In a reaction to our article,[1] in which the natural
history of cardiovascular manifestations in 52 children and
adolescents with Marfan syndrome is described, Dr
Venugopalan highlights the role of beta-adrenergic blocker
therapy in retarding the progress of aortic dilatation.[2]
As stated on page 135 of the Discussion in our article, the
use and effectiveness of this prophylactic pharmacotherapy
was well-kno...
In a reaction to our article,[1] in which the natural
history of cardiovascular manifestations in 52 children and
adolescents with Marfan syndrome is described, Dr
Venugopalan highlights the role of beta-adrenergic blocker
therapy in retarding the progress of aortic dilatation.[2]
As stated on page 135 of the Discussion in our article, the
use and effectiveness of this prophylactic pharmacotherapy
was well-known to us.[3] However, as no valid studies
proving the effectiveness of this medication in children
were available during our study period (1981-1997) and as
there were worries regarding possible adverse side-effects,
very few children or adolescents managed by the Marfan
Clinics of our hospital were prescribed beta-blockers.
The
study of Rossi-Foulkes et al,[4] reporting positive effects
of beta-blockade in a cohort of children and adolescents
with Marfan syndrome was published only after submission of
our paper. Along with the good results of similar treatment
strategies in adult Marfan patients in our hospital, this
lead us to prescribe beta-blocker therapy also in paediatric
and adolescent patients.
As most Marfan clinics will probably have adjusted their
treatment protocols in children in a similar manner, future
gathering of information on the natural history of
cardiovascular manifestations in children will hardly (if at
all) be possible. Therefore, our study offers a tool
allowing future comparison of aortic growth and
complications in untreated children with Marfan syndrome
('natural history') to those who were treated with
beta-blockers.
References
(1) van Karnebeek CDM, Naeff MSJ, Mulder BJM, Hennekam RCM,
Offringa M. Natural history of cardiovascular manifestations
in Marfan syndrome. Arch Dis Child 2001;84:129-37.
(2) Venugopalan P. Role of beta-adrenergic blockade therapy in children with Marfan syndrome and aortic root dilatation [eLetter]. Arch Dis Child 23 February 2001. http://adc.bmjjournals.com/cgi/eletters/archdischild;84/2/129#EL2
(3) Shores J, Berger KR, Murphy EA, Pyeritz RE. Progression
of aortic dilatation and the benefit of long-term
beta-adrenergic blockade in Marfan's syndrome. N Engl J Med
1994;330:1335-41.
(4) Rossi-Foulkes R, Roman MJ, Rosen SE, Kramer-Fox R,
Ehlers KH, O'Loughlin JE, Davis JG, Devereux RB. Phenotypic
features and impact of beta blocker or calcium antagonist
therapy on aortic lumen size in the Marfan syndrome. Am J
Cardiol 1999;83:1364-8.
CDM van Karnebeek, MD
MSJ Naeff, MD BJM Mulder, MD PhD
RCM Hennekam,MD PhD
M Offringa, MD PhD
Department of Paediatrics (Emma Children's Hospital) and
Cardiology
Academic Medical Centre, Amsterdam The Netherlands
I would like to draw your attention to the need for
prophylaxis against RSV in another high risk group of infants who are
being excluded at present. Infants with congenital heart diseases have
altered anatomy/physiology which make them more prone to infection with
the virus with devastating consequences. They do very badly when infected
with such a virus. While infants with normal anatomy and physiology have...
I would like to draw your attention to the need for
prophylaxis against RSV in another high risk group of infants who are
being excluded at present. Infants with congenital heart diseases have
altered anatomy/physiology which make them more prone to infection with
the virus with devastating consequences. They do very badly when infected
with such a virus. While infants with normal anatomy and physiology have
variable intensity of the disease, the group with congenital heart
disease with their limited cardiac/pulmonary functional reserve often go
into cardiorespiratory failure quickly. They need intensive care
admissions, on occasions repeatedly, to help them overcome the crisis
while awaiting surgery or in the immediate postoperative period.
My
experience in the intensive care unit looking after infants with
congenital heart diseases both pre and postop tell us that this group
might benefit from routine prophylaxis against the virus. We are yet to
conduct a study on this topic which we are planning to do in near future.
People might urgue against the idea on the ground of yet unexplored 'cost
effectiveness' aspect of such a proposal.
