluded that there is evidence, albeit from relatively poor-quality trials, that intrapartum prophylaxis reduces the incidence of neonatal sepsis, but not deaths.9 Despite this evidence, concern continues about excessive use of intrapartum antibiotics. There have been several reports that their increasing use is associated with an increased proportion of cases of neonatal sepsis caused by penicillin-resistant bacteria.10,11 Although it is sometimes difficult to prove, there is considerable empirical evidence that increased antibiotic use generally leads to increasing bacterial resistance. It is plausible that exposure to antibiotics in utero might delay colonisation of the infant gut with penicillin-sensitive anaerobes and allow penicillin-resistant facultative bacteria — many of which are potential pathogens — to become established. Recently, the CDC published revised guidelines, recommending a single strategy for prevention based on universal prenatal screening for vaginal or rectal GBS colonisation.12 The recommendation was based on a retrospective cohort study, which showed that perinatal GBS sepsis was significantly less frequent in infants of women given intrapartum antibiotics on the basis of documented GBS screening results (0.33/1000 births) than in infants of women managed on the basis of risk factors (0.59/1000 births; relative risk, 0.48; 95% CI, 0.37–0.63).13 This result is not surprising. A risk factor-based protocol cannot, by definition, prevent sepsis in infants whose mothers have no risk factors. On the other hand, the proportion of cases prevented by a protocol based on GBS colonisation depends on the sensitivity of the screening method, effectiveness of prophylaxis and compliance with the protocol.4,14 What was surprising in the CDC study was that the anticipated overall rate of intrapartum antibiotic use was similar for both prevention strategies (31% and 29%).13 In contrast, we showed that in Australia a strategy based on risk factors would lead to significantly less use of intrapartum antibiotics (18%–20% of women) than a strategy based on antenatal screening at 35–37 weeks' gestation (35%).4 This difference is apparently due to a higher incidence of risk factors in the US compared with Australia, and failure to account for women given intrapartum antibiotics during preterm labour before results of screening are available. They suggest that obstetricians in Australia should not immediately discard the option of a risk-based strategy. Neither strategy is ideal, but either, if properly implemented, can reduce the incidence of perinatal GBS sepsis. The GBS screening strategy results in at least a third of healthy young women (and their infants) being given intravenous antibiotics during labour, at significant cost and with some risks, but can achieve a lower rate of perinatal GBS sepsis.13 In Australia, with a risk-based strategy, significantly fewer women and infants would receive intravenous antibiotics. Whichever strategy is chosen, the most important determinant of its effectiveness will be compliance.

Gwendolyn L Gilbert MD, FRACP, FRCPA

Preventive treatment Inhaled corticosteroids are indicated in children with asthma who have more than mild persistent asthma or are unresponsive to non-steroidal medications after 2–4 weeks. Initial administration of 400 µg/day of chlorofluorocarbon-beclomethasone dipropionate, or budesonide, or 200 µg/day of fluticasone propionate or hydrofluoroalkane-beclomethasone dipropionate, is suggested, with subsequent titration of the dose to achieve ongoing control with the lowest dose possible. In situations where asthma control cannot be achieved with the above doses of inhaled corticosteroids, the addition of a long-acting β2-agonist, theophylline or a leukotriene antagonist should be considered. Specialist referral is recommended in children requiring high doses of inhaled steroids, regular oral steroids or in whom there is concern about possible steroid side effects. Treatment of acute asthma Systemic corticosteroid therapy is recommended for children with moderate to severe acute asthma or if there is incomplete response to β2-agonists. Initial administration of 1 mg/kg prednisolone (maximum, 50 mg) orally is suggested, and this may be repeated every 12–24 hours, depending on response. While a course of up to three days is generally sufficient, in more severe cases a prolonged course (with tapering) may occasionally be indicated. The need for recurrent systemic corticosteroid therapy for acute episodes is an indication for reassessment of the child's interval therapy.

Peter P van Asperen MD, FRACP · Craig M Mellis MD, MPH, FRACP · Peter D Sly MD, FRACP

