If sleep studeis are worth doing, they are worth doing well. The study of
sleep disordered breathing is another area of paediatrics that the UK has
stumbled to embrace.[1, 2] Sleep medicine has exponentially increased in
adults in recent years, yet in paediatrics many questions remain
unanswered.
While, van Someren et al made a valiant attempt to answer an
important question,[3] they did...
If sleep studeis are worth doing, they are worth doing well. The study of
sleep disordered breathing is another area of paediatrics that the UK has
stumbled to embrace.[1, 2] Sleep medicine has exponentially increased in
adults in recent years, yet in paediatrics many questions remain
unanswered.
While, van Someren et al made a valiant attempt to answer an
important question,[3] they did so by assessing clinical scores in
relation to a standard which was far from gold, and as such accuracy could
not be determined, only inferred. Clinical scores or simple oximetery are
limited in their ability to identify obstructive sleep apnoea (OSA), being
able to identify significant OSA but not mild/moderate cases.[4, 5] Data
is now accumulating that even mild OSA may be associated with significant
neurocognitive morbidity in children.[6, 7] Full polysomnography is the
current gold standard. The Visilab has not been satisfactorily validated
against full polysomnography, and the results presented in the paper
demonstrated a discrepancy in 2 of 10 simultaneous recordings (a 20% error
rate) with important differences in mean oxygen saturation between the two
systems (93% vs 95%). It is true that full polysomnography may not be
required in all children for the diagnosis of OSA, however this process
should be one of working down from a gold standard rather than edging up
towards it. The arguments used by van Someren against the use of full
polysomnography are weak. Children in dedicated sleep areas tolerate full
polysomnography well: In the 54 full polysomnographic OSA studies
performed in the past 6 months in this unit, sleep efficiency was a mean
of 90% (sd 8%), which includes children with frequent wakening as a result
of their OSA!
Centres in both North America and Australia have dedicated
significant funding in recent years to paediatric sleep laboratories and
the appropriate training of both nursing and medical staff through
specific specialist training criteria; the UK sadly lacks such support.
With the exception of one paediatric unit (concentrating on sleep in rare
disorders) sleep related research in the UK is linked to adults centres.
UK paediatrics needs a sleep medicine wake up call, so that standards can
be set from gold.
Steve Cunningham Margaret Harris Consultants in Paediatric Respiratory Medicine
Department of Paediatric Respiratory and Sleep Medicine Mater
Children’s Hospital Brisbane, Australia
References
(1) Shann F. Australian view of paediatric intensive care in Britain.
Lancet 1993;342:68.
(2) Wheeler R, Foote K. Pectus excavatum: studiously ignored in the
United Kingdom? Arch Dis Child 2000;82:187-8.
(3) van Someren V, Burmeister M, Alusi G, Lane R. Are sleep studies
worth doing? Arch Dis Child 2000;83:76-81.
(4) Carroll JL, McColley SA, Marcus CL, Curtis C, Loughlin GM.
Inability of clinical history to distinguish primary snoring from
obstructive sleep apnea syndrome in children. Chest 1995;108:610-8.
(5) Brouilette RT, Morielli A, Leimanis A, Waters KA, Luciano R,
Ducharme FM. Nocturnal pulse oximetry as an abbreviated testing modality
for pediatric obstructive sleep apnea. Pediatrics 2000;105:405-12.
(6) Kennedy D. Neurocognitive function in childhood obstructive sleep
apnoea syndrome (OSAS). 6th World Congress on Sleep Apnea. March 2000;
Sydney, Australia.
(7) Ali NJ, Pitson D, Stradling JR. Sleep disordered breathing: effects
of adenotonsillectomy on behaviour and psychological functioning. Eur J
Pediatr 1996;155:56-62.
I am grateful to Dr Waterston for his commentary. In order to
clarify the issues that he raised, I will confirm the following:
(1) I was suggesting that the practice in all branches of tertiary
paediatrics should be considered as a disability service from the
perspective of the family and child’s predicament. I was not confining
the proposal to traditional neurodisability.
I am grateful to Dr Waterston for his commentary. In order to
clarify the issues that he raised, I will confirm the following:
(1) I was suggesting that the practice in all branches of tertiary
paediatrics should be considered as a disability service from the
perspective of the family and child’s predicament. I was not confining
the proposal to traditional neurodisability.
(2) I was indeed specifically proposing to change the ethos of
hospital services.
(3) My consultation has been with a number of support groups which are
part of Contact a Family.
(4) I have no problem with supporting community paediatrics, providing
we are clear what it is and that it is appropriately resourced, but this
is another issue.
(5) I have no problem about supporting a community based approach to
the whole of paediatrics and have worked with research groups in India,
Bangladesh and Kenya on community based rehabilitation. Whether community
paediatrics as presently practised meets the definition of being a process
which enables disabled people and their families to function and
participate fully within their community and support the primacy of the
community in the use of resources is open to question, as Dr. Waterston I
think agrees. This process would require facilitation of a bottom up
approach, ie, giving power and resources from health, education and
social services to the community, and the research testing of such models.
