Displaying 961-1040 letters out of 1428 published
This may be due to increased testosterone.
Regarding the article by Wing et al. It is my hypothesis that the percentage of individuals of higher testosterone is increasing worldwide, more in some places than others. I suggest this is the cause of the "secular trend." Among a number of characteristics that may result from this increase in numbers of individuals of higher testosterone, I suggest increasing obesity is one. An obesity epidemic is occurring within children. (See "Obesity Epidemic in Children..." at http://www.anthropogeny.com/research.html)
Wing,et al, report that "sleep disordered breathing," "predominantly obstructive," occurs with greater frequency within obese children. I suggest this may also be due testosterone. Cistulli, et al, reported that in a 13-year-old boy that "Our data strongly suggest that the mechanism by which testosterone administration may induce or exacerbate OSA is through an influence on neuromuscular control of upper airway patency during sleep."
I suggest the findings of Wing, et al, may represent the combined effects of testosterone on "sleep disordered breathing" and obesity in the children of their study.
1. YK Wing, SH Hui, WM Pak, CK Ho, A Cheung, AM Li, and TF Fok. A controlled study of sleep related disordered breathing in obese children. Arch Dis Child 2003; 88: 1043-1047
2. Reeves-Hoche MK, Meck R, Zwillich CW. Nasal CPAP: an objective evaluation of patient compliance. Am J Respir Crit Care Med. 1994 Feb;149(2 Pt 1):530-2).
SIDS rates and risk campaigns
We were interested in the paper by Goldwater calling for a critical review of approaches to research in sudden infant death syndrome (SIDS).
We would agree that SIDS research needs to be continually re-assessed due both to difficulties in establishing this ‘diagnosis’, and to problems associated with understanding aetiological mechanisms. However, the suggestion that the fall in SIDS rates has not been due to ‘reducing the risks’ (RTR) campaigns but instead is merely ‘a reflection of natural variation’ is of great concern. Although data from Sweden and Australia are used to support this contentious proposition, examination of the data is not confirmatory.
While SIDS rates in Sweden have been less pronounced than in certain other Scandinavian countries, (at 0.3/1000 live births in 1970), by the time the Swedish back to sleep campaign was launched in 1991 the rate had risen to 1.2; it subsequently dropped to 0.4 in 1994 and has remained low ever since.[2,3] SIDS rates in Finland were lower than in Sweden, but even there the trends are similar. Examination of Australian Bureau of Statistics data also does not support Goldwater’s contention. These data clearly show continued and consistent falls in SIDS rates in all parts of Australia since information become available on risk factors (in the late 1980s). Any increases in rates have been temporary, minimal, not sustained and not statistically significant. Similar falls have been shown in many other countries. Thus, there can be no doubt that the marked decline in SIDS rates has been due to the RTR campaigns, sponsored by extremely hard working and well-motivated SIDS organisations, and not to random variation. To question the effectiveness of the RTR campaign has the potential to encourage parents to ignore well-established safety messages about infant sleeping, and thus to put their infants lives needlessly at risk.
1. Goldwater PN. Sudden infant death syndrome: a critical review of approaches to research. Arch Dis Child 2003;88:1095-1100.
2. Sudden infant death in the Nordic countries. Results of the Nordic Study of Sudden Infant Death Syndrome, 1990-1996. TemaNord, Nordic Council of Ministers, Copenhagen, Denmark. 1997:600.
3. Hauck FR. Changing epidemiology. Ch 3. In: Sudden Infant Death Syndrome: Problems, Progress & Possibilities Eds. Byard RW, Krous HF. London, Arnold. 2001; 31-57.
Address for correspondence:
Prof Roger W. Byard
Forensic Science Centre
21 Divett Place
Adelaide 5000, Australi
Phone: (618) 8226 7700
Fax: (618) 8226 7777
Atypical presentations of Kawasaki disease
The report of 2 cases of Kawasaki disease (KD) presenting with lobar pneumonia is interesting.
We have recently seen a six year old boy presenting similarly. The main feature in our case was that the child’s degree of illness was in excess of that one would expect with bilateral patchy changes on the chest Xray. Other concerns were an ESR of 80mm in the first hour, a platelet count of 495 x 109/L and CRP of 34mg/L. He developed red, dry eyes 5 days after admission with skin peeling on the 7th day. He was treated with IV Immunoglobulin and Aspirin. Within 48 hours there was dramatic resolution of his symptoms and pulmonary manifestations. An ECHO cardiogram showed normal coronary arteries.
The report by Uziel et al. underlines the need to be aware of atypical presentations of KD. However it is remarkable that despite the clinical variability of KD, the diagnosis rate in similar in different series. For example the recent study in the US gave a KS incidence of 17.1/100,000 in the <_5 years="years" age="age" group="group" in="in" us2="us2" whereas="whereas" the="the" irish="irish" incidence="incidence" was="was" reported="reported" as="as" _15.2="_15.2" _100000.3="_100000.3" agreement="agreement" relation="relation" to="to" diagnosis="diagnosis" of="of" condition="condition" is="is" converging="converging" main="main" issue="issue" now="now" being="being" atypical="atypical" cases="cases" like="like" this="this" one.="one." p="p">References (1) Uziel Y, Hashkes PJ, Kassem E, Gottesman G, Walach B. “Unresolving pneumonia” as the main manifestation of atypical Kawasaki disease. Arch Dis Child 2003;88:940-42.
(2) Holman RC, Curns AT, Belay ED, Steiner CA, Schonberger LB. Kawasaki Syndrome Hospitalizations in the United States, 1997 and 2000. Pediatrics 2003; 112:495-501.
(3) Lynch M, Holman RC, Mulligan A, Belay ED, Schonberger LB. Kawasaki syndrome hospitalizations in Ireland, 1996 through 2000. The Pediatr Infec Dis Journal 2003;22(11):959-63 .
There are few controlled studies of pedagogical devices used in patient education regarding chronic diseases like type 1 diabetes. As Briars et al points out, this area is worth further study and we agree that a critical view is needed with respect to such studies. We therefore performed this controlled study in a general hospital population following the previous study in a before-after setting at our University hospital.
Measurement of self-reported outcomes such as severe hypoglycaemia is rather difficult. In the present study we controlled for many potential flaws by using a randomised controlled design. It is a weakness, however, that the primary outcome of severe hypoglycaemia was reported only retrospectively.
Participants in intervention and control groups were given short and identical blinded information about the study, their education material and the related postal questionnaires at baseline, 12 and 24 months. Using identical questions in both groups, those surveys covered treatment variables and the patient’s use and perceived benefit of the earlier posted materials. Questions regarding events of severe hypoglycaemia were embedded in a series of different questions without highlighting any particular one. We therefore cannot see any source of bias in the information about the study design.
As described in the paper, the reduction of reported severe hypoglycaemia during the first 12 months after intervention was statistically significant. Considering only those patients responding to all questionnaires confirmed the reduction. Thus we found less than a 4% chance that random effects explained this reduction. Taking confidence intervals into account, we concluded that these data suggest a clinical effect from the intervention. A larger sample would be needed to show a significant difference in case of a smaller effect.
Moreover, the related secondary outcomes showed high frequencies of use and significantly greater perceived usefulness and learning in the intervention group, especially among those who had reported severe hypoglycaemia. We interpret this as being in favour of positive effects from the intervention. Interestingly, after 24 months, preliminary data showed a persistent reduction of severe hypoglycaemia in the intervention group, while no reduction was seen in the control and traditional treatment groups (manuscript in preparation). We interpret these preliminary data as favouring the conclusion.
Having said that, we of course agree with Briars et al that there is a chance that random variation or some kind of measurement bias could possibly explain the reduction or at least part of it. Some doubt remains from a scientific point of view and as always, new findings should be tested in independent studies. The expressed interest in this paper holds promise for further investigations in this understudied area.
Nordfeldt S, Johansson C, Carlsson E, Hammersjo JA. Prevention of severe hypoglycaemia in type I diabetes: a randomised controlled population study. Arch Dis Child. 2003;88:240-245.
Briars GL et al. Randomised controlled trial of educational video [electronic response to Nordfeldt et al. Prevention of severe hypoglycaemia in type I diabetes: a randomised controlled population study] archdischild.com 2003http://adc.bmjjournals.com/cgi/eletters/archdischild;88/3/240#567
Surfactant protein D use
We read with interest the paper by Clark and Reid  describing the potential benefits of recombinant surfactant protein D therapy.
The authors give a range of potential disease targets for surfactant protein D based therapy including neonatal chronic lung disease, cystic fibrosis, lung infections, emphysema and asthma. The authors do not however mention the potential use of surfactant protein D therapy in acute respiratory distress syndrome (ARDS) where the anti-inflammatory, immune modulation and antioxidant properties of surfactant protein D may be of benefit.
The pathologic hallmark of ARDS is diffuse alveolar damage, which results in loss of the alveolar-capillary barrier, transudation of protein -rich fluid, pulmonary oedema and hypoxemia due to intrapulmonary shunting. The mechanisms resulting are thought to be mediated by oxygen radicals, proteolytic enzymes, cytokines and complement. The most common predisposing conditions for ARDS are infection; including pneumonia and systemic sepsis, trauma, aspiration of gastric contents, near drowning and toxic inhalation.
Changes in the surfactant system in ARDS include qualitative and quantitative changes with reductions of surfactant phospholipids and increases in non-surfactant phospholipids. There is also inactivation of surfactant by leakage of various plasma proteins into the lungs.
Beneficial effects of increased oxygenation and decreased mortality due to endotracheal surfactant administration in ARDS were shown by Gregory et al. Similarly bronchoscopically administered surfactant has been also demonstrated to improve oxygenation in case studies.[4,5] The optimum route of administration and dosing schedule remains uncertain and surfactant is most commonly used as a rescue therapy in severe ARDS.
Acute respiratory distress syndrome is an important potential target for surfactant protein D based therapy.
(1) Clark H, Reid K. The potential of recombinant surfactant protein D therapy to reduce inflammation in neonatal chronic lung disease, cystic fibrosis and emphysema. Arch Dis Child 2003; 88:981- 4
(2) Greise M. Pulmonary surfactant in health and human lung diseases: state of the art. Eur Respir J 1999; 13:1455-76
(3) Gregory TJ, Steinberg KP, Spragg R, et al. Bovine surfactant therapy for patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 1997; 155:1309-15
(4) Spragg RG, Gilliard N, Richman P, et al. Acute effects of a single dose of porcine surfactant on patients with the adult respiratory distress syndrome. Chest 1994;105:195-202
(5) Walmrath D, Gunther A, Ghofrani HA, et al. Bronchoscopic surfactant administration in patients with severe adult respiratory distress syndrome and sepsis. Am J Respir Crit Care Med 1996; 154:57-62.
It is encouraging that the Royal College supports the notion that "the general paediatrician remains core to the resuscitation and stabilisation of the critically ill child" and "exposure to critically ill patients is an essential part of training", and I am glad they seek to challenge the solutions proposed. However, to dismiss them as simply unrealistic fails to heed their own goal of more imaginative teaching.
Whilst I can understand the comment, "all specialists feel theirs is essential", what is their basis for distinguishing the need for neonatal intensive care as compulsory and paediatric intensive care as not, especially now that learning opportunities for dealing with critically ill children have been so diminished by the centralization of critical care facilities? It also is somewhat paradoxical that they support the General Paediatrician as core to the resuscitation and stabilization of critically ill children, and feel a two day course is sufficient training, but demand a clinical attachment in community medicine?
I also am pleased that they support the use of simulation technology and agree that it is imperfect and expensive. It is, however, of sufficient functionality that it has a role as has been demonstrated in other countries, and hope that their comment indicating they should press for more funding is translated into action. Simulations use in addressing human factor error control is, of itself a way to deal with the exponential rise in legal costs the health service is facing, a major cause for which is human error. This alone could justify the Government providing additional funds for the proposed system. Its use to develop safer systems of operation is as useful as its use in managing the difficult airway in financial and human terms.
I applaud the attempts to introduce competence based education rather than time based, but will be interested to see how they will both define and assess these competencies. I look forward to seeing the development the Royal Colleges promise, and hope that they will be supportive when colleagues answer their call to provide inventive ways in which to deal with the training dilemma rather than dismissive.
Shaken infant trauma induced by incorrect installation of a child seat in a car
I would like to comment on the paper by de San Lazaro et al.
The authors of this paper demonstrated that violent rocking of a baby chair could produce acceleration/decelaration forces similar as those seen when violenty shaking a child and that could result in similar lesions as those seen in a true shaken baby syndrome. I recently encoutered a similar case where a 2 month old baby was placed in a maxi-cosi chair in the car. The chair was incorrectly installed (too vertically) in a manner that the child was sitting almost in an upright position. Because of warm weather, the maxi-cosy was covered with a blanket so that there was no visual control over the child during the driving. There was a car ride of 2 km with repeated acceleration and deceleration. Several hours later the child became apathic and refused to drink his milk. The child finally became comatous. On admission in the hospital, the child demonstrated all classic symptoms of a shaken baby syndrome: subdural haemorrhage with interhemisheric component, bilateral retinal haemorrhage and no external lesions. Clinical progression was infaust with development of cystic encephalopathy. One month after the initial trauma the child died of an intractible seizure. It was the this author's expert opinion that the cause of death was accidental shaking and there was no criminal prosecution.
This case demonstrates that violent shaking may be inflicted to a child by incorrect installation of a child seat in a car. This may lead to false accusations of child abuse. Therefore, it is important that paediatricians and forensic physicians have knowledge of the prior circumstances that led to the admission of a child in hopital (or death) so that accidental causes of "shaking" can be excluded. Furthermore accidental shaking by misuse or wrongful use of child seating equipment appears to be a true cause of a shaken baby-like syndrome that may simulate non-accidental injury.
Although the child's safety should be the first concern of every doctor, false accusations of child abuse may have a profound impact on parents and relatives.
(1) C de San Lazaro, R Harvey, and A Ogden. Shaking infant trauma induced by misuse of a baby chair. Arch Dis Child 2003; 88: 632-634.
Systemic effects of pimecrolimus cream
I read the article by Allen et al. with interest. I am interested in a potential systemic effect of pimecrolimus that doesn't seem to have been addressed.
I understand that the cream achieves its desired effect by surpressing the white cells in the affected area. I understand that the population of white cells migrating into the eczematous area is in continuous flux, and that these cells can re-enter the systemic circulation. I was wondering if the immune surpressive effects of pimecrolimus are lifelong for the individual white cells, and if so, why haven't there been any studies of white cell function distant from the application site, to look not for distant concentrations of the drug, but for damaged/surpressed white cells that may decrease overall immune function. As many cells are quite long lived, theoretically the effects of an application of the drug could also be long lived, and there may be systemic immune effects caused by these surpressed cells re-entering the circulation.
I ask the authors - Are you aware of any data addressing these issues?
Deficits in attention, motor control, and perception: a brief review.
I have read C. Gilberg’s paper with interest but also with concern because there to my knowledge is no scientific valid paper about children with DAMP (deficits in attention, motor control, and perception).
The term DAMP was first introduced by C. Gilberg in 1986  and based on a study of 6 years old children in Gothenburg, Sweden. The main aim of this study was to construct a screening instrument in order to detect MBD (minimal brain dysfunction) in Swedish public preschool children and analyse different aspects of the concept of MBD from a psychiatric point of view.
Unfortunately the Swedish studies by G. Gilberg have great methodological problems. In the study a non-validated questionnaire for preschool teachers was used from which the children were classified in a high load or low load index group. In the groups an unpublished number of children were included which did not have ”attention deficit” but ”conduct problems” (involving conduct problems in the definition of MBD and later DAMP the boarderline between DAMP and conduct disorder became unclear). In the final investigation, partly by selfmade non-validated tests, the 22 children from the ”high-load” group and 60 children from the low-index group (66 boys and 16 girls) were compared with a random control group, which finally consisted of 59 children (29 boys and 30 girls). Of these 141 children 42 were diagnosed as having MBD, 40 were found in the index groups, 2 in the control group, of whom one had no preschool qustionnaire ”symptoms” at all. Futhermore 3 children in the index group were diagnosed as having mental retardation, 8 of the children had psychotic behaviour to a marked degree (one of the boys was already diagnosed as having infantile autism) and two children were considered to suffer from marked depressive syndrome. So 10 of 14 children diagnosed as suffering from severe MBD, had severe psychiatric disorders which one could consider the primary diagnosis and MBD a secondary diagnosis. It could also explain the reason why children with socalled severe MBD/DAMP, autistic features were extremely common. It was the above mentioned group of 42 children who in 1986 swiched name to children with DAMP and followed till they were 22 years old. The above mentioned methodological problems also lead to a very high prevalence of DAMP, estimated to 18%, page 112 , and in one of the later studies from 2000 where C. Gilberg et co-workers suggest a new school screening examination 5 based on the earlier studies the result of the 11 factors of WISC-III the curve for control children and children with socalled DAMP is completely parallel which means that it is children with generalized developmental problems and not specific problems that is found by the new screening test. So the term DAMP is based on studies with very great methodological problems and thereby not a valid diagnosis.
In spite of this C. Gilberg now suggests a revival of the DAMP term and shifts to a new definition by combining ADHD and DCD. I would suggest that instead of confusing futher investigation one should concentrate on the ADHD diagnosis and perhaps examine if there are important subgroups e.g. children with ADHD who also have problems with motor control, of which there already are several studies.[6,7].
(1) Gillberg C. Deficits in attention, motor control, and perception: a brief review. Arch Dis Child 2003;88:904-10.
(2) Gillberg C. Attention deficit disorder: Diagnosis, prevalence, management and outcome. Pediatrician 1986;13:108-18.
(3) Gillberg C, Rasmussen P, Carlstrøm G et al. Perceptual, motor and attentional deficits in six-year-old children. Epidemiological aspects. J Child Psychol Psychiatry 1982;23:131-44.
(4) Gilberg, C. Perceptual, motor- and attentional deficit in Swedish primary schoolchildren. Some psychiatric aspects. J Child Psychol Psyciat 1983;24;377-403.
(5) Landgren M, Kjellman B, Gillberg C. Deficits in attention, motor control and perception (DAMP): A simplified school entry examination. Acta Pediatr Scand 2000;89:302-9.
(6) Pitcher TM, Piek JP, Hay DA. Fine and gross motor ability in males with ADHD. Dev Med Child Neurol 2003;45:525-535.
(7) Kalff AC, de Sonneville LM, Hurks PP et al. Low- and high-level controlled processing in executive motor control tasks in 5-6 year-old children at risk of ADHD. J Child Psychol Psychiatry. 2003;44:1049-57.
I agree with Dr Spencer that the incidence of the Paediatric Empyema is on the increase and the management of this age-old disease is dependent upon provider-based experiences. Secondly, there is no clear evidence that one modality of management is superior to the other. Therefore giving rise to controversies in the management of this disease. The pathogenesis of the disease (Empyema) is largely ignored while choosing a particular modality of the surgical intervention. As we know that when the disease advances more and more fibrous tissue gets deposited within the purulent exudate giving rise to pleural rinds. This pleural rinds restricts the lung expansion, this process starts after fibro-purulent phase when fibrinous and not fibrous adhesions exists causing loculations. While in later phase (the organizational phase) of the empyema fibrosis occurs restricting the lung expansion.
The objection I have is the use of the word early decortication. I think what author means is early debridement of the pyogenic material from the empyema cavity in the fibro-purulent phase. Some reports mentions the use Video-assisted thoracoscopic (VAT) and early decortication in the management of empyema. It is impossible to perform VAT decortication of pleural rinds, It requires formal thoracotomy to do real decortication. There is usually very little plane between firm to hard fibrous tissue restricting the lung to pass a thoracoscope. The inflamed tissue bleeds heavily hampering the vision. It is not question of experience, as we have done a number of early VAT which is definitely the way forward in reducing morbidity, risk of developing chronic empyema and hospital stay in these children. Again I feel that Fibrinolytics fail in some children because it is used late in the developing empyema process when fibrosis has commenced. Fibrinolytics is only useful in early in exudative and early fibro-purulent phases. So in essence there could be a place for all the surgical interventions only if applied to the appropriate stage of empyema. The aim of any therapy should be early intervention, that results in adequate drainage and complte expansion of lung, thus avoiding Decortication that is the excision of the pleural rinds which carries high morbidity and even mortality.
Issues potentially affecting the generalizability of Bland et al's findings
Congratulations to Bland et al. for a well-done study, well analyzed and well written up on an issue that needed to be studied the way they did it. I agree with most of their conclusions, particularly their warning that studies linking postnatal HIV transmission to feeding practices need to use more exacting methods to document the latter than most studies have used to date.
I would add to this another point: the "standardised WHO definitions" that they refer to were developed as a way of ensuring that household survey results are comparable and are not necessarily appropriate for studying the relationships between feeding patterns and certain types of morbidity. Thus the fact that the WHO definition "allows" "drops or syrups consisting of vitamins, mineral supplements, or prescribed medicines" should not be accepted unthinkingly. All of these can be provided in a contaminated or outdated form and all contain additional substances that are used as preservatives, fillers, binders, etc. While this may not matter much when studying for example the relationship between feeding patterns and concurrent patterns of diarrhea or growth, it may make a big difference when relating feeding patterns to such outcomes as allergy, micronutrient absorption--and HIV transmission.
The population Bland et al. studied is likely fairly representative of feeding patterns in wealthier rural African settings. However, in other settings their findings are less likely to hold. More importantly, their population was probably not the right one in which to compare the various measurement methods they used. The main reason for this is that there was too little variability in the duration of exclusive breastfeeding in their population. Only 17% were still exclusively breastfeeding after two weeks of age and thus able to switch category. That is, after this age so few infants change categories that high levels of sensitivity and specificity in the tools used to measure it were in a sense unavoidable. This is not to fault their study, but to point out that it needs to be repeated in other settings before generalizing from their findings.