Clinical questionA general practitioner noted that the Australian immunisation handbook1 stated that "tepid sponging of children to reduce a fever of < 41°C is no longer routinely recommended, as there is no evidence to support the efficacy of this practice". He asked whether tepid sponging is effective in lowering a raised body temperature, and whether paracetamol might be more effective in reducing body temperature if combined with tepid sponging. Search questionThe request concerned all children with raised body temperatures below 41°C. The interventions of interest were (a) tepid sponging compared with paracetamol or (b) paracetamol alone compared with paracetamol combined with tepid sponging. The ideal study design to answer this question would be a controlled trial that allocated patients at random to either (a) tepid sponging or paracetamol administration or (b) to paracetamol administration alone or in combination with tepid sponging. SearchWe conducted a PubMed search using the terms "fever", "febrile" or "temperature" combined with forms of the word "sponge" (including sponging) to identify relevant articles. To limit retrieval to methodologically rigorous studies, we applied a search filter2 that identified articles about therapy using specific research designs. Because of the time constraints of the evidence retrieval service, only articles with English abstracts published after 1989 were considered in answering the question. Summary of findingsOur search identified several studies comparing the use of tepid sponging with antipyretic drugs to reduce the body temperature of febrile children. All but one study3 specified that the subjects included were experiencing fever with temperatures in the range below 41°C. (a) A randomised controlled trial (RCT) of tepid sponging compared with oral paracetamol (15 mg/kg) found sponging was more effective in reducing body temperature only during the first 30 minutes of treatment.4 Another RCT comparing sponging with a single dose of aspirin (15 mg/kg), paracetamol (15 mg/kg) or ibuprofen (8 mg/kg) found sponging was more effective than each of the three medications during the first 30 minutes of intervention.5 After 60 minutes, the effects of each medication became superior to sponging. (b) Three studies compared the effects of paracetamol alone or combined with sponging. An RCT comparing paracetamol and paracetamol plus a 15-minute tepid sponge bath found that sponge-bathed subjects cooled faster during the first hour, but there was no significant temperature difference between the groups over the two-hour study period.6 Another RCT comparing paracetamol alone against paracetamol with tepid sponging found a greater and more rapid fall in mean temperature in the sponge plus paracetamol group. In the paracetamol-only group, 95% (n = 38) still had a temperature of 38.5°C or greater at 60 minutes, compared with 42.9% (n = 15) of the sponge-and-paracetamol group.7 An earlier study found that paracetamol plus sponging produced the greatest temperature reduction when compared with sponging or paracetamol alone, the smallest temperature reduction occurring in the group receiving sponging alone.3 We concluded that tepid sponging appears to be more effective within the first 30 minutes of treatment and has an additive effect when combined with paracetamol. OutcomeThe report was submitted to the requesting doctor, who decided to continue recommending tepid sponging in combination with paracetamol treatment to reduce body temperature in febrile children.

Vivienne F Bernath · Jeremy N Anderson · Chris A Silagy

The special healthcare needs of young people have long been recognised, but, before 1990, much of Australian adolescent medical practice was confined to small inpatient units in the major city paediatric hospitals. Other facets of adolescent healthcare — primary care, sexual and reproductive health, student health and mental health — operated independently. This was in stark contrast to North America, where the specialty of adolescent medicine had taken the lead in adolescent healthcare for three decades. Centres for Adolescent Health. Much has now changed. The establishment of Centres for Adolescent Health in Melbourne, Sydney and Auckland has signalled a broader role for adolescent medicine. Shifting disease patterns lie behind these developments. Cancer, cardiovascular disease and neuropsychiatric disorders have become health priorities in an ageing population, highlighting the need for preventive and early interventions in younger people. Adolescent disease patterns have also shifted. Infectious diseases, both blood-borne (hepatitis C, HIV) and sexually transmitted (HIV, herpes, chlamydia), pose new threats. Drug dependence, eating disorders and depression have become common. Longer survival in young people with chronic illnesses and disabilities (eg, spina bifida, cystic fibrosis) has introduced complicating psychosocial and behavioural problems. In response to these trends, adolescent medicine has embraced preventive models of care, incorporating new clinical skills and building working relationships across the spectrum of health and welfare practice. The role of specialist adolescent units has been questioned, but the number of young people admitted to hospital in the United Kingdom justifies regional adolescent inpatient units.1 In Australia, their popularity with young people (and clinical staff) and their families is a strong endorsement.2 Prevention and early intervention. The care of adolescents with chronic physical illness extends beyond the acute problems (that trigger inpatient admission) to previously undiagnosed morbidities with longer-term health implications. It is now usual to screen for psychosocial and behavioural problems affecting adherence with therapeutic regimens and, in the case of tobacco and substance misuse, possibly causing early complications. Advances in other fields of medical practice have extended the scope for prevention, with simple immunological screens for hepatitis B and C, and HIV, and vaccination for hepatitis B. So too has the introduction of clinical tools such as HEADSS, a psychosocial screen covering an adolescent's Home life, Education, recreational Activities, Drugs, Sexuality and Suicide risk/depression.3 Prevention, early diagnosis and intervention have come to dominate the care of marginalised groups, such as young offenders and homeless youth, in whom risks for blood-borne and sexually transmitted infectious diseases, substance dependence and major psychiatric disorders are very high. An emphasis on prevention and early intervention is also important in the common health problems of teenagers — depression, substance dependence, eating disorders and obesity. The greatest barrier to effective early intervention is engagement with young patients. General practitioners are the healthcare providers most commonly accessed, but most consultations are for acne, respiratory and musculoskeletal problems rather than the major causes of disease burden in this age group. Practitioner lack of confidence, skills and training in dealing with adolescent mental health and behavioural problems explains some of the unmet need. To enhance competencies in adolescent healthcare, practitioners need well-designed training based on an understanding of adolescent development, a full risk assessment, sound communication skills and a respect for confidentiality.4 With greater Medicare card ownership and the availability of longer GP consultations, adolescent access to healthcare, perhaps in the form of a "wellness" visit, would improve substantially.5 Diagnosis and intervention. New diagnostic concepts have also changed clinical practice and revealed previously under-recognised problems, such as adolescent depression and attention deficit hyperactivity disorder (ADHD) persisting beyond puberty. Prodromal and subsyndromal forms of less common disorders, such as schizophrenia and anorexia nervosa, have also been recognised. Interventions (pharmacological, educational and psychotherapeutic) used in other age groups have been adapted and shown to be efficacious in adolescents. Cognitive-behavioural treatments of depression and eating disorders, motivational interviewing for adolescent substance misuse, and pharmacotherapy for ADHD, depression or prodromal psychosis, have all shown promise in influencing short-term outcomes and even preventing the onset of fully-fledged disorders. Conclusion. Australian adolescent medicine practice has moved from being a narrow specialty to a flourishing generality, dealing with common health problems and providing a point of convergence for disciplines such as paediatrics, primary care, psychiatry, and internal medicine. The potential for an integrative approach, emphasising prevention and early intervention, is clear, but is currently constrained by a disconnection in health policies for mental health, acute care, substance misuse and services for high risk groups. The need for a coherent adolescent and youth health policy across government has never been greater.