Meanwhile considering (a) the
morbidity associated with such an infection (b) costs incurred in
postponing planned surgery and repeated intensive care admissions (c)
psychological stress of the parents I believe infants with congenital
cardiac conditions should be considered as an independent high risk group
and hence be routinely given prophylaxis.
Pearson and colleagues have presented data highlighting the use of the PIM
score as a tool for auditing paediatric intensive care unit (PICU)
performance.[1] Whilst we would agree with the authors' message that PIM has
many advantages over other scoring systems, we feel that urgent
calibration is needed before this tool is adopted as a benchmark for
performance indication in the UK.
PIM variables were develope...
Pearson and colleagues have presented data highlighting the use of the PIM
score as a tool for auditing paediatric intensive care unit (PICU)
performance.[1] Whilst we would agree with the authors' message that PIM has
many advantages over other scoring systems, we feel that urgent
calibration is needed before this tool is adopted as a benchmark for
performance indication in the UK.
PIM variables were developed predominantly from an Australian data set
(one British PICU, Birmingham participated) over 1994-1995; the data used
in Pearson's validation comes from five UK PICUs, including our own over
the period 1998-1999.[1] PIM continues to discriminate between death and
survival reasonably well giving an area under the ROC curve of 0.840 (95%
CI 0.819-0.853),[1] marginally less than the figure of 0.90 seen in the
original paper.[2] However from the 4-year period between development and
validation the model is now calibrating poorly, as evidenced by two pieces
of information from Pearson's study.[1]
First, the overall standardised
mortality ratio (SMR) is 0.87 (95% CI 0.81-0.94); this figure is
remarkably concordant across 4 of the 5 PICUs. Second, from table 2,[1] it
is possible to calculate the Hosmer-Lemeshow statistic: chi-squared = 37.41, p<_0.0001. this="this" implies="implies" poor="poor" calibration="calibration" good="good" traditionally="traditionally" represented="represented" by="by" a="a" p="p" value="value"/>0.10).
The reasons for the loss of calibration are unclear. A possible, perhaps
over-optimistic explanation is that UK units in the latter study were all
"over-performing" given that individual units demonstrated an SMR of
between 0.83 and 0.89. However it is unlikely that such a quantum leap in
the quality of paediatric intensive care delivery has occurred over the 4
years between 1994-8, given that no major treatment breakthroughs or
radical service reorganisation has occurred in this time.
More recent data
from our PICU highlights the trend towards poorer calibration, where the
PIM-derived SMR from 910 patients seen during the 2000 calendar year is
0.54 (95%CI 0.39-0.69).
The authors acknowledge the shortcomings and state that a revised version
of PIM will soon be available. However recalibration is only worthwhile if
a very broad sample of UK units participates. The UK PICOS study
(paediatric intensive care outcome study) will attempt to address this, by
collecting data used in the calculation of several scoring systems across
the whole of the UK over a one-year period commencing March 2001. From
this study it is hoped that an optimal indicator of PICU performance will
be derived.
Shane M Tibby
Ian A Murdoch
Paediatric Intensive Care Unit Guy's Hospital, London, UK
References
(1) Pearson GA, Stickley J, Shann F. Calibration of the paediatric
index of mortality in UK paediatric intensive care units. Arch Dis Child 2001;84:125-8.
(2). Shann F, Pearson G, Slater A, Wilkinson K. Paediatric index of
mortality (PIM): a mortality prediction model for children in intensive
care. Intensive Care Med 1997;23:201-7.
I read the article of Dr M Riordan on investigation and treatment of
facial paralysis in the April issue of the journal with a special
interest. It is indeed a well-composed article. However I would like to
elaborate some interesting points.
1.Although facial nerve paralysis is the commonest cause of facial
weakness, weakness of facial muscles forms another interesting spectrum of
facial w...
I read the article of Dr M Riordan on investigation and treatment of
facial paralysis in the April issue of the journal with a special
interest. It is indeed a well-composed article. However I would like to
elaborate some interesting points.
1.Although facial nerve paralysis is the commonest cause of facial
weakness, weakness of facial muscles forms another interesting spectrum of
facial weakness. Myotonic dystrophy and infantile facioscapulohumeral
syndrome can present as facial weakness. Congenital myasthenia gravis and
juvenile immune mediated myasthenia may be relevant to remember as
differential diagnosis.[1]
2.Certain infections like tuberculosis and leprosy, although uncommon
in UK, should not be ignored as we may continue to see them in immigrant
population. Tubercular meningitis may start with fever and facial nerve
palsy.[2] Infectious mononucleosis is another not too rare offender.