Finally, that mothers tended to exaggerate the duration of EBF when recalling it several months later could in part be an artefact of the slightly different method of operationalizing the definition of EBF that was used in the long-term recall. Water was the only non-milk fluid used and the extent to which other fluids (or fluids mothers did not define as "water" such as “glucose”) were given before water could be partially explanatory.
(1) RM Bland, NC Rollins, G Solarsh, J Van den Broeck, and HM Coovadia. Maternal recall of exclusive breast feeding duration. Arch Dis Child 2003; 88: 778-783 .
Education and training in the paediatric senior house officer grade
We were pleased to receive the comments from John Craig with which we largely agree. The audit we published was a retrospective one of reports received between 1997-2001. This was before many Senior House Officers (SHOs) began shift patterns of working which has become the norm in recent times. We agree that this change necessitates a different approach to education and training and we fully support the suggestions made in 'Liberating Learning'. To help tutors develop these ideas further, Janet Anderson (on behalf of the College) organised a workshop for tutors last June and another has been arranged in December.
We have also altered the 'Essential Features of an SHO Training Programme' which can be found in the new RCPCH Paediatric Training Handbook (published September 2003). Paragraph 10 now reads 'There should be three hours per week dedicated to education and training. The department should demonstrate its commitment to ongoing teaching. The format can include: tutorials, lectures, ward-based teaching and attendance in outpatients for structured teaching and feedback. Departmental meetings should be arranged so that the majority of SHOs can attend, i.e. at shift overlap times, including early morning meetings and lunch times. The educational content should be directed towards the career aims of the SHOs and sessions should be interactive whenever possible. Educational sessions should be bleep free and it should be possible to attend >70% of sessions (ie an average minimum of two hours per week)'.
In summary, we agree with John Craig's comments and the College is doing its best to support those who are delivering education and training around the UK.
(1) Craig JS and Tubman TRJ. Re education and training in the paediatric senior house officer grade [electronic response to Smith and Anderson; Education and training in the paediatric senior house officer grade: analysis of RCPCH hospital/child health visits reports, 1997–2001] archdischild.com 2003http://adc.bmjjournals.com/cgi/eletters/archdischild;88/5/450#554
Randomised controlled trial of educational video
Nordfeldt et al conclude from their randomised controlled study that severe hypoglycaemia incidence can be reduced in type 1 diabetes patients who study good quality educational videos. Examination of the premise that patient education reduces morbidity is worthy of study, both in the current setting of type 1 diabetes and in paediatric disease in general.
The current study relies on their patient’s recall of severe hypoglycaemic episodes at annual postal survey for its primary outcome measure. Patient recall might be affected by their understanding of the study design and might potentially introduce a reporting bias that suggests a beneficial effect of the educational video. In assessing such a bias it would be helpful to know what information the participants were given about their study on consenting to enter.
Despite this potential bias their data show no significant differences in hypoglycaemia incidence between their experimental groups. The author’s claimed reduction in hypoglycaemia incidence in the intervention group from 42 to 27% is therefore most logically accounted for by a fortuitously higher random incidence of hypoglycaemia in the pre- video period in the intervention group. Unfortunately no comparative data were presented for their no video control group.
There are inherent difficulties in subjecting this educational intervention to a randomised controlled study with potential biasses both in favour and against the study hypothesis. Even if the study were to have shown a clear short term effect on hypoglycaemic incidence, one would be wise to exercise caution before diverting healthcare funding to production of such video material until longer term benefit had been demonstrated. Experience dictates that educational messages are subject to a degree of decay with the passage of time. In contrast to the author’s claim that their study shows that “severe hypoglycaemia can be reduced with good quality education materials”, we interpret their data as having shown no effect of their educational material on the incidence of severe hypoglycaemia even before the waning of an educational effect, despite potential bias in favour of accepting the study hypothesis.
(1) S Nordfeldt, C Johansson, E Carlsson, and J-Å Hammersjö. Prevention of severe hypoglycaemia in type I diabetes: a randomised controlled population study. Arch Dis Child 2003; 88: 240-245.
Imprintable disorders and assisted reproductive therapies ( ART)
We read with interest Hussain and Mehta's case report in Archives of September 2003. Both cases were reminiscint of Beckwith-Weidemann syndrome in many of their features. BWS is recognised as a spectrum rather than a clear entity. A series of reports has been published [1-3] suggesting an association between conception using assisted reproduction and BWS; another showing an association with Angelman's syndrome; and finally an association with retinoblastoma, a form of cancer in which genomic imprinting is implicated in the pathogenesis. We contacted Dr Hussain and found that indeed, one of these children was conceived with IVF. Genomic imprinting, which is an epigenetic phenomenon, may well be influenced by in vitro culture media. Animal studies have already shown that manipulation of the different aspects of culture media can influence the imprinting patterns in embryos.[6,7]
We are presently studying the imprinting disorders in human in vitro fertilisation in the UK (along with other colleagues)to establish if the epidemiological evidence is robust for this association before more detailed mechanistic studies can be performed.
Where children present with unusual features such as those described in this report and an earlier report in Archives of April 2003, we recommend that the conception status should be part of the history. We understand that this is the case where families are being seen in a genetic clinic.
(1) Maher ER, Brueton LA, Bowdin SC, Luharia A, Cooper W, Cole TR, Macdonald F, Sampson JR, Barrett C, Reik W, Hawkins MM. Beckwith-Weidemann Syndrome and assisted reproductive technology. J Med Genet 2002;11:202 -204.
(2) Giquel C, Gaston V, Mandelbaum J, Siffrol JP, Flahault A, Let Bouc Y. In vitro fertilisation may increase the risk of Beckwith-Weidemann syndrome related to the abnormal imprinting of the KCNQ1OT gene. Amer J Human Genetics 2003;72:1338-1341
(3) DeBaum M, Niemitz EL, Lee MP, Feinberg AP. Association of in vitro fertilization with Beckwith-Weidemann syndrome and epigenetic alterations of LIT1 and H19. Am J Human Genetics 2003;72:156-160.
(4) Cox GF, Burger J, Lip V, Mau UA, Sperling K, Wu B, Horsthemke B. Intracytoplasmic sperm injection may increase the risk of imprinting defects. Am J of Genetics 2002;71:162-164.
(5) Moll AC, Imhof SM, Cruysberg JRM, Scouten-van Meeteren AYN, Boers M, van Leeuwen FE. Incidence of retinoblastoma in children born after in- vitro fertilisation. Lancet 2003;361:309-310.
(6) Doherty AS, Mann MRW, Tremblay KD, Bartolomei MS, Schultz RM. Differential effects of culture on imprinted H19 expression in the preimplantaion mouse embryo. Biology of Reproduction 2000;62:1526-1535.
(7) Khosla S, Dean W, Brown D, Reik W, Feil R. Culture of preimplantation embryos affects fetal development and the expression of imprinted genes. Biology of Reproduction 2001;64:918-96.
(8) Srinivasan S, Waters MJ, Rowland JE, Baxter RC, Verge CF. Hyperinsulinism and overgrowth without obesity. Arch Dis Child 2003;88(4):332-334.
Changes in education - stimulation, rather than simulation
Dr Stewart in his leading article, “Medical training in the UK”, rightly expressed concern regarding postgraduate specialist training in paediatrics in the UK. He highlights diminishing duration of training and stagnation in educational methods (dare we interpose educationalists’ mindset) as major aetiologies for looming deficiencies. Having benefited from a well-rounded formulated paediatric specialist education, which included a mandatory rotation through the paediatric intensive care unit (PICU), along with completion of general paediatric training before any subspecialisation, we advocate this approach strongly. It certainly has succoured us well on different continents.
Without exposure to PICU and/or Paediatric Accident and Emergency (A&E), where do the present paediatric trainees in the UK tangibly master care of the seriously ill child? Hopefully not entirely in the Labour Ward or while awaiting the occasional retrieval. Training time spent in the PICU has distinct educational advantages for paediatric specialist training: there is a high incidence of one-to-one teaching every working day (i.e. every day); intensivists are committed educationalists (not only out of necessity); there is a high degree of clinical exposure where recognition and assessment of critical illness is learnt and honed (ask any registrar who has rotated through a PICU); there is no place to hide – ‘your patients’ are clearly defined; management of basic life support skills, such as gaining competency in airway management, assessing sustainable respiration and effective cardiac output, is achieved; acquired skills build on the foundation of previously-received APLS training; “competence-based” assessment is inherent.
It is easier to evangalise about adjusting rotations than to effect that change. The ‘spaces’ available and those outposts needing to be filled rather than the best educational interests of the trainee(s) often govern rotations. The RCPCH may dictate training policy, but it does not fund local education or pay the trainees’ salaries. Additionally, some PICU directors may resist the imposition of a steady stream of reluctant PICU middle-graders, but the interests of children (the primary recipients of a good paediatric training scheme) need to be heeded.
Remote learning cannot substitute for direct bedside teaching and simulation techniques have been shown to be deficient(2). Paediatric trainees need real-life guidance through the subtle and dynamic challenges of clinical medicine. In our experience, there is no formula to teach ‘judgement’ in clinical decision making apart from first-hand experience under the guidance of a discerning teacher. We would advocate readjusting paediatric training rotations to include this hands-on real-life experience with critically ill children, long before breeding Consultants in Critical Simulation Care. With a structured teaching program and a logbook to ensure that all important aspects are covered, a 6-month rotation in PICU would suffice.
A central issue is whether you consider recognition of serious illness, resuscitation and stabilisation of critically ill children, and acute management of life-threatening conditions as basic, generic skills required for a specialist paediatric trainee and a general paediatrician. Would you prefer your own seriously ill child to present to a district general hospital where all the paediatric staff have these skills, or not?
(1) Stewart D. Medical training in the UK. Arch Dis Child 2003;88:655-8.
(2) Olympio MA, Whelan R, Ford RP, Saunders IC. Failure of simulation training to change residents’ management of oesophageal intubation. Br J Anaesth 2003;91:312-8.
National Survey of Childhood Tuberculosis
In the National Survey of Childhood Tuberculosis for 1998 peripheral lymph node disease (31) accounted for 32% of the total (96) cases in white children compared to 19% in the other ethnic groups.
The authors rightly state that “mycobacteria other than M. tuberculosis can cause higher rates of lymphadenitis”. Perhaps a large proportion of the cervical lymph node disease in the white group may have been due to environmental mycobacteria. It would be interesting to know how many of the white group had lymphadenitis confined to the cervical (or parotid) area, with normal chest Xrays and no contact with tuberculosis.
In the period 1982-2003, 100 patients (two thirds of whom were white) with tuberculosis were seen at the Royal Liverpool Children’s NHS Trust – Alder Hey, of whom only 8 (8%) had peripheral node disease all in the cervical area. Five of the 8 cases also had evidence of pulmonary disease. The three without pulmonary disease were non-white teenagers (when evidence of earlier pulmonary disease may have resolved). Of the two white children (2% of the total) both were young (4-6 years) and had pulmonary disease in addition.
In the period 1990-2003 we recorded 104 cases of environmental mycobacteria (which is an underestimate) virtually all in the cervical or parotid area and most were between 2-4 years of age. Only one was non-white; a two year old Bangladeshi born in the UK who had not had BCG.
Thus in Liverpool the epidemiology of tuberculous and environmental mycobacterial cervical lymphadenopathy differ in ethnic group, age range and associated pulmonary disease. The Liverpool data support the suggestion by the authors that tuberculous lymphadenitis may have been over diagnosed in the white group. In future surveys more stringent criteria for diagnosis of tuberculous lymphadenopathy might provide a clearer picture.
In the 1998 survey, of 176 cases with pulmonary disease, specimens were obtained from 64 (36%) of which 43 (67%) were culture-positive and 20 had smear-positive disease (table 4). Presumably, most of these were adolescents able to expectorate sputum. In the current Notification Form, there is provision for recording type of specimen. It would be interesting to know what proportion had gastric washings or induced sputum.
(1) Balasegaram S, Watson JM, Rose AMC et al. A decade of change: tuberculosis in England and Wales. Arch Dis Child 2003;88:772-777.
Medical Training in the UK
Re: Medical Training in the UK
We read the article by Dr Stewart with interest. Whilst we support Dr Stewart’s statements “the general paediatrician remains core to the resuscitation and stabilisation of the critically ill child” and “exposure to critically ill patients is an essential part of training”, we wish to challenge his solutions.
The apprenticeship concept is difficult to deliver within the time constraints of working and training today - we should aim for more imaginative teaching (COPMED 2002). Whilst every specialist considers that training in their subspecialty should be compulsory, solutions to designing effective teaching are not likely to be found in the creation of mandatory rotations though all specialist areas but in utilising the educational opportunities of all clinical encounters whenever they occur.
We recognise that encountering the critically ill child is an uncommon event and we strongly support the concept that all trainees undertake advanced Paediatric and Neonatal Life Support Courses. There are however also proposals for courses on Child Protection, Psychology, Human Rights, Epilepsy, Child Development, Nutrition and many more. Six to 12 months’ exposure to paediatric intensive care would take more time than the average trainee has to spare and it would be impossible to arrange rotations for all trainees. Simulators should indeed have their place in future education. At the present time, however, they are expensive and access to them is limited – we should press for more funding to be made available for educational purposes.
The College is defining competencies that Paediatricians need to acquire and is also developing more robust ways of assessing performance. Both will include the recognition and early management of the critically ill child. These will be key not only to assessing trainees but also to evaluating how training programmes deliver standards. The College has begun to run courses for Paediatricians as Educators, which will help to demonstrate ways in which creative use of time and opportunity can be integrated into a comprehensive education programme. We hope that colleagues will take advantage of these and let us know of inventive ways in which they have addressed the training dilemma.
(1) Stewart D. Medical training in the UK. Arch Dis Child 2003;88:655-658.
(2) COPMED Liberating Learning: A practical guide for learners and teachers to postgraduate medical education and the European Working Time Directive. 2002.
Re education and training in the paediatric senior house officer grade
The paper by Smith and Anderson  and the accompanying eLetters [2,3] were of interest to us because we have had two RCPCH education and training visits in the last 9 months, one for senior house officers (SHOs) and one for higher specialist trainees.
We were commended for the quality of our teaching program and we have seen an improvement in our training program and our service provision following the RCPCH team’s recommendations, thus recognising the benefits of the RCPCH visits. We would like to comment on two of the criteria used in the assessment of units, i.e. educational supervision and protected education time.
Smith and Anderson report that satisfactory educational supervision was achieved in an average of 72% (range: 36 – 100%) units.
1. This should be viewed as a disappointing result. It is possible that some of the failure in this criterion may be due to organisational and timetabling difficulties with trainees. Our concern, however, is that there may be an insufficient recognition of the Educational Supervisor’s role, whether by the College, Deanery, trainee or indeed the supervisor themselves. The Educational Supervisor is fundamental to the provision of training for junior doctors and it is important that there is access to support and training for this role. We have benefited from the training for educational supervisors provided in our region and would strongly recommend such courses to anyone providing this role.
Our unit is the tertiary referral neonatal unit in Northern Ireland. In the past year SHOs were on an eight person full shift system supported by specialist registrars (SpRs) on a "1 in 5 on-call" rota. We have just finished our first audit of attendance at the formal teaching sessions since the full shifts started. We found that the mean (SD) attendance by the SHOs was 54.4 (10.6)%, by the SpRs was 61.6 (10.4)% and by the consultants supervising the formal sessions was 67.3 (6.5)%. No-one achieved 75% attendance and only three SHOs achieved 66% or more. Smith and Anderson acknowledge that 75% attendance is virtually impossible since the introduction of shift working. Our figures bear this out and we agree with Richardson and Reddy that 75% attendance is no longer appropriate. If an attendance rate at formal teaching sessions is to be used at all for assessments, then probably 60% is more realistic with the current working patterns. Smith and Anderson are correct to stress the importance of the quality of SHO training but the absolute attendance rate is probably the least sensitive measure of this.
Richardson and Reddy appear to advocate “opportunistic teaching” as the mainstay of training. However, the formal tutorial/lecture format still remains a useful method of ensuring that a basic curriculum is covered in a given period of time. We would suggest that “opportunistic teaching” be supplemental to, rather than in place of, these formats. The strategies summarised in “Liberating Learning” are a useful framework but will require a significant change in our educational practice.
(1) Smith CP, Anderson JM. Education and training in the paediatric senior house officer grade: analysis of RCPCH hospital/child health visits reports, 1997–2001. Arch Dis Child 2003; 88:450-453.
(2) Richardson M, Reddy V. Education and training in the paediatric senior house officer grade [electronic response to Smith CP and Anderson JM, Education and training in the paediatric senior house officer grade: analysis of RCPCH hospital/child health visits reports, 1997–2001] archdischild.com 2003 http://adc.bmjjournals.com/cgi/eletters/archdischild;88/5/450#466
(3) Smith CP, Anderson JM. Authors' Reply: Education and training in the paediatric senior house officer grade [electronic response to Smith CP and Anderson JM, Education and training in the paediatric senior house officer grade: analysis of RCPCH hospital/child health visits reports, 1997–2001] archdischild.com 2003 http://adc.bmjjournals.com/cgi/eletters/archdischild;88/5/450#474
(4) The Northern Ireland Council for Postgraduate Medical and Dental Education: Educational Supervisors Workshops. http://www.nicpmde.com/Education%20Unit/Education%20Unit%20Files/SpR%20Flyer.pdf
(5) Conference of Postgraduate Medical Deans (COPMeD). Liberating Learning. London: COPMeD Publications; 2002. http://www.copmed.org.uk/publications/liberatinglearning/index.html
Childhood obesity and cancer
I read with great interest the recent review on health consequences of childhood obesity. Though they have highlighted a variety of health consequences, the influence of obesity on cancer has not been discussed.
Cancers in adulthood are associated with childhood and adolescent obesity. In a long-term follow up study, a higher prevalence of colorectal cancer was found among men who had been overweight during adolescence. Previous studies have consistently shown associations between obesity and increased risk of cancers of the endometrium, kidney, gallbladder (in women), and breast (in postmenopausal women). Adenocarcinoma of the esophagus has been linked to obesity. Though most of these studies have found associations of adult obesity with cancers, it is well known that childhood obesity may persist into adulthood, as the authors have also mentioned.
It should be noted, however, that obesity below 10 years of age was found to have a protective effect on advanced and metastatic prostate cancer  in one study. On the other hand, prostate cancer mortality rate was significantly higher among obese than non-obese  in another study. In view of these conflicting data, further studies are required.
In conclusion, childhood obesity has several health-related consequences. Cancer-related morbidity and mortality form a significant part of them. Further studies are required to get a better picture of the extent of the problem.
(1) Reilly JJ, Methven E, McDowell ZC, et al. Health consequences of obesity. Arch Dis Child 2003;88:748-52.
(2) Micozzi MS. Functional consequences from varying patterns of growth and maturation during adolescence. Horm Res 1993;39 Suppl 3:49-58.
(3) Must A, Jacques PF, Dallal GE, Bajema CJ, Dietz WH. Long-term morbidity and mortality of overweight adolescents. A follow-up of the Harvard Growth Study of 1922 to 1935. N Engl J Med 1992;327:1350-5.
(4) Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of US adults. N Engl J Med 2003;348:1625-38.
(5) Chow W-H, Blot WJ, Vaughan TL, et al. Body mass index and risk of adenocarcinomas of the esophagus and gastric cardia. J Natl Cancer Inst 1998;90:150-155.
(6) Giovannucci E, Rimm EB, Stampfer MJ, Colditz GA, Willett WC. Height, body weight, and risk of prostate cancer. Cancer Epidemiol Biomarkers Prev 1997;6:557-63.
(7) Rodriguez C, Patel AV, Calle EE, Jacobs EJ, Chao A, Thun MJ. Body mass index, height, and prostate cancer mortality in two large cohorts of adult men in the United States. Cancer Epidemiol Biomarkers Prev 2001;10:345-53.
Combined universal ultrasound screening for developmental dysplasia of the hip and neonatal hearing
We read with interest the recent articles of Dezateux et al. and Brown et al. on screening for developmental dysplasia of the hip.
Our local child health promotion group proposed an innovative service for universal neonatal hearing screening and universal ultrasound hip screening of all our 4200 babies delivered in our area. This would be a mobile community based service, provided in heath centres located within the four distinct localities and easily accessible for families without a car. Children would be invited for a combined appointment for both universal neonatal hearing and hip ultrasound screening to be undertaken at around 4 weeks of age.
The children would continue to have a neonatal clinical examination at birth, including Ortolani and Barlow tests. A combined appointment would lead to less inconvenience to parents and consequently higher uptake rates as well as providing for the possibility of reduced staff travelling costs. Information would be given to the parents during their antenatal visit and the appointment would be arranged shortly after birth via Labour Ward and recorded in the mother’s maternity notes and the parent held child health record. Parents would be informed with posters at general practitioners surgeries and the hospital antenatal clinics.
We estimated the cost of our proposed combined screening of hearing and developmental hip dysplasia to be less than £100,000 per year, described in detail in table 1.
Equipment Costs For Audiology 2@ £2,000 = £4,000 (already purchased for Sure-Start) For HipLap-top scanners 2@ £12,000 = £24,000 Total £28,000 Staff Audiology Technician 1 wte. @ £15,000 p.a. plus on costs Hip Ultrasonographer 1 wte. @ £35,000 p.a. plus on costs Hip Screening Assistant 1 wte. @ £15,000 p.a. plus on costs Total £65,000 p.a. plus on costs
Table 1 Estimated cost for combined universal hearing and ultrasound hip screening for 4200 deliveries per year
If this cost is projected to 100,000 deliveries, the proposed combined screening would cost less than £2,381,000, that works out less expensive than £4,394,515 that Brown et al. described in their study for only the universal ultrasound hip screening. We hope that the high non-attendance in community based clinics  would not affect negatively our proposed service, although we calculated in our estimation an average of 20% of non-attendance to the first appointment.