George C Patton · Lena A Sanci · Susan M Sawyer

In the arena of child health, there is no better example of efficacious and cost-effective prevention than vaccination. The World Health Organization Global Polio Eradication Initiative has resulted in a 99% decline in polio cases since 1988, half in the past two years.1 Australia has contributed by the surveillance, since 1995, of acute flaccid paralysis (AFP), under the auspices of the Australian Paediatric Surveillance Unit, and in October 2001 the Western Pacific Region, including Australia, was certified polio free.2 Haemophilus influenzae type B vaccination has dramatically reduced the incidence of meningitis in the past 10 years, and the introduction of multivalent-protein conjugate pneumococcal vaccines that are immunogenic in young children will further reduce meningitis as well as other overwhelming sepsis. Rotavirus vaccines are on phase II clinical trials, with tremendous potential to save lives in developing countries, as well as reduce morbidity in developed countries. In paediatric surgery, sophisticated new diagnostic and assessment techniques are guiding progress in acute and chronic conditions. In severe intractable epilepsy, electrode implantation and intraoperative electrocorticography, somatosensory evoked potentials and cortical stimulation allow precise localisation of seizure foci and mapping of brain function, then accurate surgical resection. Outcomes include dramatic reduction or cessation of seizures and improved behaviour. Children with spastic cerebral palsy are at high risk for secondary hip dislocation, leading to severe pain and loss of mobility. In the past, late diagnosis has meant that by the time surgery was performed the child had often been wheelchair-bound for years, with scoliosis and other musculoskeletal deformities making anaesthesia, surgery and postoperative care very difficult and potentially dangerous. Electronic gait laboratories can now be used to diagnose early signs of hip dislocation in high-risk patients, leading to preventive surgery and thus avoiding reconstructive surgery or complex salvage surgery.3 Thus, such use of the gait laboratory has the capacity to improve the general health and quality of life in children who are disadvantaged by severe physical disability. Over the past 10 years there have been dramatic findings in the neurobiological, behavioural and social sciences, leading to new understanding of the highly interactive influences of genetics and the environment on brain development and behavioural maturation in early childhood.4 There are critical periods of development when the brain is primed to respond to particular stimulation. If these sensitive periods are missed, brain structure and function is altered, sometimes with long term consequences. This concept of "use it or lose it" has long been recognised in absent language development in profoundly deaf children, or "cortical blindness" in children with uncorrected congenital cataracts. Now there is evidence for similar critical periods in early childhood for development of emotional control and self-regulation.5 There is evidence that the midlife "epidemics" of cardiovascular disease, obesity and diabetes have their origins in fetal, perinatal and early-childhood nutrition and hormonal patterning. The socioeconomic gradient of health is apparent from the very early years. Governments around the world are using such evidence to drive a multisectoral or whole-of-government approach to early childhood, linking health, education and social services to provide a more optimal environment for the healthy development of children within their families. In Australia we have strong primary care health networks, almost universal access to education from the age of about four years, and complex systems of child care, family support and other social services. We have an opportunity to build on this infrastructure as we focus priorities on children and families. Child health professionals have a particular responsibility to use evidence-based advocacy, whether in their clinics, their community or their country, for appropriate linking of all services that promote healthy development of children. The future direction for research which will make a measurable difference to children's health lies in prevention and public health — including immunisation, gene therapies, prevention of obesity, promotion of literacy, and support for families and communities in the care of the young child.

Jillian R Sewell MB BS, FRACP