3.The author has rightly pointed out the importance of careful
examination of the ear including hearing acessment. An unusual but very
interesting cause of facial weakness is presence of an intraaural tick.
Salivary glands of the tick secrete a toxin that either impairs the
synthesis or the secretion of acetylcholine in the motor end plate of facial
muscles [3]. Happily enough, the nerve weakness disappears with the
removal of the tick.
4.Perinatal traumatic facial weakness is usually a disorder of a large
term infant, delivered vaginally after a prolonged labour. Medico-legally
it is important to remember that it is more often caused by facial nerve
compression against the maternal sacrum during labour even before the
obstetricians lay their hands on the baby.[1] Although the majority recover
spontaneously, close attention to eye care is vital. It is also important
not to misdiagnose absent depressor anguli oris as facial weakness.
5.Incidence wise brain stem glioma is as important as leukemia as a
cause of facial weakness. It is interesting to point out that unlike
adults, 17% of children with neurofibromatosis type 2 can present as facial weakness.[4]
6.Although uncommon, toxins will be an important differential
diagnosis to the list of causes of facial weakness. Ingestion of ethylene
glycol, an antifreeze agent, may present with facial diplegia. Inhalation
of chlorocresol, a compound used in industrial production of heparin, is a
recognised cause of recurrent facial weakness[1]
7.Vasculitic disorders (Polyarteritis nodosa, SLE),Sickle cell anaemia
and childhood migraine can also present with facial weakness[5]
Dr Samudra Mukherjee
Senior House Officer
Department of Paediatrics
The Leeds General Infirmary
Clarendon Wing, Belmont Grove
Leeds LS2 9NS, UK
I read with great interest "An audit of RCP guidelines on DMSA scanning after UTI 1". I have recently presented a similar audit at Furness General Hospital, Barrow-in-Furness (29th March,2001), looking at DMSA scan in children with UTI.
75 children between the age group of 0-7 years who had DMSA scan, between 1st January to 31st December 2000 were included in my audit. The exclusion criteria were similar to the p...
I read with great interest "An audit of RCP guidelines on DMSA scanning after UTI 1". I have recently presented a similar audit at Furness General Hospital, Barrow-in-Furness (29th March,2001), looking at DMSA scan in children with UTI.
75 children between the age group of 0-7 years who had DMSA scan, between 1st January to 31st December 2000 were included in my audit. The exclusion criteria were similar to the published audit.[1]
The guidelines that are followed at Furness General Hospital are the Royal College of Physicians 1991 Guidelines. We have divided our patients into 2 groups. The first group included patients with risk factors associated UTI. The second group included patients without risk factors associated with UTI. Risk factors included age less than 1 year for the first UTI, associated pylonephritic symptoms and non enteric organism in the urine.[2] Like in the audit,[1] the DMSA scan positivity rate was low in only 10 of the 75 patients who underwent DMSA scan.
When risk factors are considered, 42 of our patients had +ve risk factors whereas 33 did not have risk factors. Nine of our patients who had positive risk factors had positive DMSA scan compared to only one patient with negative risk factors having positive DMSA scan. When we considered ultrasonogram and risk factors to DMSA positivity. Seven children with positive DMSA scan had positive risk factor and posiive ultrasonogram. One child with positive DMSA scan had negative risk factors but posititve ultrasound. Two children who had positive DMSA scan had positive risk factors but negative ultrasound. But no children with a negative risk factor and negative ultrasonogram together had a positive DMSA scan.
We have investigated 28 cases of UTI with negative risk factors and with negative ultrasonogram for DMSA scan and all of them had negative DMSA scan. Thus I would like to suggest on the basis of my audit that ultrasound should be performed in all children with UTI, and DMSA scan should be restricted to children with either positive ultrasound results or those with one or more associated risk factors.
Dr Tapabrata Chattopadhyay
BIBLIOGRAPHY
(1) P V Deshpande , K Verrier Jones, An audit of RCP guidelines on DMSA scanning after Urinary Tract Infection , Arch Dis Child April 2001;84:324-7
(2) R J M Coward , T L Chambers, An evidence based appraisal of investigation of childhood Urinary tract infection. Curr Paed 1999;9:215-21
The argument against the use of passive prophylaxis against RSV
infections in children with congenital heart disease (CHD) has more to
do with the lack of effectiveness and increased incidence of serious
adverse events in such 'prophylaxed' children than with its 'cost
effectiveness'. The last such attempt (Simoes EAF, Sondheimer HM, Top
FH, et al. Respiratory syncytial virus immune globuli...