(1) Dezateux C, Brown J, Arthur R, et al. Performance, treatment pathways, and effects of alternative policy options for screening for developmental dysplasia of the hip in the United Kinfdom. Arch Dis Child 2003;88:735-59.
(2) Brown J, Dezateux C, Karnon J, et al. Efficiency of alternative policy options for screening for developmental dysplasia of the hip in the United Kingdom. Arch Dis Child 2003;88:760-766.
(3) Sharp DJ, Hamilton W. Non-attendance at general practices and outpatient clinics. BMJ 2001;323:1081-2.
Shoe size, mid-arm circumference and age may be helpful in predicting weight
We read with interest the paper by Argall et al. and commend the authors on highlighting the inaccuracy with weight estimation using current methods. The authors comment that ‘further work is required to revise the methods by which weight estimation is performed; either with modifications to the formulae used to calculate weight or derivation of a new measuring tape to reflect the increasing weight of children’. In a study of 169 consecutive children aged 1-16 years seen in the outpatient department of our hospital we also found that although there was a strong linear correlation between the formula (age+4)x2 and weight (r=0.84), there was a stronger linear correlation between mid-arm circumference and weight (r=0.91). However, the best single measurement to predict weight in childhood appears to be shoe size, with a correlation coefficient of r=0.93 for an exponential curve.
Shoe size is easy to determine – either by measuring the feet of the child with a standard measure or asking the parents (in our experience most mothers know the size of their child’s feet), and although the formula to calculate weight from this is not straightforward, it can be easily calculated via a computer or PDA. If more time is available, then mid-arm circumference (MAC) provides a simpler guide, with similar degrees of precision. Using age alone, our population’s weight was best described by the formula (age+1.7)x3 although precision declines using a solely age- derived formula. The results of our study, and the formulae generated are summarised below.
Method of Prediction Mean error (kg) Percentage error (%) Standard ((Age+4)x2) 7.5 24% (Age+1.7)x3 5.4 17% (MAC (in cm) x3.6)-40 4.8 15% 6.8x e(Shoe size x 0.102) 4.5 14%
We believe that any future studies designed to validate improved methods of weight estimation should consider the use of either shoe size or mid-arm circumference as well as age.
(1) Argall JAW, Wright N, Mackway-Jones K, Jackson R. A comparison of two commonly used methods of weight estimation. Arch Dis Child 2003;88:789-90.
(2) Carroll W, Jay N, Alexander J. Towards better weight estimation in the seriously ill child – a comparison of methods. Arch Dis Child 2001;84(Suppl I):A12.
Comments regarding the ethical aspects of using radiolabelled aerosols in research
We read with interest Dr Everard’s leading article related to the ethics of using radiolabelled aerosols for research in children and wish to add our comments. There can be few areas that have been so comprehensively covered by legislation and practitioner guidance as the use of radioactivity in patients. These impose the highest standards of ethical care in diagnosis, treatment and research. The questions posed by Dr Everard are essentially those addressed by the radiation and nuclear medicine authorities through their publications and committees.
We agree wholeheartedly with Dr Everard in his conclusion that the risk of such studies appears to be extremely low. We would, however, add that it is important to consider the severity of the disease and the effectiveness of currently available therapies when making such judgements. Wheeze in infants is extremely common but thankfully it is unusual for this to become life threatening and effective therapies are already available. Cystic fibrosis remains a condition which eventually kills most affected patients and over a much shorter time scale than any conceivable adverse effects from the doses of radiation used in our study. Currently available treatments merely delay this eventuality and we would argue that it is therefore of greater practical importance for us to optimise treatment in this condition.
Dr Everard quotes his own work to claim that results similar to ours could probably have been obtained using a breathing simulator. We think that he overstates the significance of his own findings. Everard found no difference in budesonide deposition to a filter in eight normal adults compared to two experimental sites with the breathing simulator. While this may be a coarse indicator of total inhaled mass, it obviously gives no indication as to the pattern of drug delivery within the airways. It is difficult to justify extrapolation of findings from normal adults to young patients with diseased lungs and the very small number of subjects studied suggests the risk of a type two error.
Whilst we accept that more is not necessarily better in terms of some drugs, we think that this is difficult to argue in the context of nebulised Colistin. It has been used for decades in Europe without any evidence of toxicity other than subjective chest tightness and a small decrease in lung function if used without pre bronchodilation. The Danish group now routinely use twice the nominal dose quoted in our studies  and the Cystic Fibrosis Trust antibiotic group also recommends use of this higher dosage in patients over the age of two years. Everard’s own work on neutrophil elastase is of theoretical interest but does not show any evidence of clinical toxicity. This situation is significantly different to that with nebulised aminoglycosides which have been shown to have potentially very important adverse effects on renal tubular function, a fact which does not seem to have been appreciated by those conducting clinical trials on preservative free tobramycin.
We agree that further carefully designed clinical studies are required to answer outstanding questions but a multi-centred controlled randomised trial would be required to provide the necessary statistical power. The Cystic Fibrosis Trust has made admirable advances in initiating such collaborations but there are practical limitations to the number of such studies which can be performed on this patient group, and studies such as ours are a necessary preliminary before they could be initiated.
(1) Nikander K, Denyer J, Everard M et al. Validity of a new breathing simulator generating and measuring inhaled aerosol with adult breathing patterns. Journal of Aerosol Medicine 2000; 13:139-46.
(2) Dodd ME, Abbott J, Maddison J, Moorcroft AJ, Webb AK. Effect of the tonicity of nebulised colistin on chest tightness and pulmonary function in adults with cystic fibrosis. Thorax 1997; 52:656-658.
(3) Frederiksen B, Koch C, Hoiby N. Antibiotic treatment of initial colonisation with Pseudomonas aeruginosa postpones chronic infection and prevents deterioration of pulmonary function in cystic fibrosis. Pediatric Pulmonolgy 1997;23:330-335.
(4) Antibiotic treatment for cystic fibrosis. Report of the UK Cystic Fibrosis Trust Antibiotic Group. Second Edition, September 2002.
(5) Ring E, Eber E, Erwa W, Zach MS. Urinary N-acetyl-beta–D-glucosaminiadase activity in patients with cystic fibrosis on long term gentamycin inhalation. Arch Dis Child 1998;78: 540-543.
(6) Jones A, Elphick H, Pettitt E et al. Colistin stimulates the activity of neutrophil elastase and Pseudomonas aeruginosa elastase. European Respiratory Journal 2002; 19:1136-41
(7) Ramsey BW, Pepe MS, Quan JM et al. Intermittent administration of inhaled tobramycin in patients with cystic fibrosis. The New England Journal of Medicine 1999;340:23-30.
(8) Byrne NM, Keavey PM, Perry JD et al. Comparison of lung deposition of Colomycin using the HaloLite and the Pari LC Plus nebulisers in children with cystic fibrosis. Archives of Disease in Childhood 2003; 88: 715-8
We are grateful for the opportunity to respond to the important point raised by Professor Choonara regarding the optimal duration of antibiotic treatment in children with meningococcal infection.
It is undoubtedly true that meningococci are rapidly killed by appropriate antibiotics, and it is probably true that, at least in uncomplicated cases, courses of less than seven days’ duration may be adequate. However, it is not true to say that there is an adequate evidence base for recommending shorter treatment courses. The latest edition of the American Academy of Pediatrics’ “Red Book” recommends 5-7 days of antibiotic treatment.
The necessary duration of treatment has been controversial ever since antibiotic treatment was introduced; the history of the controversy in the 20th century has been thoroughly reviewed by Radetsky. His summary opinion was that all published studies had enrolled too few patients to have sufficient power to demonstrate no difference in outcome with shorter duration of treatment. The rarity of complications described by Professor Choonara is precisely the reason for this. Radetsky calculated that sample sizes of 400-1400 patients would be needed, depending on the magnitude of difference in complication rates thought to be clinically significant. Only one of the studies cited by Professor Choonara studied treatment with ceftriaxone, and this included only 32 patients with meningococcal disease. Radetsky concluded in 1990 that “…the current minimal duration [of antibiotic therapy]…is probably 7 days”, but left room for discretionary clinical judgement (“Only the patient’s response to therapy counts”). In the absence of subsequent evidence to the contrary, we cannot definitively recommend that shorter courses are safe.
(1) Choonara I. Treatment of Meningococcal Infection [electronic response to SB Welch and S Nadel, Treatment of meningococcal infection] archdischild.com 2003 http://adc.bmjjournals.com/cgi/eletters/archdischild;88/7/608#533
(2) American Academy of Pediatrics. Meningococcal Infections. In: Red Book: 2003 Report of the Committee on Infectious Diseases. 26th ed. Pickering LK, Ed. Elk Grove Village, Illinois: American Academy of Pediatrics 2003:430-6.
(3) Beeson PB, Westerman E. Cerebrospinal fever: analysis of 3575 case reports, with special reference to sulphonamide therapy. Br Med J 1943; 1:497-500.
(4) Radetsky M. Duration of treatment in bacterial meningitis: a historical inquiry. Pediatr Infect Dis J 1990;9(1):2-9.
(5) Martin E, Hohl P, Guggi T, Kayser FH, Fernex M and Members of the Swiss Multicenter Meningitis Study Group. Short Course Single Daily Ceftriaxone Monotherapy for Acute Bacterial Meningitis in Children: Results of a Swiss Multicenter Study. Part I: Clinical Results. Infection 1990:18(2):70-77.
Optimal dose of intravenous immunoglobulins in Guillain-Barre syndrome
I read with interest the recent article by Trifa et al. and appreciate their efforts to highlight an unusual complication-haemolytic anaemia-related to intravenous immunoglobulin (IVIG) therapy in Guillain- Barre syndrome (GBS). However, I have some concerns regarding the dose of IVIG used.
The usual cumulative dose of IVIG recommended in children with GBS is 2 grams/Kg.[2-4] This may be given either over two days 1 gram/kg/day)  or over five days (0.4 gram/kg/day).[2-4] Both the dosing schedules have been found to be effective in treating children with GBS. However, in one study, a faster rate of recovery was seen among those patients who received a total dose of IVIG over two days as compared to five days. Though most studies have shown benefit of IVIG in children with GBS, there are some studies where similar patterns of recovery were seen among children given supportive care alone and those treated with IVIG.
There are no adequate trials to determine if IVIG is better than placebo. Moreover, trials regarding the optimal dose of IVIG are also lacking. Therefore, it is safer to use the standard dose of IVIG (cumulative dose of 2 grams/kg) rather than 5 grams/kg as was given in this case. This is important as newer rare complications of IVIG therapy are recently being reported.
(1) Trifa M, Simon L, Hamza J, Bavoux F, Des Roziers NB. Haemolytic anaemia associated with high dose intravenous immunoglobulin therapy in a child with Guillain-Barre syndrome. Arch Dis Child 2003;88: 836-37.
(2) Kanra G, Ozon A, Vajsar J, Catagna L, Secmeer G, Topaloglu H. Intravenous immunoglobulin treatment in children with Guillain-Barre syndrome. Eur J Paediatr Neurol 1997;1: 7-12
(3) Singhi SC, Jayshree M, Singhi P, Banerjee S, Prabhakar S. Intravenous immunoglobulin in very severe childhood Guillain-Barre syndrome. Ann Trop Paediatr 1999;19: 167-74.
(4) Tekgul H, Serdaroglu G, Tutuncuoglu S. Outcome of axonal and demyelinating forms of Guillain-Barre syndrome in children. Pediatr Neurol 2003;28: 295-99
(5) Graf WD, Katz JS, Eder DN, Smith AJ, Chun MR. Outcome in severe pediatric Guillain-Barre syndrome after immunotherapy or supportive care. Neurology 1999;52:1494-7.
Repeating the search strategy in July 2003 has led to no new, relevant trials to answer this question. There has been a further descriptive study which adds to our understanding of the prognostic value of serum albumin levels in critically ill children.
Durward et al. in this journal have described the incidence of hypoalbuminaemia, its influence on anion gap and prognostic correlation in critically ill children. This is a prospective descriptive study on 134 critically ill children admitted to a tertiary paediatric intensive care unit. Their results suggest that neither admission hypoalbuminaemia nor extreme hypoalbuminaemia ( <_20 gm="gm" l="l" predict="predict" mortality="mortality" in="in" sick="sick" children.="children." this="this" result="result" is="is" contrast="contrast" with="with" the="the" adult="adult" studies="studies" which="which" describe="describe" hypoalbuminaemia="hypoalbuminaemia" as="as" an="an" independent="independent" predictor="predictor" of="of" mortality.="mortality." p="p">Reference
(1) Durward A, Mayer A, Skellett S, Taylor D, Hanna S, Tibby SM, Murdoch IA. Hypoalbuminaemia in critically ill children: incidence, prognosis, and influence on the anion gap. Arch Dis Child 2003 May;88(5):419-22.
Survival analysis by congenital anomaly sub type is needed
We commend the study by Dastgiri and colleagues  as both timely and informative. There are few published papers describing the survival of children with congenital anomalies, especially reporting survival beyond the first year of life. Those which do exist mainly describe the survival of children with Down’s syndrome  or spina bifida, but there is either limited information based on single studies for certain congenital anomaly subtypes, or no information at all. As population based information on the long-term outcome of children with a range of congenital anomalies is lacking, there is little accurate information for parents or health professionals.
Using data from a population-based register of congenital anomalies, Dastgiri and colleagues describe survival to five years of life, with 97% follow up achieved. However, the major limitation of the study is the description of survival pattern by major congenital anomaly group. Presumably the rationale for classifying cases by major group was that subtype analysis would have resulted in very small numbers. However, this analysis is misleading as the groups represent a spectrum of conditions which vary widely in their lethality. For example, neural tube defects include anencephaly, spina bifida, and encephalocele, which are known to vary greatly in outcome. Anencephaly is a lethal condition, whereas children born with spina bifida may survive many years. For example, using data from the Northern Congenital Anomaly Survey, out of 199 cases of spina bifida reported to the Survey between 1985-2001, only 31 died within the first week of life.
We agree with Dastgiri and colleagues in their call for further outcome studies. Such information from long-term prospective follow up studies is required both to give appropriate information to parents and health professionals when an antenatal diagnosis is confirmed, and also to identify factors associated with successful outcome. Many individual anomalies are uncommon and knowledge of outcomes would require data from high quality, long-standing congenital anomaly registers with good case ascertainment and consistent diagnostic coding. Analyses should be extended to go beyond five years of age and take into account the influence of clinical characteristics (e.g. presence of additional anomalies, birth weight, gender, plurality) on survival. Children born with congenital anomalies have complex health and social care needs, with cost implications for health service planning. Thus there remains the need to understand and improve the survival and quality of life for these children, and to accurately plan for their future care needs.
(1) Dastgiri S, Gilmour WH, Stone DH. Survival of children born with congenital anomalies. Arch Dis Child 2003;88:391-94.
(2) Leonard S, Bower C, Petterson B, Leonard H. Survival of infants born with Down’s syndrome: 1980-96. Paed & Perinat Epidemiol 2000;14:163-71.
(3) Wong L-YC, Paulozzi LJ. Survival of infants with spina bifida: a population study, 1979-94. Paed & Perinat Epidemiol 2001;15:374-78.
(4) Northern Regional Survey Steering Group. Fetal Abnormality: an audit of its recognition and management. Arch Dis Child 1992;67:770-74.
Ineffective intervention and pointless investigation after childhood urinary tract infection
Wheeler and colleagues are to be applauded for putting another nail in the coffin of the routine MCUG, a distressing and potentially harmful intervention which has been imposed on thousands of unhappy children, with the best of intentions, but, unfortunately, based upon assumption, anecdote and extrapolation.
Unless something has been left out of the reporting of the International Reflux Study (IRS), Wheeler et al. are incorrect in stating that "a randomised comparison between surgical treatment and antibiotic treatment has not been performed". Surely the IRS was in fact just such a study showing no useful benefit of one intervention over the other both in terms of frequency of UTI or scarring. It could well be argued that the absence of benefit for the addition of surgery to antibiotic prophylaxis shown in the Birmingham Reflux Study (BRS) over and above antibiotic treatment is likely to indicate that surgery is ineffective. If that is the case, then the absence of a difference in the IRS between surgery alone and antibiotics alone may well indicate, not so much that both are equally effective as that both are equally ineffective!
It is noteworthy that 14 years ago Professor White, co-author of the BRS, suggested that a controlled trial of antibiotic prophylaxis would now be ethical. Nevertheless, antibiotic prophylaxis with trimethoprim is a relatively innocuous intervention and, pending such a good controlled trial, it would, perhaps, be a brave paediatrician who would deny this during infancy and maybe up to 2 years. Surprisingly, this is exactly the practice of many following a normal MCUG, notwithstanding the continuation of UTI following surgery and the complete absence of reflux in 30% of infants with abnormal DMSA scans following UTI.
Anecdotally this DGH unit is not unusual in having abandoned the MCUG as an investigation performed with the sole indication of UTI - despite consensus recommendations! The practice in this unit following infantile UTI remains to provide prophylaxis to all infants up to two years. Investigation, however, in the presence of normal renal ultrasound examination (US) and urinary stream is limited to annual BP, urine testing for protein and US to monitor renal growth until a single DMSA scan can be performed at 4 years. Outside this age group DMSA is only performed in the presence of symptomatic pyelonephritis or abnormal ultrasound.
(1) Jodal U et al. Infection pattern in children with vesicoureteral reflux randomly allocated to operation or long-term antibacterial prophylaxis. The International Reflux Study in Children. J Urol 1992;148:1650-1652.
(2) Birmingham Reflux Study Group. Prospective trial of operative versus non -operative treatment of severe vesico-ureteric reflux in children: five years observation. BMJ 1987;295:237-241.
(3) White RHR. Vesicoureteric reflux and renal scarring. Arch Dis Child 1989;64:407-412.
(4) Gleeson FV, Gordon I. Imaging in urinary tract infection. Arch Dis Child 1991;66:1283.
(5) Vernon SJ et al. New renal scarring in children who at age 3 and 4 years had normal scans with dimercaptosuccinic acid: follow up study. Br Med J 1997;315:905-9.
(6) Rickwood A et al. Current imaging of childhood urinary infections: prospective survey. Br Med J 1992;304:663-5.
Short course treatment for meningococcus - a warning
I am concerned that Professor Choonara suggests that an evidence-based approach would suggest that a 4-day course of intravenous antibiotic treatment (benzylpenicillin or ceftriaxon) is sufficient for meningococcal meningitis. In support of this recommendation he mentions two studies totalling perhaps 63 patients in all who received antibiotic treatment for 4 days in total and amongst whom there were no relapses. Based on this number of cases the 95% confidence interval of the probability of an adverse event where no adverse event occurred is 4.7% or about 1 in 20 cases.[1,2] Given the serious consequences of undertreatment of meningococcal meningitis I would be unwilling to accept such odds. In my view further studies are necessary before such a recommendation can be made with confidence.
(1) Hanley JA, Lippman-Hand A. If nothing goes wrong is everything all right? JAMA 1983;13:1743-5.
(2) Eypasch e, Lefering R, Kum CK, Troidl H. Probability of adverse event that have not yet occurred: a statistical reminder. Br Med J 1995;311:619-20.
Cycle helmets and legislation
Lee and Mann urge paediatricians to be advocates for accident prevention and make the case for legislation for cycle helmet use in children and young people. I am all for advocacy for cycle use but have strong doubts over the role of legislation. At the same time as the June editorial, the Cyclists’ Touring Club magazine was writing a critique of legislation. This is not the first such critique and Lee and Mann do not mention previous BMJ correspondence, e.g. Hillman. Lee and Mann’s main thesis is that helmet use reduces risk of brain injury and that education alone is not sufficient to prevent the majority of brain injuries. Both these points of view are open to question. According to Franklin, large population studies show no discernible reduction in fatal or serious injuries relative to cycle use in countries where helmet use has become significant; in the USA, an increase in helmet wearing from 18% to 50% of cyclists between 1991 and 2001 was associated with a 40% increase in risk of head injury. In Australia, the absolute number of head injuries fell but this was proportionately less than the decline in cycle use.
A key question is whether legislation leads to fewer people cycling. If this is the case then it is counterproductive: as the CTC point out, the health benefits of more people cycling without helmets are greater than the gain in head injury reduction of fewer people cycling with helmets. As an advocate of better health for children I will urge for measures to encourage cycling and walking in children rather than compulsory helmets which could be seen as victim blaming, unless it is part of a package of measures including traffic calming, traffic reduction measures and separation of cyclists from motorists. I will continue to wear a helmet myself and shall encourage usage locally, but don’t believe the evidence is yet adequate to support population measures , either for children or for everyone.
(1) Franklin J. Heads up. CycleAug/Sept 2003.
(2) Hillman M. Cycling offers important health benefits and should be encouraged. BMJ 1997;315:490.
We are glad Dr Redfern found our article of interest.
We agree on most points. For clarity, the fact that there are difficulties inherent in comparing the nutritional adequacy of human milk with that of infant formula does not detract from our main point, namely that more research is required regarding the possible differing nutritional needs of formula versus breast fed infants at the onset of weaning. Regarding the anecdotal evidence, in Winchester mothers not wishing to continue exclusive breast-feeding beyond 4 months cite practical rather nutritional concerns. These are based on a belief that a little solid food given to breast fed babies between 4 and 6 months of age leads to increased contentment and longer gaps between night breast feeds-important considerations at a time when many mothers are returning to work.
We thank Drs Odeka and Wong for their interest in our article.
(1) Redfern L. Weaning infants, encouraging breast feeding [electronic response to KD Foote and LD Marriott, Weaning of infants] archdischild.comhttp://adc.bmjjournals.com/cgi/eletters/archdischild;88/6/488#531
(2) KD Foote and LD Marriott. Weaning of infants. Arch Dis Child 2003;88:488-492.
(3) E Odeka and L Wong. Weaning of infants; timing should be individualized [electronic response to KD Foote and LD Marriott, Weaning of infants] archdischild.comhttp://adc.bmjjournals.com/cgi/eletters/archdischild;88/6/488#510
Pantoea agglomerans septic arthritis following lemon tree thorn injury
We read with interest the recent report by Kratz et al. about a patient with Pantoea agglomerans septic arthritis following a palm tree thorn injury.
We would like to add a child we recently attended at the National Children’s Hospital of Costa Rica. A 9-yr-old healthy boy was admitted to our hospital 3 days after suffering a penetrating injury in his left knee with a lemon tree thorn, after falling from a tree. He developed fever of 38°C the evening of the trauma, but had no other complains. The morning after, fever persisted and he developed knee pain, local erythema, and difficulty to walk. Symptoms persisted for 2 days more before seeking medical attention. On admission to the orthopedic emergency room, temperature was 38°C, and his left knee was swollen, warm, painful, had evidence of effusion and limited range of motion, and he was not able to walk. No local bruises or lesions were visible. Rest of physical examination was normal. A radiograph of the knee did not showed abnormalities or any foreign body. An arthrocentesis was performed that night and a moderate amount of yellowish fluid was obtained and sent for culture. Synovial fluid analysis showed low glucose (8 mg/dL), increased lactate dehydrogenase (1.195 IU/L) and protein (6.4 g/dL); Gram stain was negative. Blood cultures were taken and empiric intravenous therapy with oxacillin and gentamicin was initiated for suspected knee septic arthritis.
Peripheral blood count only revealed mild neutrophilia, and sedimentation rate was 38 mm/h. The day after, symptoms worsened; a repeat arthrocentesis revealed a serosanguineous and purulent synovial fluid and consequently, an arthrotomy with drainage was done. Surgical findings revealed a grossly purulent fluid, synovial changes consistent with knee septic arthritis, and no foreign bodies were visible. A Penrose drainage was left for two days. After 3 days of admission, synovial fluid culture was positive for Pantoea agglomerans (susceptible to amikacin, ceftazidime, cefepime, ciprofloxacin, cefotaxime; and resistant to ampicillin). Oxacillin and gentamicin were discontinued and intravenous ceftazidime (150 mg/kg/day) was started and continued for 9 days. Blood cultures were negative. Fever disappeared the day after surgery and symptoms resolved progressively. After 15 days of admission, he was discharged home to complete treatment with oral cefixime for one more week. At follow up, no complains or sequelae were documented. Very few cases of P. agglomerans septic arthritis after penetrating trauma have been reported in children, as recently addressed by Kratz and colleagues.
We reviewed the literature [1-6] and found no previous reports of P. agglomerans septic arthritis after lemon tree thorn penetrating injury. This microorganism should always be considered after any thorn-associated septic arthritis, as delay in diagnosis and initiation of treatment is common [1-6] and risk of osteomyelitis also exists.
(1) Kratz A, Greenberg D, Barki Y, Cohen E, Lifshitz M. Pantoea agglomerans as a cause of septic arthritis after palm tree thorn injury; case report and literature review. Arch Dis Child 2003;88:542-4.
(2) Flatauer FE, Khan MA. Septic arthritis caused by Enterobacter agglomerans. Arch Intern Med 1978;138:788.
(3) Strömqvist B, Edlund E, Lidgren L. A case of blackthorn synovitis. Acta Orthop Scand 1985;56:342-3.
(4) Vincent K, Szabo RM. Enterobacter agglomerans osteomyelitis of the hand from a rose thorn: a case report. Orthopedics 1988;11:465-7.
(5) Olenginski TP, Bush DC, Harrington TM. Plant thorn synovitis: an uncommon cause of monoarthritis. Semin Arthritis Rheum 1991;21:40-6.
(6) De Champs C, Le Seaux S, Dubost JJ, Boisgard S, Sauvezie B, Sirot J. Isolation of Pantoea agglomerans in two cases of septic monoarthritis after plant thorn and wood sliver injuries. J Clin Microbiol 2000;38:460-1.
Short-term versus long-term thromboprophylaxis
We read with great interest the commentary of Dr Thomas concerning our case of a healthy nine-year-old child affected by venous thromboembolism (VTE), with persistent residual venous thrombosis at one year of follow-up. The comments were pertinent and were appropriate for publication at the same time due to the relevance of the case, both for its unique presentation and for the problems it raised regarding diagnosis and treatment. We proposed ad interim long-term anticoagulant therapy. Dr Thomas proposed that the child's parents and medical attendants be alerted to offer short-term thromboprophylaxis at times of increased thrombotic risk in the future.
However, in our opinion, the decision to persist with intermittent thromboprophylaxis remains problematic with this child. Dr Thomas underestimated the possible existence of a thrombophilic condition, observing that:
(1) it had not been shown conclusively that the VTE was a primary event, and should therefore be presumed to have been provoked by the previous infectious disease;
(2) combined thrombophilia had not been demonstrated conclusively;
(3) the risk of recurrent events among patients with multiple thrombophilic traits is unknown; and
(4) the lack of recanalisation of the vein probably does not contribute to risk.
(1) To address Dr Thomas' observations, we will add further argument. We agree that the nature of the first VTE (provoked or unprovoked) should be the principal consideration in prescribing subsequent long-term secondary antithrombotic prophylaxis. However, we doubt that the VTE in this child, which occurred after an acute respiratory-tract infection, can be confidently classified as provoked. A number of cases of VTE following Varicella or measles infections are cited in the PubMed reference http://www.ncbi.nlm.nih.gov/entrez/query.fcgi; moreover, acute pharyngitis or tonsillitis can be complicated by thrombophlebitis of the internal jugular vein (Lemierre syndrome). This was not the case in our patient. Of course, endothelial injury due to viral infection cannot be ruled out as an event triggering VTE, but on the basis of the above considerations, in our opinion the thrombogenic stimulus was very mild.
(2) Dr Thomas stated that the laboratory results were inconclusive in corroborating the existence of a double thrombophilic defect, and compared the protein S and homocysteine values of our patient with some ranges for these parameters cited in the literature. Our diagnosis of thrombophilia in this child was made not only on the basis of these absolute values, which we found abnormal relative to ranges observed in our laboratory, but also from the family history, which showed the relevant genetic background. The father had greatly increased levels of homocysteine (141 ƒÝmol/L) and was homozygous for the C677T polymorphism in the MTHFR gene (as was the child). The mother had an obvious free protein S deficiency (41%). Such a laboratory diagnosis conformed to the clinical presentation, in so far as VTE is rare in the overall paediatric population and among child carriers of a single thrombophilic abnormality. This prompted us to consider our patient, from a clinical point of view, to be affected by a severe thrombophilic condition.
(3) Both the thrombophilic traits observed in this patient have been associated per se with an increased risk of recurrent VTE.[3,4] Moreover, the association of multiple thrombophilic defects is a well established risk for recurrent VTE.[5,6] Obviously, if mild hyperhomocysteinaemia is corrected, then carriership of protein S deficiency becomes the only non-removable risk factor. However, carriers of protein S deficiency remain possible candidates for indefinite anticoagulation.
(4) Finally, citing the paper by Prandoni et al, Dr Thomas stated that only the presence of prothrombotic defects increases the risk of recurrent VTE. This is a misinterpretation of the work of Prandoni et al, because this report clearly states that multivariate analysis of their prospective cohort of patients with VTE produced a hazard ratio for a recurrent event among patients with residual thrombosis of 2.4 (95% CI, 1.3,V4.4), of 2.5 in patients with unprovoked first VTE (95% CI, 1.4,V4.4), and of 3.1 in patients with thrombophilia (95% CI, 1.8,V5.2), when compared with patients with secondary thrombosis. Furthermore, at least two other research groups have confirmed that the presence of residual vein thrombosis is predictive of a recurrent event,[8,9] independently of the presence of inherited thrombophilia. We agree with Dr Thomas that the absence of VTE in the family history and the doubt that this was a truly unprovoked occurrence of VTE should be carefully weighed in the therapeutic decision. However, the considerations discussed above prompted us at the time to recommend long-term antithrombotic prophylaxis, after careful counselling of the child's parents and evaluation of their compliance.
(1) Zannolli R, Mazzei MA, Sacco P, Turchetti V, Amato T, Battistini S, Berardi R, Volterrani L, De Stefano V, Morgese G. Posterior knee pain: primary symptom of a small non-occlusive venous clot. Arch Dis Child 2003;8:728-30.
(2) Tormene D, Simioni P, Prandoni P, Franz F, Zerbinati P, Tognin , Girolami A. The incidence of venous thromboembolism in thrombophilic children: a prospective cohort study. Blood 2002;100:2403-5.
(3) Engesser L, Broekmans AW, Briet E, Brommer EJ, Bertina RM. Hereditary protein S deficiency: clinical manifestations. Ann Intern Med 1987;106:677-82.
(4) Eichinger S, Stumpflen A, Hirschl M, Bialonczyk C, Herkner K, Stain M, Schneider B, Pabinger I, Lechner K, Kyrle PA. Hyperhomocysteinemia is a risk factor of recurrent venous thromboembolism. Thromb Haemost 1998;80: 566-9.
(5) Nowak-Gottl U, Junker R, Kreuz W, von Eckardstein A, Kosch A, Nohe N, Schobess R, Ehrenforth S; Childhood Thrombophilia Study Group.Risk of recurrent venous thrombosis in children with combined prothrombotic risk factors. Blood 2001;97:858-62.
(6) Bauer KA. Management of thrombophilia. In State of the Art 2003, XIXth Congress of the International society on Thrombosis and Haemostasis. J Thromb Haemost 2003; 1:1429-34.
(7) Prandoni P, Lensing AW, Prins MH, Bernardi E, Marchiori A, Bagatella P, Frulla M, Mosena L, Tormene D, Piccioli A, Simioni P, Girolami A. Residual venous thrombosis as a predictive factor of recurrent venous thromboembolism. Ann Intern Med 2002;137:955-960.
(8) Piovella F, Crippa L, Barone M, Vigano D'Angelo S, Serafini S, Galli L, Beltrametti C, D'Angelo A. Normalization rates of compression ultrasonography in patients with a first episode of deep vein thrombosis of the lower limbs: association with recurrence and new thrombosis. Haematologica 2002;87:515-22.
(9) Cosmi C, Legnani C, Cini M, Valdre L, Guazzaloca G, Coccheri S, Palareti G. Thrombophilia and residual vein thrombosis are independent risk factors for recurrent venous thromboembolism. J Thromb Haemost 2003;suppl: abstract OC150.
Prevalence of autism: no evidence for the conclusion
In view of the widespread British media coverage of this study last week in advance of its publication it is interesting to discover how weak its claims actually are:
"The prevalence of autism, which was apparently rising from 1979 to 1992, reached a plateau from 1992 to 1996 at a rate of some 2.6 per 1000 live births. This levelling off, together with the reducing age at diagnosis, suggests that the earlier recorded rise in prevalence was not a real increase but was likely due to factors such as increased recognition, a greater willingness on the part of educationalists and families to accept the diagnostic lable, and better recording systems. The proportion of parents attributing their child's autism to MMR appears to have increased since August 1997."
In effect the conclusion of this paper is a hypothesis for which it has produced no evidence. It is hard to see why the levelling off of a trend is evidence of the trend being in itself illusory - this is a logical 'non-sequitur'. Nor has the paper produced any evidence that the rising trend was due to better recognition, or that there was some institutional movement that reached fruition in mid-90s which led to a tailing off of the trend. It is curious that this is an interpretation which has to be read into the statistics and no one has actually been able to corroborate an institutional drive to diagnose more cases of autism during this period from conventional documentary sources. The 'discussion' cites no external evidence for this. The only certain trend in regard to diagnostic style identified is that it happens younger, but this is also entirely consistent with higher incidence leading to greater familiarity in turn leading to faster diagnosis. In fact nothing has been shown at all.
The issue of the rising prevalence of autism has been tied spuriously to the issue of the MMR and autism. These may be to many minds connected concerns but the perception that autism is rising is not dependent on the conviction that it is being caused by the MMR. Whether the MMR vaccination can cause autism is surely anyhow a clnical issue which cannot be resolved by reviewing data from public health records, although there have been many such publications in this field. As the paper itself points out this kind of data can be misleading, but not only in the way it suggests. For instance, bad local reactions to vaccination may go unreported while parents' accounts of their child's development may be diluted by the tendency of medics to repeat stereo- typical histories (comparing notes with other parents this seems to be a common experience although there is no doubt it is all done in good faith).
The incidence of autism has certainly increased; a full explanation of the reason for this is most important.
Treatment of Meningococcal Infection
It is disappointing to see that Welch and Nadel  recommend seven days treatment with antibiotics for children with uncomplicated meningococcal infection. An evidence-based approach would support the use of four days intravenous therapy. There have been two clinical trials that have evaluated the duration of therapy. A prospective study of four days treatment with intravenous benzylpenicillin for 50 consecutive patients (adults and children) with meningococcal meningitis was published in 1986. Two patients died within the first 36 hours of therapy and one elderly patient developed aspiration pneumonia requiring penicillin therapy beyond four days. The remaining 47 patients were cured and no relapses occurred.
Another study randomised 31 children with meningococcal meningitis to either four or eight days treatment with ceftriaxone. The duration of therapy had no effect on outcome. Neurological sequelae were related to the severity of the illness on presentation.
The meningococcus is highly sensitive to antimicrobial agents including benzylpenicillin, cefotaxime and ceftriaxone all of which are used successfully in treatment. Complications, in particular subdural effusion, are uncommon in meningococcal disease. In an era of evidence based medicine, there is no clinical indication for the routine treatment of all children with meningococcal septicaemia or meningitis for more than four days.
(1) Welch SB, Nadel S. Treatment of meningococcal infection. Arch Dis Child 2003;88:608-614.
(2) Viladrich PF, Pallares R, Ariza J. Four Days of Penicillin Therapy for Meningococcal Meningitis. Arch Intern Med 1986;146:2380-2382.
(3) Martin E, Hohl P, Guggi F et al. Short Course Single Daily Ceftriaxone Monotherapy for Acute Bacterial Meningitis in Children: Results of a Swiss Multicenter Study. Part I: Clinical Results. Infection 1990;18:70-77.
(4) Schaad UB, Nelson JD, McCracken Jr GH. Recrudescence and Relapse in Bacterial Meningitis of Childhood. Pediatrics 1981;67:188-195.
We thank Drs Loh et al. for their comment  to our letter.
We wish to clarify that our letter was to share our own experience and it reflected our perspective during a very turbulent period when we had to deal with SARS. It highlighted practices which were carried out at our institution, a tertiary teaching hospital, in tandem with Singapore's efforts against SARS. Although there was a SARS-designated hospital, all other hospitals were fully geared in the frontline battle against the disease. There were adult patients diagnosed with SARS at our hospital who were eventually transferred to the designated hospital. Doctors and nurses from our department contributed to the paediatric team based at the SARS- designated hospital as part of our nation's fight against the virus. We therefore have first-hand knowledge that there was no mortality or paediatric patients who required assisted ventilation. This, together with the relatively fewer number of paediatrics patients compared to adults, led us to hypothesize that the coronavirus causing SARS might affect children differently, and cause a milder form of disease. Data from other countries with outbreak appear to be similar to our observation. However, this does not imply that we have over-reacted in our preventive measures in children. On the contrary, as was pointed out in our letter, even paediatricians should keep their guard and remain vigilent at all times (as we are even now), not knowing if children may be a carrier-source. The changes to our lives brought on by SARS affected all Singaporeans, with medical personnel shouldering much, including the responsibility of caring for the sick, and learning more about the disease.
(1) Lik Eng Loh, Janil Puthucheary, Irene Chan, Oh Moh Chay. Re Childhood SARS in Singapore [electronic response to Bever et al. Childhood SARS in Singapore] archdischild.com 2003 http://adc.bmjjournals.com/cgi/eletters/archdischild;88/8/742#524
(2) Van Bever H, Hia C, Swee Chye Q. Childhood SARS in Singapore. Arch Dis Child 2003;88:742.
Weaning infants, encouraging breast feeding.
The review by Foote and Marriott on infant weaning  was of interest especially in the light of the recent adoption by the UK Department of Health of 6 months as the age for the introduction of complementary foods.
The authors make a number of comparisons between artificial feeding and breast milk that deserve comment. They make the point that the nutrient density of cows milk based formula is less than that of breast milk, highlighting particularly the lower iron content of breast milk. There are inherent difficulties in analysing the composition of breast milk and making comparisons with formula feeding. Breast milk differs in its composition throughout lactation, depending on factors such as the infant’s age, frequency of feeding, time of day, etc. It is indeed the case that the iron content is lower in breast milk, but the presence of the transfer protein lactoferrin makes iron in breast milk more easily absorbed. Hence the iron concentration in artificial formulae is higher to compensate for less efficient absorption.
The authors cite anecdotal evidence from their Winchester clinic that mothers who breast-feed would rather discontinue than maintain exclusivity. It would be interesting to assess the understanding of those mothers about the nutrient composition of breast milk. Anecdotal experience from my own practice (Salford, Greater Manchester) is that many mothers believe that, apart from the colostrum produced in the first few days of lactation, formula feeding and breast-feeding are nutritionally pretty much the same. They are unaware of issues such as the bioavailability and better absorption of nutrients from breast milk. This belief that there is no great advantage to breast-feeding beyond a few weeks underpins decisions on how long to breast-feed their infants.
I strongly agree with the authors that encouraging more mothers to breast-feed is an imperative in the UK. There is also a need to give parents more specific information on the nutritional and immunological benefits of breast-feeding, not just in the antenatal period but also once lactation is established, when mothers are pondering decisions on the duration of breast-feeding and the timing of introduction of solids.
The authors point to social and cultural factors in the UK, which would make a major change in weaning policy difficult. They suggest that the best interests of infant health would be better served by encouraging more mothers to breast feed, rather than promoting exclusivity for 6 months.
I would add the observation that social and cultural factors in the UK are not conducive to breastfeeding beyond a few weeks of age. I would suggest that the short duration of breast-feeding in the UK, and the early introduction of solids, both stem from ignorance of the advantages of breast milk. Promoting a greater knowledge of the nutritional advantages of breast-feeding would address both problems, and permit the public to challenge the prevailing social climate, which leads to short periods of breast-feeding and premature weaning.
(1) Foote KD, Marriott LD. Weaning of infants. Arch Dis Child 2003;88:488-492.
The reflections of Stewart on the state of training for general paediatricians in the acute stabilization of critically ill children will hopefully fuel much needed debate and change. Whilst agreeing with the many shortfalls of the current system which he identifies, however, I believe that the solution should not be focussed around the paediatric intensive care unit (PICU).
The majority of resuscitation and stabilization of children happens outside the PICU. My experience of talking to general paediatricians is that the increasing emphasis on tertiary intensive care units makes them feel increasingly deskilled, as opposed to enhancing their training opportunities and support. Rather than deskilling paediatricians, their specialist local expertise should be enhanced, encouraged and acknowledged.
Acute Paediatrics, as practiced in a District General Hospital (DGH), is different in context, resources and management goals from that practiced on the tertiary PICU. By definition, intensivists see children who have been assessed as being critically ill by another clinician. The general paediatrician has to decide who, amongst the many children they see, should be brought to the attention of an intensivist. The intensivist is accustomed to managing crisis situations with a full array of back-up both in terms of equipment and personnel. The general paediatrician has to work within the constraints of limited local resources and be able to utilize them to their maximum potential. Stabilization and timely transfer (if required) are the goals of care in the district hospital, whereas in focus on the intensive care unit moves to ongoing physiological support and medium-term management to optimise outcome.
The validity of acute paediatrics as a special interest for the general paediatrician has been affirmed by the growing number of posts advertised for paediatricians with an interest in emergency medicine, or able to take on a liaison role with the Emergency Department. As this area of interest develops further, these paediatricians will be best placed to provide training both for Senior House Officers (SHOs) and Specialist Registrars (SpRs) and also their other consultant colleagues. They will also be in a position to facilitate more effective multi-disciplinary training, with local Emergency Medicine and Anaesthesia staff, and to work around local logistical issues. 6 months of PICU training may be of interest to some, but will not necessarily expose the trainee to situations similar to those that they will face as a general paediatrician. The north American practice of rotation through the PICU for 1 or 2 months during residency may provide enough exposure at an SHO level for the trainee to assimilate some foundational principles and identify some of their own ongoing learning needs. As the length of training shortens, it is crucial to distil those aspects of experience and skill acquisition that an SpR would hope to gain from PICU placement into a more focussed form. The use of technology, such as simulators, and audio-visual feedback in the local context certainly has potential to do this. As Stewart points out, the growing use of telemedicine does allow the tertiary intensivist to collaborate as a part of the medical team in acute settings in the DGH, usually prior to then retrieving the child. As local training would need to involve all team members, the intensivist does have a role to play in this context. As local clinicians identify their training needs, intensivists may well be invited to offer specific expertise, but should not drive the educational agenda.
Training the trainees
As a junior doctor in training, I can’t agree more strongly with Dr Stewart. I am presently a senior house officer in Paediatric Intensive care and I feel strongly that all junior doctors should have an opportunity to work in an Intensive care unit. This is regardless of whether they view themselves as intensivists or general paediatricians in the long run.