The argument against the use of passive prophylaxis against RSV
infections in children with congenital heart disease (CHD) has more to
do with the lack of effectiveness and increased incidence of serious
adverse events in such 'prophylaxed' children than with its 'cost
effectiveness'. The last such attempt (Simoes EAF, Sondheimer HM, Top
FH, et al. Respiratory syncytial virus immune globulin for prophylaxis
against respiratory syncytial virus disease in infants and children with
congenital heart diease. J Pediatr 1998;133:492-9), albeit with a
different product (RSV-IGIV) showed no statistically significant decrease
in RSV hospitalisation in children with CHD. On the other hand, there
was a significantly higher incidence of unanticipated cyanotic episodes
and of poor outcomes after surgery among children with cyanotic CHD.
The IMpact-RSV Study Group's trial of Palvizumab (Pediatrics
1998;102:531-7)) did not include children with CHD, and in the light of
the RSV-IVIG experience, direct extrapolation of the safety od Palvizumab
from the non-CHD group to children with CHD is fraught with danger. Any
intended evaluation of the newer monoclonal antibody in children with CHD
will therefore need careful risk/benefit analysis, and will need close
independent data monitoring committee for detecting such adverse events.
We read with interest the article on the need for and the role of a co-
ordinator in the provision of child health surveillance (CHS)[1] and
particularly the need to work with the Primary Care Team in developing
quality standards.
We have used such standards in City and Hackney for the past 5 years.
When a General Practitioner (GP) applies to join the CHS list the
Consultant Community Paediatrician...
We read with interest the article on the need for and the role of a co-
ordinator in the provision of child health surveillance (CHS)[1] and
particularly the need to work with the Primary Care Team in developing
quality standards.
We have used such standards in City and Hackney for the past 5 years.
When a General Practitioner (GP) applies to join the CHS list the
Consultant Community Paediatrician for that practice visits and discusses
these standards, advising the GP to attend a CHS course and local clinics.
We audited these standards by asking GP’s attending the weekly post -
graduate teaching to complete a questionnaire.
19 (56%) of the 34 GP’s attending that session completed the
questionnaire. Of these, 68% were registered for CHS, 90% had attended a
CHS course but only 47% locally.
The number of under-five’s registered with these practices ranged
from 120 to 1000. 63% held dedicated child health clinics but only 53% had
clerical support to deal with the Personal Child Held Record.
68% had suitable scales, 79% a height measure (mostly described as
permanent and attached to a wall). Age appropriate toys were available in
63% of surgeries. 90% had a dedicated vaccine fridge but the community
pharmacist had visited only 5% to give advice.
79% of the responders had the local CHS Manual; only 63% had the Area
Child Protection Committee Guidelines. 68% had received child protection
training but only 13% within the last 5 years.
It would be difficult to generalise to all the GP’s from this self-
selected group who may have been interested in the CHS lecture that day or
keen to receive PGEA hours. Currently 55% of GP’s are on the CHS list in
this area and our sample exceeded this with 68% being accredited. However
it is clear that even amongst a group where high numbers are accredited
the standards that most paediatricians would consider to be essential, for
example, an adequate pair of scales or recent child protection training,
are not always met.
The Primary Care Trust has a responsibility to ensure adequate
standards in primary care and we have a responsibility to support high
quality CHS. We hope that this study will help to improve standards if it
is extended to include all GP’s and the findings acted upon with
managerial support.
Yours sincerely,
Emma Devereux and Deborah Hodes.
References
(1) Blair M, The need for and the role of a co-ordinator in child health
surveillance/promotion. Arch Dis Child 2001;84:1-5.
I write with regard to the recently published protocol for treating
attention deficit/ hyperactivity disorder.[1] I would like to comment
specifically on a few points.
The authors suggest a trial of an elimination diet if the history
suggests that dietary factors might be significant, drawing on one paper
to suggest that 'there is evidence for the effectiveness of an
individually constru...
I write with regard to the recently published protocol for treating
attention deficit/ hyperactivity disorder.[1] I would like to comment
specifically on a few points.