In my opinion training courses such as APLS and NALS are brilliant when a structured approach is needed for an acutely unwell infant or child. However intensive care training makes one extremely meticulous when monitoring simple trends such as fluid balance, urine output and vital parameters. Personally I hope this training would help me in the future to anticipate worrying trends in my patients even before things get seriously wrong. In addition intensive care units are an excellent model for the full shift system and train doctors in systematic handovers.
At a SHO level, there are very few training posts in paediatric Intensive care. At the same time it would be quite intimidating and unsettling to work as a registrar in Intensive care with no prior training. Centralisation of intensive care units inadvertently leads to other units having a low threshold for transferring patients. While stabilising the sick child is a priority task, there are often too many people at hand (including registrars and consultants in A&E, paediatrics and anaesthesia) playing a vital role. The poor SHO in paediatrics is often out of all the “action.”
Hands on experience is essential between APLS and NALS courses which are repeated every 3 years. Are mannequins and simulators an acceptable alternative?
(1) Stewart D. Medical training in the UK. Arch Dis Child 2003;88:655-658 .
Frequency of child abuse in sudden infant death
Whilst it is reassuring to know that the numbers of infants dying suddenly in N & E Yorkshire have fallen dramatically, apparently following the introduction of a preventive programme, in my opinion, the prevalence of maltreatment as a cause of sudden infant death remains uncertain.
I do not think that the method of ascertainment as described in Stanton's paper is sufficiently sensitive to provide a reliable numerator. This inadequacy is underlined by Stanton's own acknowledgement that in two of the families where two siblings died "in circumstances suggestive of maltreatment of MSBP", "there were no reasons to question the initial daignosis of SIDS in the first deaths, even in retrospect".
Moreover, it is very surprising that despite a dramatic fall in the numbers of sudden infant deaths associated with prone sleeping, there was no change in the proportion of infants dying in suspicious circumstances. Does Dr Stanton believe that there has been a parallel decline in the frequency of child abuse?
Author's reply to Winrow
My thanks to Dr Winrow for pointing out that all disciplines are affected by the contraction of training time. Consultants all over the country are struggling to maintain the standards of care for the future in the face of increasing demands on their own time and reduced time in which to train.
However, rather than obscure the wider issue I hope to draw attention to it. This issue affects us all. The rotation of trainees through intensive care is not a compartmentalisation of training as the experience is applicable to all trainees, and also addresses the loss of continuity with the sickest of patients that Dr Winrow refers to.
Whilst the issue of continuity of care in its widest sense is a major one, affecting PICU as much as general paediatrics, the comment that the initial resuscitation of critically ill patients is “the easy bit” and that certification in PALS or APLS is sufficient must be a reference to how “easy” it is to get wrong. Inefficient resuscitation has far reaching consequences on patient outcome, which, of course, the referring team does not see as the patients are taken away by the retrieval team.
The introduction of simulation centres is not a cure-all. However, it is a component of a strategy to improve the efficiency of training. The Human Patient Simulator is appropriate for Critical Care, but the educational approach can assist in training all future doctors. Unfortunately, most physicians are not aware of what is available. The simulated patient (both mannequin and computer based) can enhance (not replace) “real” clinical experience, and can even be used to assist in obtaining the longitudinal experience Dr Winrow feels is being lost. Our options are limited, either the duration of training is extended once more, or we seek alternatives to improve educational efficiency. The use of technology can be a useful aid in improving our use of time. If implemented correctly, it may redress the balance between time available, and the need for clinical excellence. It may however, require a new way of thinking about medical education.
(1) Winrow AP. The problem is greater than PICU training [electronic response to Stewart D, Medical training in the UK] archdischild.com 2003 http://adc.bmjjournals.com/cgi/eletters/archdischild;88/8/655#522
Re Childhood SARS in Singapore
Van Bever et al. have described their experience with Paediatric SARS in Singapore. We are concerned that some facts were not highlighted.
Their institution, the National University Hospital (NUH) was not designated to be a centre for the care of SARS in Singapore, it was therefore not surprising that they did not encounter any cases. They failed to mention in their detailed summary of the protective measures employed by their hospital, the key measure employed by the Singapore government to prevent the spread of SARS. In an effort to contain and curb the spread of this highly contagious coronavirus all cases of suspected SARS, based on travel to afflicted countries and/or positive contact history with the appropriate symptomatology, clinical and radiological findings, were re-directed to Tan Tock Seng Hospital (TTSH), the only SARS designated hospital in Singapore. Physicians were required to refer any suspected SARS patients there for care and isolation. Although TTSH does not have a paediatric unit, a team from KK Children’s Hospital, the largest paediatric centre in Singapore, were based there to care for all paediatric cases. There were over 70 paediatric patients seen and investigated for the possibility of SARS. The findings are reported elsewhere (Paediatric SARS in Singapore, J Puthucheary et al, manuscript submitted for publication), and describe several cases of adult-to-child transmission within family clusters, with no child-to-child or child-to-adult transmission.
Their statement that SARS is mainly a disease of adults and adolescents is not incorrect, but the same may be said for any number of infectious agents; nevertheless it has enough significance within children to be a concern to paediatricians. The initial suggestion that the measures put in place may have been an over-reaction does not fit with the data compiled in TTSH and available through the Singapore Ministry of Health, demonstrating a significant reduction in transmission associated with the adoption of the described measures.
The Archivist draws our attention to the widespread application of peanut containing oils in UK infant care practices and recent research linking this to the current levels of peanut allergy. Mustard oils are applied to infants in much of South Asia in the first months of life. In Nepal by my observation this practice is generally carried out daily in direct sunlight as an adjunct to massage. I am not aware of an equivalent phenomenon of mustard oil sensitisation. Does this support the hygiene hypothesis or is this accounted for by intrinsic differences between mustard oil and peanut oil?
The problem is greater than PICU training
Whilst I agree with much of what Stewart discusses, his leading article is at danger of obscuring a wider malaise in training by its call for all trainees to experience and, by extension, staff regional PICUs. Potentially every specialty within Paediatrics could add its voice in this way resulting in the compartmentalisation of training.
Consultants working in district general hospitals recognise that many PICU patients originate in their hospitals and are then transferred to the PICUs. Paediatric trainees in the DGH therefore do have the chance to experience the recognition and supervised stabilisation of sick patients prior to retrieval to the PICU. In my experience most paediatric trainees have already undergone a plethora of certificated courses of the PALS, NALS and APLS variety and are therefore well versed in the mantra espoused on these courses. This is the "easy bit".
A more pressing problem in the debate surrounding education is how we can train future consultant colleagues during their Specialist Registrar years in the aspects of patient management that extend beyond the end of their shift. It is more than a loss of continuity of patient care. The chance to experience and understand the totality of patient care, whether in-patient or outpatient, has been lost. Trainees largely see cross-sectional fragments of care but rarely the longitudinal aspects. The damage inflicted by the New Deal has been a loss of cumulative experience. Experience is difficult to obtain from study days. No amount of clinical simulators will confer such everyday clinical experience and real life decision making. Current medical education fails the trainees by preventing the acquisition of experience derived from shouldering supervised clinical responsibility, which equips us for the "now what do I do" part of medicine.
(1) Stewart D. Medical training in the UK. Arch Dis Child 2003;88:655-658.
Meningitis without rash – a suitable group for Dexamethasone?
We read with interest the article by Bashir and colleagues  on the diagnosis and treatment of bacterial meningitis. Within this article they commented that they favour the empiric use of dexamethasone in developed countries for children with suspected meningitis.
The metanalysis by McIntyre et al  showed that the benefits for dexamethasone were greatest for H. influenzae meningitis, with a possible, though non-significant, benefit in pneumococcal meningitis. One practical solution to ensure that steroids are given to children with meningitis who may benefit from them, is to give dexamethasone to all children who present with meningitis without a petechial rash. Indeed, our local policy recommended dexamethasone to be given before antibiotics to children with meningitis and no rash, and we therefore audited its use.
We performed a retrospective review of all children with >10 white cells/mm3 in their cerebrospinal fluid (CSF), admitted to Birmingham Heartlands Hospital between Jan 1998 and Aug 2002. Children were excluded if they had a non-blanching rash on admission or if their discharge diagnosis was not meningitis. CSF was cultured using standard microbiological methods and examined for viruses by PCR.
In our study 108 children were identified; median age 7 yrs. Causes of meningitis were: Viral 41 (enterovirus 40), bacterial 22 (Meningococcus 13, Hib 1, Pneumococcus 4). Sixteen children received dexamethasone, but only two prior to the first dose of antibiotic. If, as McIntyre et al. suggest, only those with Haemophilus or pneumococcal meningitis may benefit from the use of dexamethasone, then this might have benefited only 5/108 (i.e. 1 in 22) children. None of those who may have benefited were given dexamethasone with or before the first dose of antibiotics. Local policy in our unit has now changed so that dexamethasone is only being administered if Haemophilus is seen on gram stain of the CSF. With the present controversy surrounding the use of dexamethasone it may be that routine use of steroids as an adjunctive treatment for children with meningitis without rash should be reconsidered or, at the least, individualised.
(1) H El Bashir, M Laundy, and R Booy. Diagnosis and treatment of bacterial meningitis. Arch Dis Child 2003;88:615-620.
(2) McIntyre P. Berkey C. King S. Schaad U. Kilpi T. Kanra G. Odio Perez C. Dexamethasone as adjunctive therapy in Bacterial Meningitis. A meta-analysis of randomised clinical trials since 1988. JAMA 1997;278(11):925–931.
(3) Makwana N, Riordan A. Retrospective study of Meningitis presenting without a rash over a four-year period to determine the most likely aetiology (Abstract). Current Paediatrics; in press.
Only wholeness leads to clarity
Authors Lee and Mann argue for law compelling use of cycle helmets by children to prevent road deaths and serious injuries. This observer is surprised that the peer reviewers allowed publication of material lacking evidence either that the actual risks faced by child cyclists justify compulsion, or that the real world results of helmet compulsion in other countries justify compulsion in this country. These shortcomings are typical of papers in the medical literature that attempt to address the issue of cyclist safety. I believe these chronic shortcomings are primarily the consequence of the failure of the peer review process.
In the first place, it is irrational that consideration of helmet laws for children is restricted only to cycling, or even begins with cycling. Although, tragically, around 30 child cyclists have been killed on public roads annually in recent years, typically 110 child pedestrians are killed annually. Estimates of death risk per KM travelled derived from standard data sources  do not suggest child cyclists face greater risks than child pedestrians in most age groups. It is any case evident that the average child is almost four times more likely to become a serious casualty whilst walking rather than cycling. The peer reviewers ought to have insisted on a more general discussion of the risks faced by children in transport. This would have placed the injuries to cyclists in context and enabled priority, surely the basis of any systematic approach to public health interventions.
In the second place the evidence for the effectiveness of cycle helmets is split by an interesting contradiction. The authors cite research based on case-control trials reporting that helmeted cyclists were much less prone to serious head injuries than the bareheaded, at least at the time and in the locality of the research work. However, there is also a substantial body of evidence based on population-level studies of head injuries with increasing helmet use. These studies consistently fail to show material benefit for cyclist populations that took up helmet wearing. This was even true in New Zealand, where cyclists responded willingly to helmet promotion, with voluntary use reaching 60% even before the well-obeyed law of Jan 1994 came into force. The famous helmet laws for the states of Australia brought into effect during 1990-94 drew a similar null result upon close analysis. In the United States, population-level data gathered by the Consumer Product Safety Commission (a US government organisation that strongly promotes helmet use) shows that the risk of head injury per US cyclist increased by 40% during the 1990s, while helmet use increased from under 20% to at least 50% of cyclists. The omission of such evidence places a serious question mark against the competence of the peer reviewers in this case.
The hiatus between clinical trials and population-level results is of scientific interest and draws the curiosity of inquiring minds. Ignoring the hiatus smothers the existence of a mystery. This is unscientific.
It must be added by-the-by that studies of reported casualties in Britain have revealed a disturbing tendency towards increasing severity of injury with increasing helmet use. This has been observed at the national level  and for London, where helmet use grew much earlier than the national average. Edinburgh has been identified as having the highest level of helmet use in the country. An ongoing analysis of reported casualties by the author has revealed increasingly severe injuries after 1995, especially for child cyclists. These increases cannot be accounted for by worsening road conditions, since this would have been revealed in pedestrian injury trends. It is not absolutely clear whether the effect is coincidence or consequence, but fair peer review ought to have insisted on some commentary on whether helmet use has influenced reported road casualties. The objective is, after all, to reduce deaths and serious injuries in road crashes.
That helmet use has failed to improve reported road casualties is not surprising. A cycle helmet is designed to meet the event of a simple fall at speeds below 12 mph. Such a mild crash is unlikely to incur serious injury when road riding. Safety campaigners are pressing helmets to an application for which they were not intended. The ethics of this are questionable, a point peer reviewers should have highlighted. The use of helmets is more relevant off-road or “at play”, stunt riding on BMX or MTB type machines. The use of helmets in such situations is perhaps to be encouraged, although parental supervision should come first. On the other hand, these comparatively high-risk activities are the consequence of children being denied the freedom to cycle for transport. Riding sensible road bikes on public streets either is, or ought to be, a safe mode of travel for children, not rationally to be distinguished from walking.
In summary, the peer review process has failed to stop incomplete evidence being presented as reliable knowledge. The readership may in consequence be led into two levels of misconception:
1. the factoid that child cyclists are more at risk from motor traffic than child pedestrians;
2. the factoid that cycle helmets can protect children in road traffic accidents. A famous line from Schiller comes to mind as apt to the occasion:
Nur die Fuelle fuehrt zur Klarheit.
[Only wholeness leads to clarity]
Let us hope, for the sake of the public understanding of cycling, that in future peer reviewers apply this wisdom. There will be resurgence of children walking and cycling only when the perceived danger from motor traffic in urban areas is addressed. Proposing compulsory use of inappropriate safety equipment evades this simple truth. Public health interventions must focus upon the source of the perceived danger, not burden the innocent with the consequences of adult licentiousness.
(1) Lee AJ, Mann NP. Cycle helmets. Arch Dis Child 2003;88:465-466.
(2) The Department for Transport. Road Accidents in Great Britain; the Casualty Report. The Stationery Office, London, various years.
(3) The Office of National Statistics. The National Travel Survey. The Stationery Office, London, various years.
(4) Scuffham P, Alsop J, Cryer C, Langley J. Head injuries to bicyclists and the New Zealand helmet laws. Accident Analysis and Prevention 2000;32:565-73.
(5) Robinson D. Head injuries and bicycle helmet laws. Accident Analysis and Prevention 1996;28:463-75.
(6) Barnes J. A Bicycling Mystery; Head Injuries Piling Up. New York Times, July 29th 2001.
(7) Wardlaw M. Three lessons for a better cycling future. BMJ 2000;321:1581-5.
(8) Pedal cyclist casualties in Greater London. London Research Centre Factsheet 76. London, Aug 1997.
Meningococcal Sepsis: an alternative hypothesis
In their article on the pathophysiology of meningococcal sepsis Pathan et al. highlight their view that thrombosis is the principal etiology of the purpuric rash that is so characteristic of meningococcal sepsis. As the explanation for this they cite the well-described procoagulant state found in the severe form of the disease and the impairment in the thrombolytic pathway.
Evans  who studied five patients with severe meningococcal sepsis originally suggested the association between the rash and procoagulant state. He described disseminated intravascular coagulation with a histological picture of acute vasculitis, intracapillary thrombus and fibrin deposition. Thus the procoagulant state was associated with the rash of severe meningococcal sepsis. However in a recent consensus statement, in which one of the present authors was on the panel, it was not only noted that it was surprising that so little thrombosis was seen histologically but also that histologists had difficulty showing clot occlusion. Later in the same statement they argue that this lack of thrombus is misleading, suggesting that the thrombus may have been lysed and thus not seen at the time of autopsy. Yet in this present review article they comment that thrombolysis is impaired. It was this impairment in thrombolysis, which led to the use (albeit unsuccessfully) of tissue plasminogen activator in severe meningococcal disease.
In a recent article Kaptchuk discusses interpretative bias on research evidence, in particular plausibility and mechanism bias. The assumption that the procoagulant state and purpura, in occurring together in meningococcal disease, are thus linked by thrombosis could be an example of mechanism bias, particularly as this is not confirmed histologically. There is also a danger in that all other data is interpreted assuming that thrombosis is the mechanism resulting in purpura. It is important to step back occasionally and examine the original hypothesis and reassess whether it is sound. We have previously argued for an alternative mechanism to thrombosis as a cause of the necrotic skin lesions. This hypothesis has the advantage in providing an explanation for the rapid onset of shock, the rash and hypocalcaemia found in meningococcal septicaemia.[5,6] The loss of calcium into the subcutaneous tissue (acute calcifylaxis or acute tissue necrosis) is classically associated with the same histological picture as seen in meningococcal disease. The intracapillary thrombosis as first described by Evans is more compatible with that seen in calcifylaxis and is unlikely to be severe enough to result in severe necrotic lesions. We have suggested that those children with severe meningococcal sepsis and rash have an excess of protease activity, which overwhelms the antiprotease response resulting in albumin cleavage and calcium release into the tissues.
It is difficult to question long held ideas and what we have published is only a hypothesis and may be incorrect. However we feel that it does warrant examination and may advance understanding of the disease if shown to have some validity.
(1) Pathan N Faust SN Levin. Pathophysiology of meningococcal meningitis and septicaemia. Arch Dis Child 2003;88:601-607
(2) Bernard G Artigas A Dellinger P et al. Clinical expert round table discussion (session 3) at the Margaux Conference on critical illness: The role of activated protein C in severe sepsis. Critical Care Medicine 2001 ;29:S75-S77.
(3) Evans RW Glick B Kimball F et al. Fatal intravascular consumption coagulopathy in meningococcal sepsis. Am J Med 1969;46:910-918
(4) Kaptchuk TJEffect of interpretive bias on research evidence. BMJ 2003;326:1453-1455.
(5) Holland PC, Thompson D, Hancock SW, Evans SW, Hodge D, Shires S. Degradation of albumin in meningococcal sepsis. Lancet 2001;357:2102-2104.
(6) Holland PC, Thompson D, Hancock SW, Hodge D. Calciphylaxis, proteases and purpura-an alternative hypothesis for the severe shock, rash and hypocalcaemia associated with meningococcal sepsis. Critical Care Med 2002;30(12):2757-2761.
Therapeutic implications of sex differences in asthma and atopy.
With great interest I read the review by M Osman  on the sex- related differences of prevalence and severity of asthma and atopy before and after puberty.
Dr Osman postulates that testosterone and female sex steroids directly affect the immunological respons to e.g. allergens. If these hormones do play a role at physiological levels in vivo there is, indeed, most certainly a reason to consider what the therapeutical implications are. However, there is at least one other good physiological explanation for the changes in the reported prevalence and severity of asthma during childhood and adolescence. There is convincing evidence that airway patency in neonates and infants is reduced in males compared to females, and that this lasts till puberty. Because of the small size of the bronchial tree, infants are especially vulnarable to any increase in airways resistance. As symptoms may be considered the top of the iceberg, the higher reported morbidity of respiratory disease in male infants may simply mean that they develop symptoms earlier in the disease process than females do. During puberty, airway growth and function in males exhibits a growth spurt that surpasses that of females, and men have larger airways than females in early adulthood.[2-6] These biological phenomena help to explain not only why male infants and children demonstrate more morbidity from bronchiolitis, Cystic Fibrosis, asthma and infectious disease in general, but also why this reverses after puberty.[7,8] In addition, factors such as gender-related differences in exposure to outdoor and indoor allergens and air pollution may play an additional role. I think these aspects should have been addressed in this review article as well.
(1) Osman, M. Therapeutic implications of sex differences in asthma and atopy. Arch Dis Child 2003;88:587-90.
(2) Merkus, PJ, GJ Borsboom, W Van Pelt, PC Schrader, HC Van Houwelingen, KF Kerrebijn, PH Quanjer. Growth of airways and air spaces in teenagers is related to sex but not to symptoms. J Appl Physiol 1993;75:2045-53.
(3) Martin, TR, RG Castile, JJ Fredberg, ME Wohl, and J Mead. Airway size is related to sex but not lung size in normal adults. J Appl Physiol 1987;63:2042-7.
(4) Gibellino F, DP Osmanliev, A Watson, NB Pride. Increase in tracheal size with age. Implications for maximal expiratory flow. Am Rev Respir Dis 1985;132:784-7.
(5) Merkus, PJ, AA ten Have-Opbroek, PH Quanjer. Human lung growth: a review. Pediatr Pulmonol 1996;21:383-97.
(6) Becklake, M. Gender differences in airway behaviour (physiology) over the human lifespan. Eur Respir Mon 2003;25:8-25.
(7) Postma, D. Gender differences in the natural history of pulmonary disease. Eur Respir Mon 2003;25:74-81.
(8) Hibbert M, Lannigan A, Raven J, Landau L, Phelan P. Gender differences in lung growth. Pediatr Pulmonol 1995 ;19:129-34.
Pathological demand avoidance syndrome or psychiatric disorder?
In the recent issue of the Archives, Newson et al. make the case for a distinctive "pathological demand avoidance syndrome". This arose out of the work by the authors in a clinic for children with problems in communication.
These children are described as having a tendency to avoid or resist ordinary demands, to have surface sociability but a lack of sense of identity, pride and shame, labile mood, impulsivity led by need to control, language delay, obsessional behaviour and some sort of - usually "soft" - neurological involvement. The syndrome is not a recognised psychiatric disorder in either ICD-10 or DSM-IV classification systems.
How well do the authors make the case for this new syndrome? Some of the features outlined (for example sense of identity, price and shame) would be specially difficult to identify reliably. Others are suggestible of a number of different child and adolescent psychiatric disorders as described in ICD-10 and DSM-IV (WHO, 1991; APA, 1994).[2,3] From the authors' descriptions, the impression is that these children are likely to have had co-morbid developmental and psychiatric problems, varyingly including oppositional defiant and/or hyperkinetic disorder or social anxiety disorder of childhood. In some cases the features described may have been precursors of a schizotypal disorder. The paper does not however make a case for the validity or specificity of the syndrome in relation to these disorders.
The paper helpfully draws attention to the clinical variability amongst children with communication disorders. However, it would seem regrettable if new syndromes were to be used in clinical practice without consideration of whether an established psychiatric diagnosis would have been appropriate, as this will create confusion for parents and others involved. Better integration of paediatric and child psychiatric services working with children with developmental communication disorders should help reduce the likelihood of this happening.
(1) Newson E, Le Marechal K, David C. Pathological demand avoidance syndrome: a necessary distinction within the pervasive developmental disorders. Arch Dis Child 2003; 88:595-600.
(2) APA. Diagnostic and statistical manual of mental disorders, 4th Edition. DSM-IV. Washington: APA, 1994.
(3) WHO. ICD-10 classification of mental and behavioural disorders. London: Churchill Livingstone, 1991.
(4) Roberts S, Garralda E, Renfrew D. Schizotypal disorder among child and adolescent mental health users. Journal of the American Academy of Child and Adolescent Psychiatry 2001;40:1366.
Height screening at school
We applaud the honesty of Banerjee et al. in reporting on their review of community height screening. They found that the quality of measurement was poor but perhaps this is not surprising, since there seems to have been little investment in training or quality monitoring. We wish to make two points in reply to the commentary by Betts.
Firstly, we emphasise that the reason we have questioned the value of whole-population growth monitoring  is not that measuring is often badly done. Technique could undoubtedly be improved. It is rather that when analysed as a screening process, the maximum potential yield, sensitivity and specificity of growth monitoring are disappointing, even when carried out to a high standard.
Second, we have looked in detail at the question of obtaining mid- parental height to improve the performance of growth screening in the community. We concluded that the judgements that have to be made require a degree of sophistication that belongs, for the present, in a specialist clinic, not in whole population screening programmes. Indeed, the value of target height in detecting 'hidden' pathology was recently examined in a cohort of short children and its usefulness called into question.
The essential ingredients for early recognition of abnormal growth are a knowledge of how to assess growth as part of routine paediatric consultation in primary care, a readiness to listen to parental worries and quick, easy referral to specialist services when in doubt. Current evidence suggests that the additional yield of a whole-population growth screening programme would be modest and that a high price would be paid in false positives.
Consultant in Community Child Health, Islington PCT and Great Ormond Street Hospital
Professor of community paediatrics, Sheffield
Linda D Voss PhD
Peninsula Medical School, Plymouth Campus
(1) Hall DMB and Elliman D (Eds) Health For All Children. 4th edition. Oxford: OUP; 2003.
(2) Mulligan J and Voss LD, Non-familial short stature. Arch Dis Child 2000;83:369
Weaning of infants; timing should be individualized
I read with interest the review by Foote and Marriott about weaning practices. I agree with some of the general sentiments and do suggest that more research is needed to fully understand the reasons for advocating a stance.
Weaning as a process, enables the nutritional needs of a rapidly growing child to be met. The growth in infants double by 5 months and expected on average to treble by 1 year. Adequate dietary provision to meet this demand is therefore essential. There should be a balance between energy, protein and vitamin provisions. The process of weaning, enables solids to be gradually introduced and the dependence on milk decreased as the main source of nutrition.
The process of weaning is applied in various ways by different cultures and this area would need to be understood and researched if we are to be consistent with the advise we give. Should the weaning practise be same for all cultures? Do we have enough information to give an affirmative answer? The WHO, has recommended that babies should be exclusively breast fed for 4-6 months. While this may be ideal in the developing world, difficulty implementing this in the industrial world may make this impractical.
The practice of weaning is not in doubt but the timing needs individualizing as a concept for it to work. The first COMA report recommends that weaning should start from 4–6 months and the 2nd and 3rd reports on present day practice, acknowledge the wide range of growth rates after birth and suggests that weaning may start from as early as 3 months. This is a view I share. Infants utilize breast milk efficiently and by age of 6 months this will be inadequate. There are suggestions that the poor development of head control at 3 months may have a bearing on the lack of adequate suck and swallow at his age but by 4 months the improved neck control enables feeding in an upright position in a chair. By 5 months pureed foods can be taken and these babies can form a bolus before swallowing. I believe that early initiation of solids may facilitate acquisition of these skills. Another reason for discouraging early weaning, is the belief that renal and gut immaturity may not be efficient at handling the materials in weaning diets. The evidence for this assertion is weak. A review of the age at which 1st solids were introduced in the UK  showed that 19% were offered by 8weeks, 68% by 3 months, and 94% at 4 months. Solids may be offered earlier than parents acknowledge, since they are aware that it is contrary to professional advise. This diversity should encourage professionals to recognise the need to build on this practise in order to improve it. There are issues of antigenic load on the gut, but the science and understanding of food allergies still needs further studies. Weaning should be an enjoyable and supportive process for child and parents and the specific needs of the infant, parent and culture must be considered at all times. Weaning as a process should be individualized and supported with good evidence to facilitate successful outcome. The place for research into cultural weaning practices, the components of weaning feeds, and effect of early ‘antigen attack’ are essential. Weaning should be considered from the ages of 4–6 months and this may be offered early if the infant’s need cannot be met wholly by milk. If an infant at 6 months is not weaned, the nutritional intake is likely to be inadequate.
(1) Foote KD, Marriott ID. Weaning of Infants. Arch Dis Child 2003;88;488-92.
(2) Department of health & social security Present day practice in Infant feeding; 3rd Report. London: HMSO, 1988.
(3) White A, Freath S, O’Brien M. Infant feedingLondon: HMSO, 1992.
(4) Sullivan SA , Birch LL. Infant dietary experience and acceptance of solid foods. Pediatr 1994;93: 271-7.
Re: Response to Jan et al
We would like to take this opportunity to thank Jan and colleagues for responding to our article. It is acknowledged that the team at the Melatonin Research Group has the longest experience worldwide in the use of melatonin in children with neurodevelopmental disability.
The paper they refer to  includes a randomised controlled trial (RCT) of fast-acting vs. controlled release melatonin. Only the first 16 patients took part in the RCT, "in the remainder of the patients CR was studied on a clinical basis". As our question addressed whether or not melatonin was effective, rather than comparing different formulations of melatonin, this article was excluded.
We would also take issue with Jan's comments regarding epilepsy. The Sheldon study  commenced as an open consecutive recruitment study but was abandoned due to concern about side effects. The study Jan refers to is a simple case series of six children with epilepsy, in whom seizures appeared to reduce in five. If both these reports are accurate, then melatonin has both pro- and anti-convulsive effects, and it is still important to be cautious with its use.
We are delighted to learn that the group is currently involved with an RCT of melatonin in children with neurodevelopmental disorders and chronic sleep disorders, and wholeheartedly agree that more clinical research is needed. We will be very happy to review and update our Archimedes report when this trial is complete.
(1) Jan JE, Hamilton D, Seward N, et al. Clinical trials of controlled release melatonin in children with sleep-wake cycle disorders. J Pineal Res 2000;29:34-39.
(2) Sheldon SH. Pro-convulsant effects of oral melatonin in neurologically disabled children. Lancet 1998;351:1254.
(3) Peled N, Shorer Z, Peled E, Pillar G. Melatonin effect on seizures in children with severe neurologic deficit disorders. Epilepsia 2001;42:1208-10.
Response to is melatonin likely to help children with neurodevelopmental
Last year, Archimedes, a new format, was launched by Archives of Disease in Childhood for offering "practical, best evidence based answers to practical, clinical questions". One of the first questions was : "Does melatonin help developmentally delayed children with sleep problems?". Since the conclusions of this brief article are now on the Internet and physicians have access to them, our Melatonin Research Group has felt obliged to make some comments.
There is indeed a paucity of prospective randomised controlled studies on melatonin treatment of chronic sleep disorders in children with neurodevelopmental disabilities. While we are presently involved in such a study, it needs to be pointed out that. in addition to a number of issues, it is extremely difficult, time-consuming and expensive to do this research because of the inherent difficulties with the multidisabled population.
The statement that melatonin is ineffective in sleep fragmentation and early morning wakening is no longer correct. Regular, exogenous melatonin has a half life of approximately 1 hour, therefore it is eliminated from the body within 3-5 hours. This is why it is most effective for sleep phase onset delay. With the recent marketing of controlled release melatonin formulations, it has become clear that they may be helpful in eliminating sleep fragmentation and early morning wakening. Wiley and Phillips have excluded from their survey the only clinical article dealing with this issue.
Based on a brief letter in the Lancet, caution was advised in the use of melatonin in epilepsy. Willey and Phillips accepted this statement despite the fact that this was an uncontrolled case report of only a few children. This finding has since been contradicted. Furthermore, melatonin is occasionally used to treat certain types of seizures because of its anticonvulsant properties.
The child in the Willey and Phillips letter was visually impaired. With increasing loss of vision, the prevalence of chronic sleep difficulties tends to increase because the retina has a direct input into the suprachiasmatic nucleus (sleep clock) which controls pineal melatonin secretion. In the sleep-wake cycle disorders of visually impaired individuals, melatonin treatment can be quite successful, in fact at times it is the only effective therapy. There was also a suggestion that melatonin is a sedative medication. It is a chronobiotic hormone, with minimal sedative properties, but it should not be used as a hypnotic drug. The authors should have pointed out that, since children with neurodevelopmental disabilities can have a wide range of sleep disorders, with different aetiologies, only a selected number of children should respond to this treatment.
There is extensive literature on the pharmacokinetics of melatonin as it relates to the sleep of individuals with or without disabilities and also under normal and abnormal circumstances. Without discussing the basic physiology, it is difficult to understand the reasons for the therapeutic applications of melatonin. There is a potential danger in the Archimedes format, which offers simple answers to complex questions. We need further research that would help us identify which children would and would not benefit from melatonin treatment.
(1) Willey C, Phillips B. Is melatonin likely to help children with neurodevelopmental disability and chronic severe sleep problems? Arch Dis Child 2002;87:260.
(2) Jan JE, Hamilton D, Seward N, et al. Clinical trials of controlled release melatonin in children with sleep-wake cycle disorders. J Pineal Res 2000;29:34-39.
(3) Sheldon SH. Pro-convulsant effects of oral melatonin in neurologically disabled children. Lancet 1998;351:1254.
(4) Peled N, Shorer Z, Peled E, Pillar G. Melatonin effect on seizures in children with severe neurologic deficit disorders. Epilepsia 2001;42:1208-10.
We congratulate Keith Ross and his colleagues who have achieved what many other districts have failed to. Their use of an asthma card as a prescription and health care plan is, we agree, an example of good practice that works well. However, their experience illustrates exactly the point we were trying to make. In order to circumvent the legal problems they have persuaded themselves and colleagues in Wolverhampton that their system complies with the current regulations. It is by no means clear that this is the case. Other districts that have introduced an emergency inhaler scheme have interpreted the law in different ways. The result is inconsistency with no possibility of any authoritative body being able to produce clear guidance. Our argument was that as emergency inhalers for school are a safe and effective preventive measure for a substantial public health problem, it ought to be straightforward to introduce them. This needs to be acknowledged by the Department of Health. We would draw comparison with the introduction of defibrillators in public places. All it took was their inclusion in the NHS plan and there they are, despite considerably less evidence of either their safety or effectiveness.
(1) Ross KR, Heap E, Kalra D, Moore A, Rayner R. Emergency asthma inhalers in schools [electronic response to Reading R et al. Emergency asthma inhalers in school] archdischild 2003 http://adc.bmjjournals.com/cgi/eletters/archdischild;88/5/384#502
Fosfomycin for osteomyelitis?
We were interested to read the recent article by Corti et al. examining the use of fosfomycin for infective osteomyelitis.
Whilst fosfomycin has good gram-positive including anti- staphylococcal and gram-negative coverage it is only available in the intravenous preparation. Concern regarding the emergence of resistance means that in our hospital it is reserved for resistant / relapsing infections and always given in combination.
British readers should realise that fosfomycin is not routinely available in the UK and has to be specially imported. It was originally marketed in the UK as a once a day therapy for urinary tract infections but proved too expensive.
We feel that the title of the article and the conclusion are misleading as they imply that fosfomycin should be used as an alternative first line therapy in osteomyelitis. This is in comparison to the last paragraph of the discussion where it is stated that following this study their hospital policy for osteomyelitis therapy is intravenous flucloxacillin followed by oral clindamycin. We agree that flucloxacillin is a good choice as initial intravenous therapy but feel that it is also a good option for when intravenous is changed to oral therapy.
Which antibiotics are chosen depends on susceptibility of organisms, antibiotic penetration and ease of administration. The causative organisms and their relative frequencies are similar in this study to those we found in Newcastle between 1991 and 1999; Pathogens were identified in 26/63 (41%) children with osteomyelitis; Staphylococcus aureus 85%, Streptococcus pneumoniae 7.5% and Salmonella sp. 7.5%. It is because of this and other similar data that we would add an intravenous beta-lactam antibiotic into the initial empiric regime e.g. amoxycillin or cefuroxime. The relatively long intravenous courses used in this study (2.5 weeks in fosfomycin group) are disparate to our experience and that of a number of European centres in that short intravenous followed by relatively long oral antibiotics courses has many advantages and do not result in increased relapse rates.[2,3]
The final point is that this study is significantly underpowered to detect any difference between fosfomycin and the others therapies (failure rate of 2/103 (2%)). Using the higher relapse rate from adult studies of approximately 15% [4,5] then to detect an arbitrary 10% improvement or worsening in outcomes / relapse rates with 80% certainty if two therapies are compared approximately 280 or 500 patients would need to be enrolled. In conclusion whilst fosfomycin has good anti-microbial coverage we feel that in the UK its limited supply and the unavailability of an oral preparation mean that conventional beta-lactam antibiotics should remain the main stay of osteomyelitis therapy. We acknowledge that comprehensive evidence based guidelines for acute osteomyelitis therapies are lacking. We are at present developing best evidence guidelines for the British Paediatric Allergy Infection and Immunology Group (BPAIIG).
(1) Corti N, Sennhauser FH, Stauffer UG, Nadal D. Fosfomycin for the initial treatment of acute haematogenous osteomyelitis. Arch Dis Child 2003;88(6):512-6.
(2) Peltola H, Unkila-Kallio L, Kallio MJ. Simplified treatment of acute staphylococcal osteomyelitis of childhood. The Finnish Study Group. Pediatrics 1997;99(6):846-50.
(3) Davies EG, Elliman DAC, Hart CA, Nicoll A, Rudd PT. The Child with Bone or Joint Infection. Manual of Childhood Infections, 2nd Edition. London: WB Saunders, 2001:69-71.
(4) Pechere JC, Delisle R. Open study of ceftazidime in serious infections due to multiply- resistant bacteria. J Antimicrob Chemother 1983;12 Suppl A:181-8.
(5) Weinberg WG. Safety and efficacy of teicoplanin for bone and joint infections: results of a community-based trial. South Med J 1993;86(8):891-7.
(6) Altman DG. Clinical trials; Sample size. Practical Statistics for Medical Research. Chapman & Hall, 1991: 455-460.
Sudhir Kumar writes an excellent review of the likely pathology of cerebral malaria. They state that Mannitol should not be used routinely, an opinion with which I agree. They say however, it should be used judiciously, but on what evidence do they make this summation, and on what clinical indication? I assume this opinion is based on clinical experience. It was anecdotal evidence that led me to search the literature and submit the published article. The evidence for if, and when, to use Mannitol is lacking, so in the meantime it cannot be recommended, judiciously or otherwise.
(1) Kumar S. Intravenous mannitol should not be routinely recommended for cerebral malaria [electronic response to Tomlinson RJ and Morrice J, Does intravenous mannitol improve outcome in cerebral malaria?] archdischild.com 2003 http://adc.bmjjournals.com/cgi/eletters/archdischild;88/7/640#496
Risk assessment from single procedures
I read with interest the article by the team from Southampton. They described an elegant strategy for the retrieval of impacted central venous lines. However they describe the technique as safe based on a single reported procedure. As a rough guide in order to achieve a 10% level of risk of an adverse event with 95% confidence then around 28 uncomplicated procedures are required. How would one quote the risk based on a single procedure to parents giving consent?
Broadly speaking adverse events can be divided into two groups; predictable and unforeseen. Though we may try and minimise predictable events the unforeseen, by definition, require a certain degree of experience (i.e. trial and error)to identify. As a profession we must learn by the lessons of the past and realise that what may appear to be an excellent idea may have hidden pitfalls not easily appreciated. It really is meaningless to describe small numbers of procedures as "safe" particularly in this case since the technique involved forming an externalised loop with fine wire through the great vessels.
Re: This palm tree does not usually cause thorn injury
I thank Dr D'Souza for his comment.
The date palm may, indeed, look like the coconut palm in it's form. But the shape of the date palm thorns are different, as can be seen in figure 3. Those thorns are vicious and can cause severe penetrating injuries (As worse as getting hit by a falling dried coconut...).
(1) D'Souza NA. This palm tree does not usually cause thorn injury [electronic response to A Kratz et al. Pantoea agglomerans as a cause of septic arthritis after palm tree thorn injury; case report and literature review] archdischild.com 2003 http://adc.bmjjournals.com/cgi/eletters/archdischild;88/6/542#493
Emergency asthma inhalers in schools
We were interested in the review by Reading et al. In Wolverhampton we are fortunate in having had a schools asthma policy in place since 1994 which includes supplying emergency inhalers to schools for use when the pupil’s own inhaler is not available.
The policy was initiated by two hospital paediatricians with an interest in asthma and was quickly incorporated into the local Respiratory Care Group. The involvement of enthusiastic school nurses with a special interest and training in asthma and the support of the community paediatricians have been invaluable.
Initially, an approach was made to the Director of Education who was of the view that giving inhaled treatment to known asthmatics could be considered to fall within the school staff acting in loco parentis. Every state school in the borough was offered a visit from a hospital paediatrician and a children’s asthma nurse to present the theory and practise of using emergency asthma inhalers. Every school was supplied with a short acting beta-agonist (pMDI plus spacer), a protocol including dosage, and authorisation signed by a hospital paediatrician, community paediatrician and the lead school nurse for asthma. An annual update is given to the school nurses and they (or the lead school nurse) in turn annually train or retrain the school staff as required.
Pupils with asthma are identified by the school nurse and each child given an individual asthma card with their emergency treatment detailed. Written consent for a named pupil to be given the emergency inhaler is obtained from the parent and authorised by a paediatrician. This is in effect the prescription. These individual, but standard, health care plans for children with asthma are not “a logistic nightmare” but straightforward to administer and conform to the joint Health and Education guidelines for supporting pupils with medical needs in school.
A school nurse led audit in 2003 confirmed that all schools held a register of use, with a named person from the school staff being designated by the head teacher.
Although our policy may not comply strictly with the letter of the law, there is clear clinical responsibility and we ensure that all children with asthma have ready access to emergency treatment in school.
Senior School Nurse (Wolverhampton City PCT)
New Cross Hospital, Wolverhampton, WV10 0QP
New Cross Hospital, Wolverhampton, WV10 0QP
Consultant Community Paediatrician (Wolverhampton City PCT)
New Cross Hospital, Wolverhampton, WV10 0QP
New Cross Hospital, Wolverhampton, WV10 0QP
Keith R Ross
New Cross Hospital, Wolverhampton, WV10 0QP
(1) Reading R, Jones T, Upton C. Emergency asthma inhalers in schools. Arch Dis Child 2003;88:384-386.
(2) Department of Health and DfEE. Supporting Pupils with medical needs a good practice guide. Department for Education and Employment 1996.
High dose fluticasone and adrenal suppression
Following the editorial by Russell  recommending a short synacthen test for asthmatics receiving fluticasone in a daily dose of 1000 mcg or above, we undertook a computer search of our records of asthmatic patients.
Asthmatics have approximately 4000 consultations per year with our team. We identified 190 children taking inhaled fluticasone either alone or in combination with salmeterol. Of these 21 were on daily doses of 1000 mcg or over and one was on a dose of 500 mcg daily having previously been on 1000 mcg for 8 months. Two had taken oral prednisolone within the last month and were not investigated because of possible adrenal suppression due to the oral steroid. Of the remainder, 13 were female and 6 were male. Their ages ranged from 7.79 years to 18.54 years (mean 13.0 years). Only one patient was on concomitant intranasal fluticasone. Twelve were using Diskus dry powder inhalers, five a metered dose inhaler with a spacer (volumatic) and one a metered dose inhaler alone. A short synacthen test was performed on all 19 patients and was normal in all as judged by a rise of 200 nmol or a peak of 500 nmol.
One of the authors has cared for asthmatic patients since the introduction of inhaled steroids in the early 1970s and has seen only one asthmatic patient suffer an Addisonian crisis. The crisis followed acute cessation of long continued oral prednisolone. While the recent reports of adrenal suppression in asthmatics on high dose inhaled corticosteroids indicate that this serious side effect must be kept in mind when caring for such patients, our experience is that it is not a common occurrence. Further information regarding the prevalence and risk factors for this complication would be of benefit to clinicians and might rapidly be obtained by using the British Paediatric Surveillance Unit's ‘Orange Card’ reporting system.
(1) Russell G. Inhaled corticosteroids and adrenal insufficiency. Arch Dis Child 2002;87:455-6.
(2) Todd GRG Acerini CL Ross-Russell R, et al. Survey of adrenal crisis associated with inhaled corticosteroids in the United Kingdom. Arch Dis Child 2002;87:457-61.