The authors suggest a trial of an elimination diet if the history
suggests that dietary factors might be significant, drawing on one paper
to suggest that 'there is evidence for the effectiveness of an
individually constructed elimination or oligoantigenic diet'. In fact
there have been a number of good double-blind placebo-controlled trials of
dietary interventions in ADHD. Changes in mood state (eg. irritability)
rather than ADHD symptoms per se have been shown in response to foods in a
minority of subjects. However food intolerance is very unlikely to be the
sole cause and dietary intervention alone is rarely helpful and may be
harmful. In any case a repeated single-blind challenge (at a minimum) is
required.[2]
The assertion that intelligence testing is 'relatively
straightforward' and can be carried out by non-psychologists is
problematic. Cognitive functioning is extremely complex and difficult to
measure reliably or meaningfully. Some paediatricians with an interest can
be trained to use (and interpret) certain standardised psychometric tools,
aware of their limitations. However if there is academic under-achievement
the child deserves a formal psychometric assessment by an educational
psychologist, including academic achievement testing, to identify
strengths and weaknesses to develop an individualised program of remedial
tuition.
The authors suggest trying psychological interventions before a trial
of medication. This goes against the grain of published evidence.[3] If
the diagnosis is clear and there is significant disability, then a trial
of stimulant medication should be considered early, and instituted
alongside behavioural interventions.
The suggestion to 'Check hearing clinically' runs contrary to the
accepted wisdom that clinical assessment of children’s hearing is
notoriously unreliable. Finally pervasive developmental disorder is listed
as a co-morbidity, whereas in fact it is an exclusion criterion according
to DSM-IV (the authors provide partial DSM-IV diagnostic criteria).
1. Hill P, Taylor E. An auditable protocol for treating attention
deficit/ hyperactivity disorder. Arch Dis Child 2001;84:404-409
2. Breakey J. The role of diet and behaviour in childhood. [Review]
Journal of Paediatrics & Child Health1997;33:190-4.
3. Arnold LE, Abikoff HB, Cantwell DP et al (MTA Co-operative Group). A
14-month randomized clinical trial of treatment strategies for attention-
deficit/ hyperactivity disorder. Arch Gen Psychiatry 1999;56:1073-86.
Dr Daryl Efron
Royal Children's Hospital
Tel: 61-3-9345-5522
Fax: 61-3-9345-5900
e-mail: efrond@cryptic.rch.unimelb.edu.au
Dr Tibby and Dr Murdoch note that, in our study of paediatric
intensive care units (PICUs) in the UK [1], PIM discriminated well between
children who died and children who survived, with an area under the ROC
curve of 0.84. However, they are concerned that PIM had "poor
calibration" because the standardised mortality rate (SMR) in the UK units
was 0.87 (95% CI 0.81-0.94) - that is, the actual number of deaths was
only 87...
Dr Tibby and Dr Murdoch note that, in our study of paediatric
intensive care units (PICUs) in the UK [1], PIM discriminated well between
children who died and children who survived, with an area under the ROC
curve of 0.84. However, they are concerned that PIM had "poor
calibration" because the standardised mortality rate (SMR) in the UK units
was 0.87 (95% CI 0.81-0.94) - that is, the actual number of deaths was
only 87% of the number predicted by PIM. In fact, this figure is almost
identical to the PIM SMR for all PICUs in Australia in 1997-99, where the
SMR was also 0.87(95% CI 0.81-0.92). It is very encouraging that PIM gives
such similar results in Australia and the leading PICUs in the UK, as it
suggests that standards are comparable between the two groups of units and
that PIM
performs similarly in Australian and UK children.
It is normal for SMRs to fall with time as intensive care improves,
and for mortality prediction models to need recalibration. This has
happened with PRISM [2], MPM [3] and APACHE [4], as well as PIM. Despite
Dr Tibby and Dr
Murdoch's reservations, the fact that the SMR has fallen by a similar
amount in both Australia and the UK suggests that standards of care have
improved in PICUs in those countries in recent years.
Dr Tibby and Dr Murdoch point out that the Hosmer-Lemeshow test gives
a low p value for PIM's performance in the UK data. This test divides the
sample into 10 groups, ranging from very low to very high risk of death,
and compares the actual number of survivors and non-survivors in each
group
with the number predicted by PIM. Because PIM predicts too many deaths in
the leading units in the UK, it follows that the number of actual deaths
differs from the number predicted - so the Hosmer-Lemeshow p value is low.