We were interested to read the letter from Playfor in which he detailed the fatal consequences of iatrogenic hyponatraemia following administration of intravenous 4% dextrose/0.18% saline to a young child with moderate dehydration.
We were reminded of a similar though less severe case which led us to change our unit policy in a manner exceeding that recommended by Playfor.
A 3 year old child was admitted with viral gastroenteritis and moderate dehydration. An attempt at oral rehydration was unsuccessful due to persistent vomiting, and intravenous fluids were commenced. Her initial biochemistry showed sodium 136, potassium 4.0, urea 10.1, creatinine 67. The fluids were prescribed by a trainee doctor, who prescibed 4% dextrose/0.18% saline at a maintenance rate. This was continued overnight until reviewed on the consultant ward round the following morning when the fluid prescription was changed to 2.5% dextrose/0.45% saline. Repeat biochemistry showed the sodium was 127. The child made an uneventful recovery with gradual normalisation of the sodium concentration.
Review of this potential “near-miss” critical incident led us to conclude that there is no necessity for 4% dextrose/0.18% saline to be stocked on the general paediatric unit. 2.5% dextrose/0.45% saline can be used safely as standard rehydration or maintenance fluids in the vast majority of children. We removed 4% dextrose/0.18% saline from the ward stocks and have not used it since. We felt that this would avoid the possibility of individual prescribing error causing an event such as that described by Playfor. In the busy general paediatric unit where this incident occurred we have had no further instances of iatrogenic hyponatraemia in the 3 years since we took this decision.
(1) Playfor S. Fatal iatrogenic hyponatraemia. Arch Dis Child 2003;88:646-7.
Re: Tell me a story
I applaud Rudolf and Storr for writing their paper and the Archives for having the courage to publish it. The Medical literature after all represents only a fraction of literature as a whole.
After a busy day trawling through evidence based websites it would be wonderful to have access to a different source of intellectual refreshment. May I suggest that the RCPCH website develops a “reading room,” an archive of children’s books, adding them as they come out of copyright or if that is not possible imbeds links to where these can be found. Literature is one of the best that things life can offer us. It enriches us in many different ways alluded to in Rudolf and Storr’s paper.
In many ways non medical literature is just as important for our professional development as being up to date with the current medical literature and indeed they compliment each other. By giving us insight, the benefit of others’ experience and wisdom, both enable us hopefully to be better informed in our decisions and actions and consequently be better doctors.
(1) MCJ Rudolf, E Storr. Tell me a story ... What can paediatricians gain from reading stories? Arch Dis Child 2003;88:635-637.
Intravenous mannitol should not be routinely recommended for cerebral malaria
I read with great interest the recent article by Tomlinson et al. Authors feel that intravenous mannitol may improve the outcome in patients with cerebral malaria, though there are no randomized controlled trials on the subject. However, I would like to make certain observations.
Cerebral oedema in cases of cerebral malaria is often multifactorial. Main pathogenic mechanisms include cytoadherence of parasitized erythrocytes to the endothelium (mechanical hypothesis), and neuronal injury by malarial toxin and excessive cytokine (tissue necrosis factor- alpha) production (cytotoxic hypothesis). The cytotoxic hypothesis seems to be the most important factor, which in turn may get triggered by the sequestration of parasites. Several associated systemic complications such as hypoglycemia, hypovolemia, hyperpyrexia, renal failure, and lactic acidosis may contribute to the pathogenesis of cerebral oedema. Recurrent seizures that occur commonly in cerebral malaria could also cause a worsening of cerebral oedema.
Brain imaging studies in cerebral malaria have demonstrated an increased brain volume, which has been thought to be secondary to sequestration of parasitized erythrocytes and compensatory vasodilatation rather than from edema. Other imaging studies have demonstrated, in addition to brain swelling, widespread low-density areas suggestive of ischaemic damage. The patterns of damage were consistent with a critical reduction in cerebral perfusion pressure, hypoglycaemia, or status epilepticus.
Mannitol acts by causing a plasma expansion, thereby increasing the cerebral blood flow (CBF). In addition, mannitol may cause cerebral vasodilatation. Increased CBF and vasodilatation may worsen cerebral oedema as mentioned earlier. Furthermore, mannitol is contraindicated in hypovolemia, renal failure, and pulmonary edema; which are common complications seen in cerebral malaria.
In view of the above, mannitol should not be used routinely but may be used in emergency situations for rapid lowering of raised intracranial pressure (ICP). It is important not to discontinue mannitol abruptly as it may lead to a rebound intracranial hypertension. Another method that could be used to rapidly lower the ICP is mechanical ventilation (hyperventilation)-induced hypocapnia. Vasoconstriction caused by hypocapnia helps in reducing the ICP. This method is also avoided long- term as prolonged vasoconstriction may lead to reduced cerebral perfusion, thereby worsening the cerebral ischaemia, as noted earlier.
Additionally, other factors, which may contribute to cerebral oedema such as hyperpyrexia, hypovolemia, seizures, hypoglycaemia, renal failure and lactic acidosis, should be identified and promptly treated.
In conclusion, mannitol cannot be routinely recommended for lowering ICP in cases of cerebral malaria. Adequate treatment for lowering ICP in cerebral malaria would include mechanical-ventilation-induced hypocapnia, judicious use of mannitol and treatment of precipitating factors.
(1) Tomlinson RJ, Morrice J. Does intravenous mannitol improve outcome in cerebral malaria? Arch Dis Child 2003; 88: 640-641.
(2) Garg RK. Cerebral malaria. J Assoc Physicians India 2000; 48:1004-13.
(3) Gachot B, Vachon F. Physiopathology of cerebral malaria. Presse Med 1995; 24:642-6.
(4) Looareesuwan S, Wilairatana P, Krishna S, et al. Magnetic resonance imaging of the brain in patients with cerebral malaria. Clin Infect Dis 1995;21:300-9.
(5) Newton CR, Peshu N, Kendall B, et al. Brain swelling and ischaemia in Kenyans with cerebral malaria. Arch Dis Child 1994; 70: 281-7.
Antibiotic resistance in urinary tract isolates and risk of renal scarring.
Lakhani and Gransden  stated in their article that in urinary tract infection the initial use of an antibiotic the urinary tract isolate is resistant to will through a delay in effective treatment lead to an increased risk of renal scarring. The authors concluded that nitrofurantoin should replace trimethoprim as the first line antibiotic for treatment of urinary tract infection (UTI) in childhood because of the high rate of trimethoprim resistance. We recently presented  data from a case control study investigating the influence of delay of treatment associated with trimethoprim resistant UTI on renal scarring. We compared 23 children with and 101 children without renal scarring after their first UTI. The prevalence of renal scarring in patients with trimethoprim resistant organism initially treated with trimethoprim was 3/18 (17%) and 20/106 (19%) in patients, treated with the appropriate antibiotic (p=1.0). In patients with trimethoprim resistant organism treated with trimethoprim as antibiotic of first choice the delay in effective treatment ( median and range) in patients with renal scarring was 4 days (1-5) and in patients without renal scarring 2 days (0-8) (p=0.46). Our conclusion is, that having a prompt response to microbiological sensitivity testing did not delay the effective treatment of a UTI significantly and did not increase the risk of renal scarring. This was supported by a recent review, which concluded that in studies, in which therapy was not more delayed than a week, there was no effect of treatment delay on the risk of renal scarring. We therefore have not changed our policy using oral trimethoprim as antibiotic of first choice in treating UTI in patients beyond infancy, tolerating oral antibiotics and not affected by septicemia.
(1) Ladhani S, Gransden W. Increasing antibiotic resistance among urinary tract isolates. Arch Dis Child 2003;88:444-5.
(2) Eisenhut M, El Masri F, Murphy P, Jones CA. Risk factors for renal scarring in children with urinary tract infection-a retrospective case control study. Arch Dis Child 2003; 88 (Suppl I): A72.
(3) Jakobsson B, Jacobson SH, Hjaelmas K. Vesico-ureteric reflux and other risk factors for renal damage: identification of high-and low-risk children. Acta Paediatr Suppl 1999;431:31-9.
Why starve? Give what the child needs!
Acute gastroenteritis being an inflammatory process, many physicians advice a rest to bowel during the phase and in the convalescence.
Outcome of it will be definitely affected by diet as diet was the sole factor causing the gastroenteritis. SO diet cant be stopped. Gradual introduction of food is a vague term as the question of 'how gradual introduction?' makes it irrelevant.
Its agreeable by all that we require more liquids to counter the ongoing losses and the dehydration; eventually landing up in semisolid or liquid diet in early management of gastroenteritis at least till dehydration ceases to exist. Normal diet can be started provided the gastroenteritis is not a sequale of a chronic disease like malabsorption syndrome.
Feeding doesnot stop or slow down the gastroenteritis but it just helps in tackling dehydration. Gastroenteritis, either viral or bacterial has its own course and may require specific medicines which definitely help in reducing the duration and frequency of motions in gastroenteritis.
Whatever diet is given (slow or gradual) should satisfy the necessary caloric requirement and the fluid requirement of dehydration.
This palm tree does not usually cause thorn injury
The article by Kratz et al. highlights an important and frequently missed cause of arthritis secondary to thorn injury in children.
The picture on the cover of this particular issue of the ADC drew my attention to your article. After reading it however, I would like to point out to the readers that the palm tree in the photograph on the front cover resembles the coconut palm which in my experience does not cause such an injury. I have spent my entire childhood in a coconut growing area of the world and went on to specialise in Paediatrics after my basic medical training. I did not come across such a cause of septic arthritis in children until I moved to a date palm growing country. In this region thorn injury from the date palm was a well known cause of chronic septic arthritis in children.
I would like to ask if other readers have any experience with this form of injury from the coconut palm. The reason I am seeking this clarification is that coconut palm trees are a common feature of many tourist resorts in the Far East. My impression is that these are very benign trees with little risk of such an injury. One may of course be unfortunate enough to be hit by a falling dried coconut which is a different issue!
(1) A Kratz, D Greenberg, Y Barki, E Cohen, and M Lifshitz. Pantoea agglomerans as a cause of septic arthritis after palm tree thorn injury; case report and literature review. Arch Dis Child 2003;88:542-544 .
Adequate treatment of neurocysticercosis
We read with interest the recent article by Rao and Lessing. They have presented two cases of symptomatic seizures secondary to solitary cerebral cysticercus granuloma.
We would like to make certain observations. First, the authors state that they made a diagnosis based on radiological findings and positive serological tests in the first patient. They are absolutely right in their approach, however it may give an erroneous impression that serological tests are required for the diagnosis. Serological tests for neurocysticercosis are of limited value as they often lack sensitivity and specificity. Diagnostic criteria based on brain imaging have been described  and later validated. According to these criteria, solitary cysticercus granulomas measure less than 20 mm in diameter, may be associated with edema but not severe enough to displace the midline, and they occur in patients with seizures who have a normal neurological examination, and no evidence of an active systemic disease. When those lesions resolve spontaneously, either disappearing or transforming into a calcified nodule, the diagnosis of neurocysticercosis is almost certain. The images provided by the authors fulfill most of these findings and a repeat imaging is advisable to look for resolution of the lesion.
Second, authors have managed these children without any treatment. Although the patients remained seizure-free, current guidelines  state that antiepileptic drugs are required for all these patients as they are prone to have a seizure recurrence. Prophylactic therapy with antiepileptic drugs however may be stopped after normalization of brain imaging in patients who have remained seizure-free. There is a general agreement that antiparasitic therapy with albendazole or praziquantel is not required for solitary enhancing cysticercus lesions. (5) Hence, we agree with the authors on not prescribing antiparasitic therapy in the cases presented.
(1) K R S Rao and D Lessing. Neurocysticercosis in West London. Arch Dis Child 2003;88:471.
(2) O. H. Del Brutto, V. Rajshekhar, A. C. White Jr et al. Proposed diagnostic criteria for neurocysticercosis. Neurology 2001;57:177-183
(3) Rajshekhar V, Haran RP, Prakash GS, Chandy MJ. Differentiating solitary small cysticercus granulomas and tuberculomas in patients with epilepsy. Clinical and computerized tomographic criteria. J Neurosurg 1993; 78:402-7.
(4) Rajshekhar V, Chandy MJ. Validation of diagnostic criteria for solitary cerebral cysticercus granuloma in patients presenting with seizures. Acta Neurol Scand 1997;96:76-81.
(5) Garcia HH, Evans CA, Nash TE et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev 2002;15: 747-56.
One child whitewash
The recent article "The One Child Policy" by W X Zhu  notes that: "a strict one child per family policy is imposed in the cities." However, the article downplays the severity of the abuse, and even falsely claiming that: "in 30 pilot counties the policy has been lifted."
In May, 2002, the US State Department looked at several of these United Nations Population Fund (UNFPA) so-called model counties, and found that they retained coercive elements in law and practice. The UNFPA seeks to help China to cover attrocities by claiming reform.
An independent investigation revealed destruction of homes as common practice in one of these pilot counties for women who decide for themselves when to give birth.
Coercive abortion is a crime against humanity. It was one of the crimes that Adolph Eichmann was sentenced to death for. China is not shifting away from coercion. Your journal should not support this cover-up.
A proposal for the pathophysiology of Bochdalek herniation
I read the article with interest, having managed a case in a seven month female in the last month.
This case presented with an acute onset of symptoms - three days of vomiting, the last bilious, and bloody diarrhea. Fluid resuscitation was required. There were no respiratory symptoms, the chest Xray was normal, the abdominal Xray revealing dilated bowel loops. An intussusception was suspected and she was transferred to a surgical centre, however abdominal ultrasound and GI contrast enemas were not diagnostic.
She underwent an exploratory laparotomy which revealed large colon and part of the spleen in the left hemithorax. The gut was viable and she made an uneventful recovery. Malrotation was present.
This case does not correspond to acute herniation prior to presentation, or acute incarceration of previously herniated bowel, (as described in the article), as the initial chest Xray on presentation was normal. The asociation of a diaphragmatic hernia with malrotaion is described in the literature, case series document varying frequencies ranging from 3- 50%.[1-3]
We propose that in this case malrotation predisposed to increased interabdominal pressure and eventual herniation through a congenital defect. It is not clear form the literature if this has been described elsewhere.
(1) Singh S et al. Delayed presentation of congenital diaphragmatic hernia. Pediatric Emergency Care 2001; 17(4):269-71.
(2) Newman BM et al. Presentationof congenital diaphragmatic hernis past the neonatal period. Archives of Surgery 1986;131 (7):813-6.
(3)Elhalaby EA et al. Delayed presentationof congenital diaphragmatic hernia. Pediatric Surgery International 2002; 18(5-6):480-5.
Re: Amitraz poisoning
First of all, I would like to thank Dr Bosnak for his contribution and comments that include very useful and important information. The clinical findings about amitraz poisoning occur depending on the dosage.[1,2]
However, the another study should be conducted to investigate whether the density of amitraz solution has any effect related to the clinical severity of amitraz poisoning cases. Actually, the real factor that affects the intensity of the clinical findings of the amitraz poisoning regardless of the density of the solution is the amount of amitraz ingested by the child per kg or per m2.
It will not be totally acceptable approach to state that dopamine contraindicates for amitraz poisoning cases. However, as advised previously it would be a more appropriate approach to give a 10 times reduced dopaminin dosage under careful supervision and monitoring of patients who use medicine inhibits MAO, since it allows a closer monitoring for the side effects. As a matter of fact, dopamin is rarely necessary for amitraz poisoning. The necessity of dopamine usage was mentioned in only 16 of the 154 cases (excluding the study by Bosnak et al) reported. (3/11 cases of the study by Yaramiþ et al, 10/24 cases of the study by Aydin et al, 1/2 cases of the study by Doðanay et al, 2/9 cases of the study by Yilmaz et al ).
The study that is mentioned by Bosnak in the last paragraph and that includes a case of 16 children with amitraz poisoning could not been founded since only the journals in Index Medicus, EMBASE and SCI-Expanded databases were searched. Therefore, number of amitraz poisoning cases in the literature has gone up to 170 from 154 by the addition of these 16 recently discovered cases. It is really worth paying attention that most of the cases reported are from Turkey. Moreover, on February of 2003 another amitraz poisoning case of 8 children was reported in Turkey.
(1) Ulukaya S, Demirag K, Moral AR. Acute amitraz intoxication in human. Intensive Care Med 2001;27:930–3.
(2) Yilmaz HL, Yildizdas DR. Amitraz poisoning, an emerging problem: epidemiology, clinical features, management, and preventive strategies Arch Dis Child 2003;88:130–4
(3) Gunes B (Ed). FarmaList Türkiye Týbbi Ýlac Rehberi. FarmaTip Yayincilik, 5th edition. Ankara, 2000.
(4) Yaramis A, Soker M, Bilici M. Amitraz poisoning in children. Hum Exp Toxicol 2000;19:431–2.
(5) Aydin K, Per H, Kurtoglu S, et al. Amitraz poisoning in children. Eur J Pediatr 2002;161:349–50.
(6) Doganay Z, Aygun D, Altintop L, et al. Basic toxicological approach has been effective in two poisoned patients with amitraz ingestion: case reports. Hum Exp Toxicol 2002;21:55–7.
(7) Bosnak M, Soker M, Dikici M et al. Amitraz Intoxication in Children. New J Med 1997;14:155-7.
(8) Caksen H, Odabasi D, Arslan S, et al. Report of eight children with amitraz intoxication. Hum Exp Toxicol 2003;22: 95-7.
Thyroid disease is part of the 22q11 deletion Syndrome
We read with interest Greeenhalgh's report  of recommended investigation and management of children with chromosome 22q11 microdeletion.
In this report no mention is made of thyroid disease. We would like to suggest that diseases of the thyroid can be a significant cause of morbidity in these children and that screening for thyroid disease should be considered part of their management. Scuccimarri and Rodd  have highlighted the importance of thyroid dysfunction associated with 22q11.2 deletion syndrome including congenital hypothyroidism, dysgenesis of the thyroid gland and childhood onset hypothyroidism. In 1997 Ryan et al  presented data on 558 patients from European centres with 22q11.2 deletion in which 4 patients were found to have hypothyroidism. Hyperthyroidism in the form of Grave's disease is being increasingly reported and in 2001 Kawame et al.  reported a series of such patients. We also reported a case of primary hypothyroidism presenting as hypothyroid myopathy in a 2 year 7 month old boy with 22q11 deletion. Most recently Weinzimer  reviewed hormonal disorders in patients with 22q11 deletion. He discussed reports with incidences of hypothyroidism of 0.7% to 7% occurring in patients with 22q11 deletion, mentions the well documented autopsy findings of congenital anomalies of the thyroid gland and the emerging reports of other autoimmune conditions associated with the 22q11deletion. As signs of thyroid disease may be difficult to interpret in children with the chromosome 22q11.2 deletion, thyroid function testing should be considered part of the medical management.
(1) K L Greenhalgh, I A Aligianis, G Bromilow, H Cox, C Hill, Y Stait, B J Leech, P W Lunt, and M Ellis. 22q11 deletion: a multisystem disorder requiring multidisciplinary input. Arch Dis Child 2003;88:523-524 .
(2) Scuccimarri R, Rodd C. Thyroid abnormalities as a feature of DiGeorge Syndrome: a patient report and review of the literature. J Pediatr Endocr Metab 1998;11:273-276.
(3) Ryan AK, Goodship JA, Wilson, DI, Philip N, Levy A, Scidel H et al. Spectrum of clinical features associated with interstitial chromosome 22q11 deletions: a European collaborative study. J Med Genet 1997;34(10):798-804.
(4) Kawame H, Adachi M, Tachibana K, Kurosawa K, Ito F, Gleason M. Graves' Disease in patients with 22q11.2 deletion. J Pediatr 2001;139:892-5.
(5) Preece J, Smith R. Thyroid disease in children with 22q11.2 deletion syndrome. J Pediatr 2002;141(2):297.
(6) Weinzimer S. Endocrine aspects of the 22q11.2 deletion syndrome. Genet Med 2001;3(1):19-22.
On Gatrad's summary of New Testament teachings about circumcision
Unfortunately, Gatrad, Sheiky and Jacks did not get it right in their summary of New Testament teachings about circumcision.
While it is true that Jesus was circumcised, John's Gospel quotes him as making a very pointed dig at circumcisers. He mentioned how his critics circumcised on the sabbath day and retorted: 'Why are you angry with me for making a man whole and complete on a sabbath?' (John 7: 23, Jerusalem Bible0. The early church rejected any requirement for circumcision at the first Church council (Acts 15).
Therefore, the rejection of circumcision did not originate with St Paul. At first, Paul circumcised a man to make him more acceptable to the Jews (Acts 16: 1-3). However, in his letters, he turned against circumcisers with increasing anger, finally admonishing Christians to beware of the mutilation (Philippians 3: 2). In fact, Paul was so angry with those pushing circumcision that he wished they would castrate themselves (Galatians 5: 12).
This would be of purely religious interest except that Paul's anger at circumcisers has a very contemporary resonance. He said that some were into circumcision for the money (Titus 1: 11-12) That has been noted in connection with circumcision today.[2-4]
Paul specifically said that those who pushed circumcision on others '... desire to have you circumcised that they may glory in your flesh.' (Gal. 6: 13, RSV)
It is this glorying in the flesh that should be a concern to every person concerned with the welfare of children.
Take this professor of urology:
'In regard to the esthetic aspects of circumcision my associate, Professor Willard E. Goodwin, has commented that "circumcision is a beautification comparable to rhinoplasty," and that the circumcised organ "appears in its flaccid state as an erect uncircumcised organ - a beautiful instrument of precise intent.' 
Or what about this comment from a professor of Medicine and a professor of Nursing?
"What is sexier about a circumcised penis?