However, Table 2 in our paper shows that the ratio of observed to expected
deaths was similar across the 10 groups [1], so that the recalibrated
model is likely to fit well. The fact that the Hosmer-Lemeshow test gives
a low p value does not necessarily mean that a model (such as PIM) is
invalid -
it often means only that the standard of care in the test PICUs differs
from that in the units in which the model was derived.
The PICUs that contributed the data from which the PIM score was
derived were all leading units that deliver a high standard of care, so
the score reflects best practice in 1994-1996 when the data were
collected. We are
recalibrating PIM using data from units in the UK and Australia, and the
new model will be available this year. Unfortunately, the quality of
paediatric intensive care is not uniform in the UK, and there is evidence
that some units do not perform at an optimal standard [5-7]. Surely it
would be preferable for the UK to use an international standard based on
best practice (such as PIM), rather than the average of good and not-so-
good units from the whole of the UK (PICOS). The UK should aim for best
practice rather than being content with average practice.
Yours sincerely
Frank Shann Gale Pearson
(1) Pearson GA, Stickley J, Shann F. Calibration of the paediatric
index of mortality in UK paediatric intensive care units. Arch Dis Child
2001;84:125-8
(2) Pollack MM, Patel KM, Ruttimann UE. PRISM III: an updated pediatric
risk of mortality score. Crit Care Med 1996;24:743-52
(3) Lemeshow S, Teres D, Klar J, Spitz Avrunin J, Gehlbach SH, Rapoport J.
Mortality probability models (MPM II) based on an international cohort of
intensive care unit patients. JAMA 1993;270:2478-86
(4) Knaus WA, Wagner DP, Draper EA, Zimmerman JE et al. The APACHE III
prognostic system: risk prediction of hospital mortality for critically
ill hospitalized adults. Chest 1991;100:1619-36
(5) Pearson G, Shann F, Barry P, Vyas J et al. Should paediatric intensive
care be centralised? Trent versus Victoria. Lancet 1997;349:1213-7
(6) Bennett NR. Provision of paediatric intensive care services. Br J Hosp
Med 1997;58:368-71
(7) De Courcy-Golder K. A strategy for development of paediatric intensive
care within the United Kingdom. Intens Crit Care Nurs 1996;12:84-9
I read with interest the report on ulceration of the palm due to
playing Nintendo [1] since I have published an almost identical case: a 9-
year-old girl sustained ulceration of the palm from playing "Mario Party"
on the Nintendo 64 video game console [2] (please access publication and
photos on http://www.mja.com.au/public/issues/173_11_041200/koh/koh.html
). This game caused the injury because some players tend to use...
I read with interest the report on ulceration of the palm due to
playing Nintendo [1] since I have published an almost identical case: a 9-
year-old girl sustained ulceration of the palm from playing "Mario Party"
on the Nintendo 64 video game console [2] (please access publication and
photos on http://www.mja.com.au/public/issues/173_11_041200/koh/koh.html
). This game caused the injury because some players tend to use their
palms to rapidly rotate the joystick. I would like to share several
important lessons with your readers who may be writing up unusual clinical
cases.
Whilst writing up our case I did a search for "Nintendo" in PubMed
(National Library of Medicine) [3] and found cases of repetitive strain
injuries including nintedinitis of the elbow, wrist and neck, Nintendo
induced incontinence and epilepsy. There were no reports in PubMed of
ulceration associated with playing Nintendo. I therefore submitted in
October 2000 a case report of "ulcerative nintendinitis". The publication
[2] attracted a lot of pre-Christmas 2000 media interests including 17
radio interviews. One interviewer suggested that the injury must surely
be an exceedingly rare occurrence. A radio listener advised that I access
the Internet search engine Altavista to look for sites on "Nintendo".
This I did and easily found two relevant sites. One was a press release
[4] on 8th March 2000 by the Attorney General of New York: following 90
complaints of hand injuries including blisters and cuts, Nintendo of
America agreed to provide up to four protective gloves to each owner of
the video game "Mario Party". Nintendo of America is committing US$80
million for the gloves in North America.
The second site is a chat site for users of video games. I accessed
their discussions for the 8th March 2000 (on the same day of the press release
from the Attorney General of New York) and found 28 postings where the
authors mentioned that they had blisters of their hands / thumbs whilst
playing video games.[5]
When I read the article in your Journal I keyed in "Nintendo" and
also my name in Pubmed (accessed 1st May 2001) and found that whilst your
article was listed in Pubmed, the report in the Medical Journal of
Australia was not. [6]
My experiences with the Internet suggest that clinical conditions,
which have not been reported by doctors, may already have been described
elsewhere on the Internet. This is the second example of the benefits of
accessing the Internet when one is writing up a rare clinical case.[7]
Another point is that not all publications are listed in Pubmed. The
above reiterated the importance of using other Internet search engines to
complement the usual search in PubMed when it comes to reporting unusual
clinical cases.
Yours sincerely,
Koh T.H.H.G., BA (Oxon), MA, MBBChir(Cantab), FRCPCH, FRACP,
Senior Specialist in Neonatal Paediatrics
Kirwan Hospital, Thuringowa QLD 4817 Australia
Phone 0747730363 Fax 0747732103 guan_koh@health.qld.gov.au
References:
1. Wood J. The "How!" sign--a central palmar blister induced by
overplaying on a Nintendo console.
Arch Dis Child. 2001 Apr;84(4):288.
In a reaction to our article,[1] in which the natural history of cardiovascular manifestations in 52 children and adolescents with Marfan syndrome is described, Dr Venugopalan highlights the role of beta-adrenergic blocker therapy in retarding the progress of aortic dilatation.[2] As stated on page 135 of the Discussion in our article, the use and effectiveness of this prophylactic pharmacotherapy was well-kno...
I would like to draw your attention to the need for prophylaxis against RSV in another high risk group of infants who are being excluded at present. Infants with congenital heart diseases have altered anatomy/physiology which make them more prone to infection with the virus with devastating consequences. They do very badly when infected with such a virus. While infants with normal anatomy and physiology have...
Pearson and colleagues have presented data highlighting the use of the PIM score as a tool for auditing paediatric intensive care unit (PICU) performance.[1] Whilst we would agree with the authors' message that PIM has many advantages over other scoring systems, we feel that urgent calibration is needed before this tool is adopted as a benchmark for performance indication in the UK. PIM variables were develope...
Dear editor,
I read the article of Dr M Riordan on investigation and treatment of facial paralysis in the April issue of the journal with a special interest. It is indeed a well-composed article. However I would like to elaborate some interesting points.
1.Although facial nerve paralysis is the commonest cause of facial weakness, weakness of facial muscles forms another interesting spectrum of facial w...
I read with great interest "An audit of RCP guidelines on DMSA scanning after UTI 1". I have recently presented a similar audit at Furness General Hospital, Barrow-in-Furness (29th March,2001), looking at DMSA scan in children with UTI. 75 children between the age group of 0-7 years who had DMSA scan, between 1st January to 31st December 2000 were included in my audit. The exclusion criteria were similar to the p...
Dear Editor,
The argument against the use of passive prophylaxis against RSV infections in children with congenital heart disease (CHD) has more to do with the lack of effectiveness and increased incidence of serious adverse events in such 'prophylaxed' children than with its 'cost effectiveness'. The last such attempt (Simoes EAF, Sondheimer HM, Top FH, et al. Respiratory syncytial virus immune globuli...
We read with interest the article on the need for and the role of a co- ordinator in the provision of child health surveillance (CHS)[1] and particularly the need to work with the Primary Care Team in developing quality standards.
We have used such standards in City and Hackney for the past 5 years. When a General Practitioner (GP) applies to join the CHS list the Consultant Community Paediatrician...
Dear Editor,
I write with regard to the recently published protocol for treating attention deficit/ hyperactivity disorder.[1] I would like to comment specifically on a few points.
The authors suggest a trial of an elimination diet if the history suggests that dietary factors might be significant, drawing on one paper to suggest that 'there is evidence for the effectiveness of an individually constru...
Dr Tibby and Dr Murdoch note that, in our study of paediatric intensive care units (PICUs) in the UK [1], PIM discriminated well between children who died and children who survived, with an area under the ROC curve of 0.84. However, they are concerned that PIM had "poor calibration" because the standardised mortality rate (SMR) in the UK units was 0.87 (95% CI 0.81-0.94) - that is, the actual number of deaths was only 87...
I read with interest the report on ulceration of the palm due to playing Nintendo [1] since I have published an almost identical case: a 9- year-old girl sustained ulceration of the palm from playing "Mario Party" on the Nintendo 64 video game console [2] (please access publication and photos on http://www.mja.com.au/public/issues/173_11_041200/koh/koh.html ). This game caused the injury because some players tend to use...
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