"Perhaps visualizing the glans, the urinary meatus, and the corona without them being hidden under a foreskin is arousing. After all, such is the appearance of an erect penis, and sexual imagery of the erect penis involves exposure of the glans.
"While the foreskin of an uncircumcised penis can be retracted, the circumcised penis exists in exposed beauty whether flaccid or erect." 
'Beautiful instrument'? Exposed beauty? Isn't this the language of desire rather than medicine?
Most doctors would be concerned by these comments. The words are warning signs that the profession should not ignore.
(1) 'tout entier 'in the French Jerusalem Bible, 'every whit whole' in the King James Version.
(2) Phoenix New Times, 24 April 2003, 'Rent a patient. Need some quick cash? Everyone makes a killing when doctors and clinics scam the insurance companies. http://www.phoenixnewtimes.com/issues/2003-04-24/ feature.html/print.html Accessed 1 June 2003
(3) 'Hospital Offers Cut-Rate Surgery to Boost Business' Reuters News Service, 23 August 2002. http://www.cirp.org/news/reuters08-23-02/
(4) "I have some good friends who are obstetricians outside the military, and they look at a foreskin and almost see a $125 price tag on it," says Wiswell. "Each one is that much money. Heck, if you do 10 a week, that's over $1000 a week, and they don't take that much time." Dr Thomas E. Wiswell, quoted in Betsy A. Lehman. 'The Age Old Question of Circumcision'. Boston Globe, Boston, Massachusetts, 22 June 1987:41.
(5) Joseph J. Kaufman, M.D., professor of surgery/urology, University of California School of Medicine, Los Angeles in 'Should circumcision be done routinely? in Medical Aspects of Human Sexuality, December 1967, page 30
(6) Williamson, Marvel L., Ph.D., R.N. and Williamson, Paul S., MD. Women's preference for penile circumcision in sexual partners. Journal of Sex Education and Therapy, Vol. 14, No. 2 (Fall/Winter 1988): pp. 8-12. http://www.geocities.com/HotSprings/2754/womenpre f.html and with a critical commentary http://www.circumstitions.com/Iowa.html
Voiding dysfunction in Duchenne muscular dystrophy
We read with interest the report by MacLeod et al who described urinary symptoms in 46 (62%) of 74 male children with Duchenne muscular dystrophy (DMD).
The authors comment that:
"The neurological basis for this dysfunction is difficult to explain."
Daytime incontinence, urinary frequency, and urgency were reported in 22 (48%), 14 (30%), and 18 (39%) of the 46 boys, respectively. These symptoms suggest the possibility of urge syndrome, a common problem in children that does not have any obvious neurological cause. The pathogenesis of urge syndrome is incompletely understood, but voiding postponement is common in these children and might play an aetiologic role. Voiding postponement is more common in children with neuromuscular disorders because the physical disability impairs access to a bathroom. There are many reasons why access to a bathroom is impaired or why these children might choose to postpone voiding. Wheelchair patients require specialized bathroom facilities and might require assistance, neither of which might be available. Even for "ambulatory" patients, getting on and off a toilet is often a labour- intensive and time-consuming process for many of these children. Requesting assistance for such a personal task might be difficult or embarrassing for some children.
Children with urge syndrome commonly demonstrate squatting behavior, which is a learned response to minimize incontinence associated with an unwelcome detrusor contraction. Children with DMD have proximal muscle weakness and might be limited in their ability to squat or otherwise to develop muscular strategies to cope with an unwelcome detrusor contraction.
(1) Macleod M, Kelly R, Robb SA, Borzyskowski M. Bladder dysfunction in Duchenne muscular dystrophy. Arch Dis Child 2003;88:347-349.
(2) Robson WL, Leung AK, Bloom DA. Daytime wetting in childhood. Clin Pediatr 1996;35:91-98.
Once upon a time . . .
I very much enjoyed reading Storr and Rudolf's review of literary perspectives on childhood. Appropriately enough, Charles Dickens loomed large. 'Oliver Twist' is the first novel in the English language that takes a child as its central character. The book is also polemical and the early chapters are very much an attack on the working of the New Poor Law, a series of measures introduced to cut down the cost of the poor by precluding the able-bodied pauper from relief and by making the life of the workhouse as unappealing a prospect as possible. Dickens strongly objected to the fact that by consigning sexes to different quarters within the same workhouse, the need for family life among the poor and needy was totally disregarded. He satirised the new dietary provisions in Oliver's asking for " . . some more", no doubt provoked by angry memories of his own deprivation and separation from family in childhood, and his obsessive comparison of the need for food and the need for love.
In fact, there is much in Dickens to interest paediatricians. 'Our Mutual Friend' published in 1864 even contains a brief description of what it was like in Great Ormond Street Hospital, opened twelve years earlier. He describes the admission of a sick orphan to " . . a fresh airy room . . a little quiet bed and a little platform over his breast on which to arrange toys . . . doll's houses, woolly dogs, tin armies, Moorish tumblers, wooden tea-things, and the riches of the earth". Dickens was very clear that childhood experiences fundamentally influenced the way people behaved as adults. Pleasant Riderhood in 'Our Mutual Friend' is a pawn shop owner and grown up daughter of a reprobate father. Dickens makes allowances for her mercenary and predatory nature in stating, " . . observe how many things were to be considered according to her own unfortunate experience. Show her a wedding and she only saw two people taking out a regular licence to quarrel and fight. Show her a Christening, and she saw a little heathen personage . . (who) was not in the least wanted by anybody, and would be shoved and banged out of everybody's way, until it should grow big enough to shove and bang . . . Show her a live father and she saw a duplicate of her own father, who from infancy had been taken with fits and starts of discharging his duty to her, which duty was always incorporated in the form of a fist or leathern strap, and being discharged, hurt her". 'Our Mutual Friend' portrays a London of wastelands, of disconnection and alienation, and a society dominated by financial speculation and commodity fetishism. As a cautionary tale warning against the moral dangers of greed and materialism it has lost none of its relevance.
(1) Ackroyd P. Dickens. London: Vintage, 1999: 231.
(2) Ackroyd P. Dickens. London: Vintage, 1999: 232.
(3) Dickens C. Our Mutual Friend. Ware: Wordsworth Editions Limited, 1997: 310.
(4) Dickens C. Our Mutual Friend. Ware: Wordsworth Editions Limited, 1997: 331.
Clinically relevant data needed to inform prescribing decisions
Ladhani and Gransden are right to encourage other units to review local data on antibiotic resistance among urinary tract isolates. There is not adequate evidence to suggest one antibiotic is superior to others in presumptive therapy of urinary tract infection (UTI). Local antibiotic susceptibility patterns should thus help make the antibiotic choice. However I have two major concerns about their conclusions:
1. They do not demonstrate the clinical significance of their data and
2. Empiric use of nitrofurantoin is not justified by their data.
1. Clinical relevance of resistant organisms. One study shows that the bacteriological cure rate in UTI is the same irrespective of whether the infecting bacteria were sensitive or resistant to the antibiotic given. The clinical significance of antibiotic resistant urinary tract isolates thus needs to be shown.
Like Ladhani and Gransden we were concerned that 17% of urinary tract isolates cultured in our hospital were trimethoprim resistant. We therefore reviewed the case notes of 21 children with trimethoprim resistant urinary tract isolates. Of these 21, eight were found not to have a urinary tract infection, despite having a bacterial culture of 105 colony-forming units of a single species per ml urine. Most of these were samples collected in urine bags. 85% of positive cultures of urine specimens obtained from a bag are false positive results. We have now abandoned the use of urine bags. Of the 13 thought to have UTI, seven were on trimethoprim prophylaxis and had breakthrough infections. Only six children had clinically significant trimethoprim resistant urinary tract isolates and were not on trimethoprim prophylaxis; none developed renal scaring.
Our data suggest antibiotic resistant urinary tract isolates in children occur mainly in false positive urine samples and those on antibiotic prophylaxis. Studies in adults have shown that trimethoprim resistance is independently associated with exposure to trimethoprim, antibiotics other than trimethoprim and prior UTI.[3,4] Ladhani and Gransden do not report if urine bags were used to collect specimens, nor how many antibiotic resistant urinary tract isolates were not genuine urine infections, nor which children were on prophylaxis or had had previous treatment for UTI.
For the community isolates there is also a potential for bias. A recent New Zealand study concluded that “actual resistance rates are significantly less than those derived from routine pooled laboratory specimens, and when used in an intention to treat calculation to inform empiric prescribing, become even less significant”. Many general practitioners (GPs) will not send a urine culture from a child with a suspected UTI. They may be more likely to send samples if the child fails to respond to empirical antibiotic treatment. This will thus falsely raise the proportion with antibiotic resistant isolates. GPs may also use urine bags leading to false positive results.
2. Empiric use of nitrofurantoin. The suggestion that nitrofurantoin should be the first line empiric treatment for UTI in children should be reviewed. Children taking nitrofurantoin have significantly more adverse effects than those taking trimethoprim. Nitrofurantoin needs to be taken 4 times a day, this is associated with lower adherence levels than regimens dosed once or twice daily. Nitrofurantoin also costs about 60 times as much as trimethoprim or cefalexin.
Unfortunately, no data is given on sensitivity to cefalexin. This antibiotic is commonly used for UTI, is cheap and has a very acceptable taste. This might be a better alternative should trimethoprim be inappropriate.
Ladhani and Gransden have provided some useful data on antibiotic resistance. “While collection of these routine data is essential to provide early warning of emergent resistance, a truly representative rate should be determined to inform prescribing decisions if resistance appears to be increasing”.
Proper trials of empiric antibiotic treatment in children with UTI are required. Until these are done our experience shows that local audit of cases notes of children with antibiotic resistant urinary tract isolates is simple and helps provide data on which to base local antibiotic guidelines. I would encourage other units to do it.
(1) Downs SM. Technical Report: Urinary Tract Infections in Febrile Infants and Young Children. Pediatrics 1999;103(4).
(2) Ferry S, Burman, LG, Holm SE. Clinical and bacteriological effects of therapy of urinary tract infection in primary health care: relation to in vitro sensitivity testing. Scandinavian Journal of Infectious Diseases 1988;20:535–44
(3) Steinke DT, Seaton RA, Phillips G, MacDonald TM, Davey PG. Prior trimethoprim use and trimethoprim-resistant urinary tract infection: a nested case-control study with multivariate analysis for other risk factors. J Antimicrobial Chemotherapy 2001;47:781-787.
(4) Sotto A, De Boever CM, Fabbro-Peray P, Gouby A, Sirot D, Jourdan J. Risk factors for antibiotic-resistant Escherichia coli isolated from hospitalized patients with urinary tract infections: a prospective study. J Clin Microbiol 2001;39:438-44.
(5) Richards DA, Toop LJ, Chambers ST, Sutherland MG, Harris BH, Ikram RB, Jones MR, McGeoch GR, Peddie B. Antibiotic resistance in uncomplicated urinary tract infection: problems with interpreting cumulative resistance rates from local community laboratories. NZ Med J 2002;115:12-4.
(6) Williams GJ, Lee A, Craig JC. Long-term antibiotics for preventing recurrent urinary tract infection in children. In: The Cochrane Library, Issue 4, 2001. Oxford: Update Software.
(7) Claxton AJ, Cramer J, Pierce C. A systematic review of the associations between dose regimens and medication compliance. Clin Ther 2001;23:1296-310.
Hypothalamic hamartomas: syndromes and surgery
The recent article by Ng et al. and the accompanying commentary  address the notion that girls with precocious puberty should undergo cranial imaging to exclude a CNS malformation.
One consideration not discussed in that article or the commentary is that hypothalamic hamartomas can be part of a malformation syndrome, most commonly Pallister -Hall syndrome. Because this disorder can be subtle (minimal post- axial polydactyly with metacarpal fusion, bifid epiglottis, and anal stenosis) it can be missed. The disorder is inherited in an autosomal dominant pattern, so the recurrence risks may be substantial. Conversely, if a child with any of these anomalies develops precocious puberty, there is no doubt that cranial imaging is indicated.
The issue of surgery for hypothalamic hamartomas is challenging. My experience with Pallister-Hall syndrome combined with published data on children with non-syndromic hypothalamic hamartomas  show that these lesions are malformations, not tumors. No patients in these series have experienced visual axis compromise in spite of having enormous hamartomas, some as large as 4 cm and associated with developmental distortion of the optic tracts and chiasm. In several instances, I have urged families to refuse planned surgical interventions and these children have done well. Although the commentary focuses on the cost of the MRIs, the greater cost may be that of unnecessary neurosurgery and its subsequent morbidity, sometimes including lifelong hormonal replacement. Avoiding one unnecessary neurosurgical procedure may save more than the cost of 100 MRIs.
Note: The opinion expressed here is that of the author and does not necessarily represent the opinion of the institutions with which he is affiliated.
(1) Ng SM, Kumar Y, Cody D, et al. Cranial MRI scans are indicated in all girls with central precocious puberty. Arch Dis Child 2003 88(5): 414-417.
(2) Biesecker LG, Graham JM Jr. Pallister-Hall syndrome. J Med Genet 1996 Jul;33(7):585-9.
(3) Biesecker LG, Abbott M, Allen J, et al. Report from the workshop on Pallister-Hall syndrome and related phenotypes. Am J Med Genet 1996 Oct 2;65(1):76-81.
(4) Feuillan PP, Jones JV, Barnes KM, et al. Boys with precocious puberty due to hypothalamic hamartoma: reproductive axis after discontinuation of gonadotropin-releasing hormone analog therapy. J Clin Endocrinol Metab 2000 Nov;85(11):4036-8.
Vitamin K deficient bleeding in cystic fibrosis
The report by Drs Verghese and Beverley of the 9 week old infant with cystic fibrosis (CF) who presented with late vitamin K deficiency bleeding (VKDB) was very interesting. However the quoted prothrombin time (PT) and normal range was confusing.
A PT of > 10 seconds could be normal, since the normal reference range for PT in healthy 1 month old term infants is 10.6 – 13.1. Yet the PT in this infant must have been very prolonged, for this is a hallmark of VKDB. I wonder whether in quoting their result and range, the authors were in fact referring to the international normalised ratio (INR) rather than PT? The INR is a ratio obtained from the PT of the patient’s plasma divided by that of control plasma. It should be used to monitor oral anticoagulant therapy rather than to report PT tests in patients with liver disease or bleeding diatheses.
It would be of interest to know exactly which oral vitamin K preparation the infant received. The currently recommended regime for oral prophylaxis is mixed micellar (MM) Konakion (Roche) in multiple 2 mg doses. This infant received two 1 mg doses of vitamin K prior to the bleeding. Infants with malabsorption may be more prone to VKDB with lower than recommended oral doses or with (unlicensed) oral preparations other than MM whose absorption may be inferior. Regardless, just as oral prophylaxis has proven ineffective for many infants with cholestatic liver disease, it has failed to protect this infant against late VKDB.
The authors concluded that universal neonatal CF screening may have prevented this life-threatening complication. Another interpretation is that a policy of universal intramuscular prophylaxis may have prevented this case of late vitamin deficiency bleeding.
(1) Verghese T, Beverley D. Vitamin K deficient bleeding in cystic fibrosis Arch Dis Child 2003;88:553.
(2) Andrew M, Paes B, Milner R, et al. Development of the human coagulation system in the full-term infant. Blood 1987;70:165-72.
(3) Department of Health. Vitamin K for newborn babies. London: HMSO, 1998 (PL/CMO(98)3. Available at http://www.doh.gov.uk/cmo/cmo98_3.htm
(4) Von Kries R, Hachmeister A, Gobel U. Can 3 oral 2 mg doses of vitamin K effectively prevent late vitamin K deficiency bleeding? Eur J Pediatr 1999;158 Suppl 3:S183-6.
Malaria chemoprophylaxis in children: practical problems
I am writing in response to the article on fever in returned travellers  that highlights the disappointing uptake of malaria chemoprophylaxis in travellers.
I wish to point out the practical problems associated with malaria chemoprophylaxis in children. The medications used for chemoprophylaxis varies depending on the area travelled to. A combination of weekly chloroquine and daily proguanil is the standard recommendation for travellers to South Asia. Mefloquine is recommended when travelling to areas of chloroquine resistant falciparum malaria but is associated with a lot of side effects. Maloprim (a combination of pyrimethamine and dapsone) is the only other chemoprophylaxis for falciparum malaria chemoprophylaxis in children under 12 years of age. Chloroquine is the only medicine available in syrup form, but the syrup is extremely bitter. All the other medications are available in tablet forms and have to be crushed and given to children under 2 years of age. The recommended duration of chemoprophylaxis is 1 week prior to travel to 4 weeks after return to UK.  Many families residing in the UK and visiting their countries of origin stay abroad for a minimum of three to four weeks. This would mean that the desirable duration of chemoprophylaxis would vary between seven to eight weeks. As we can imagine, it can be incredibly difficult to get a young child under 2 years of age to comply with this child unfriendly chemoprophylaxis for this length of time. It is highly likely that many parents would try for a while and give up. This would account for the poor uptake of malaria chemoprophylaxis.
We can only improve the compliance to malaria chemoprophylaxis by production of more child friendly medications or an effective malaria vaccine. This will reduce the cases of imported malaria in children in the United Kingdom.
(1) NS West, FAI Riordan. Fever in returned travellers: a prospective review of hospital admissions for a 2 ½ year period. Arch Dis Child 2003; 88:432-434.
(2) British National Formulary. Prophylaxis against malaria.
(3) PHLS, Malaria reference laboratory. Guidelines for prevention of malaria-2001.
Authors' Reply: Education and training in the paediatric senior house officer grade
We were pleased to receive the comments from Martin Richardson  about our article  because it allows us to clarify the College's position on education in the modern NHS. Our survey of College Visit reports covered the period 1997 to mid 2001 which was before most departments introduced shift patterns of working. The article was written many months ago and this inevitably resulted in some of our comments becoming outdated.
The RCPCH agrees that training methods need to change to accomodate new patterns of working and the Liberating Learning document is very helpful in this regard. The College is organising a number of workshops for College Tutors to further develop these themes.
In line with this, the new Paediatric Training Handbook, which will be published in the next few months, has been changed. One of the essential features of an SHO training programme now reads: 'There should be three hours per week dedicated to education and training. The department should demonstrate its committment to ongoing teaching. The format can include: tutorials, lectures, ward-based teaching and attendance in outpatients for structured teaching and feedback. Departmental meetings should be arranged so that the majority of SHOs can attend, i.e. at shift overlap times, including early morning meetings and lunch times. The educational content should be directed towards the career aims of the SHOs and sessions should be interactive whenever possible. Educational sessions should be bleep free and it should be possible to attend >70% of sessions (i.e. an average minimum of 2 hours per week).'
We hope this addresses the concerns which were outlined in Martin Richardson's letter.
(1) Richardson M, Reddy V. Education and training in the paediatric senior house officer grade [electronis response to Smith CP and Anderson JM, Education and training in the paediatric senior house officer grade: analysis of RCPCH hospital/child health visits reports, 1997–2001] archdischild.com 2003 http://adc.bmjjournals.com/cgi/eletters/archdischild;88/5/450#466
(2) Smith CP, Anderson JM. Education and training in the paediatric senior house officer grade: analysis of RCPCH hospital/child health visits reports, 1997–2001. Arch Dis Child 2003; 88:450-453.
The one child family policy in China and the gender ratio
Zhu points out the favorable effects of the One Child Family Policy (OCFP) on China’s demographic problems and on the population. In our opinion, the considerable, unfavorable consequences of the OCFP are not sufficiently taken into consideration in the article. One of the major problems is the gender imbalance of Chinese population. The gender ratio mentioned by Zhu refers to the entire population, but the data regarding the gender ratio at birth (GRB) show a much more alarming situation. According to the official China’s 2000 Census data, that Zhu does not mention, 117 male children are born every 100 female babies in China, and in some provinces –such as in Hainan- the GRB (male:female) rises up to 135:100. GRBs over 113:100 have been reported in China’s official figures since the late 1980s  and the phenomenon seems therefore to be increasing. It’s widely recognized that this abnormal GRB is the direct consequence of the OCFP: in a culture in which a strong traditional preference for boys exists, the OCFP determined the spread of prenatal sex selection practices against female fetuses, through the use of ultrasounds and selective abortion. The underreporting of female births, that Zhu presents as a cause of the abnormal gender ratio, has not been documented. If it existed and was so relevant as to skew the GRB by 10%, we should hypothesize that also the data about the decline of fertility rate in China are substantially biased. Although the OCFP does not seem to be the cause of negative effects on health and psychological conditions for the many only children born in China following the introduction of the policy, yet it is likely to cause them social problems in the next years. Indeed, if China’s family planning policy is not modified so as to reduce GRB, in the next future about one sixth of Chinese young male adults -and up to one third in some rural areas- won’t have the possibility to create a family and to have children, due to the lack of women to marry.
(1) Zhu W X, The One Child Family Policy. Arch Dis Child 2003;88:463-464. (2) Plafker T. Sex selection in China sees 117 boys born for every 100 girls. BMJ 2002;324:1233.
(3) Gu B, Roy K. Sex Ratio at Birth in China, with Reference to Other Areas in East Asia: What We Know. Asia-Pacific Population Journal 1995;10:17-42.
(4) Hesketh T, Qu J D, Tomkins A. Health effects of family size: cross sectional survey in Chinese adolescents. Arch Dis Child 2003;88:467-471.
Guidelines already there
This was a very useful example of evidence based medicine. However, we already have advice as to the answer to this question from the British Thoracic Society. The child concerned need not have had a chest Xray at presentation. The guidelines state that "Chest radiography should not be performed routinely in children with mild uncomplicated acute lower respiratory tract infection". (Strength of recommendation [A], ie Ia/Ib level of evidence.)