I was proposing a much more confined revolution of tertiary medicine which
let the users and community into the action reorganising the difficulties
and influence that the people in tertiary services face.
Brian G R Neville
Professor of Paediatric Neurology
The article from the Netherlands by Cappendijk and Hazebroek[1] has again confirmed what is already known in clinical
practice. A recent paper from the Leicester Royal infirmary[2] is almost
identical.
As the authors pointed out, the factors determining the diagnostic
delay are numerous and often cannot be influenced. However, I agree with
their statement that “in a child with abdominal pai...
The article from the Netherlands by Cappendijk and Hazebroek[1] has again confirmed what is already known in clinical
practice. A recent paper from the Leicester Royal infirmary[2] is almost
identical.
As the authors pointed out, the factors determining the diagnostic
delay are numerous and often cannot be influenced. However, I agree with
their statement that “in a child with abdominal pain which do not settle
quickly, appendicitis should be excluded by early and if necessary
repeated surgical consultations”.[1]
The vermiform appendix varies from 2 cm to 24 cm in length, the
average being about 9 cm. It is longer in the child than in the adult. The
position of the appendix shows a high variation in children. [3, 4] This
variation in the location of the appendix in the abdomen explains the
variation of symptoms seen with acute appendicitis. If the appendix is
retrocaecal or located in the posterior portion of the abdomen,
localisation of the pain and tenderness on examination occur late if at
all. If the appendix is posterior in the pelvis, the pain may localise
only to the lower abdomen. And tenderness to palpation is poorly
localised. The diarrhoea of appendicitis is most common in patients with a
low-lying appendix in proximity to the colon and rectum.[5]
We recently saw a 9-year-old boy presenting with maximum tenderness
in the left iliac fossa. There was a 31-hour history of generalised
abdominal pain followed by vomiting. He was referred to the surgeon with
the diagnosis of generalised peritonitis. Examination under anaesthesia
revealed a mass in the left iliac fossa. Laparotomy confirmed a
generalised peritonitis resulting from a left iliac fossa abscess. This
was from a ruptured appendix, the tip of which was in the left iliac
fossa.
References
(1) Cappendijk VC, Hazebroek FWJ. The impact of diagnostic delay on
the course of acute appendicitis. Arch Dis Child 2000;83:64-6
(2) Williams N, Bello M. Perforation rate relates to delayed presentation
in childhood acute appendicitis. J R Coll Surg Edin 1998;43: 101-2
(3) Bakheit MA, Warille AA. Anomalies of the vermiform appendix and
prevalence of acute appendicitis in Khartoum. East Afr Med J 1999;76:338-40
(4) Johnston TB, Whillis J. Gray’s Anatomy 1942; 28th Edition, Longmans,
Green and Co.
(5) Shandling B, Fallis JC. Acute appendicitis. In Nelson’s Textbook of
Paediatrics. 1992; 14th Edition, Behrman R. W.B. Saunders Company
Dr Stephen Kwame Dotse
115 Nab Wood Drive
Shipley, West Yorkshire BD18 4AP, UK
Partsch, Aukamp and Sippell propose that increased testicular
temperature in early childhood might affect later spermatogenesis. They
suggest that 'disposable' nappies could contribute to this and demonstrate
a significant difference between the scrotal skin temperature recorded in
infants using 'disposable' nappies and washable cotton nappies. They
mention in their introductory paragraph that other environ...
Partsch, Aukamp and Sippell propose that increased testicular
temperature in early childhood might affect later spermatogenesis. They
suggest that 'disposable' nappies could contribute to this and demonstrate
a significant difference between the scrotal skin temperature recorded in
infants using 'disposable' nappies and washable cotton nappies. They
mention in their introductory paragraph that other environmental factors
may be important in the deterioration seen in male reproductive health
over recent years, but do not relate any of these factors to disposable
nappies.[1]
There are many concerns about the use of 'disposable' nappies in
addition to increasing scrotal temperature that may impact on future
fertility and general health. The 'disposable' nappy consists of a plastic
outer layer, a layer of superabsorbant chemicals and inner liner. Nappies
are not subject to government controls or independent testing and
'disposable' nappy manufacturers do not need to disclose the
contents.[2][3]
Recently concern has been raised about the presence of Tributyl Tin (TBT) in 'disposable' nappies. Greenpeace and Women's Environmental
Network have commissioned research which showed that there were
significant levels of TBT in many brands of 'disposable' nappy, including
those on sale in the UK.[4][5] Babies may be in contact with up to 3.6
times the WHOs estimated tolerable daily intake. TBT is an environmental
pollutant which is used in anti-fouling ship paint. It is known to disrupt
the endocrine and immune function of marine shellfish and there are
international plans to phase out its use.
The superabsorbant chemicals used include sodium polyacrylate
crystals which form a gel in contact with urine. This gel can be seen on
the skin in contact with it and there are particular concerns about this
entering the body through broken skin in the nappy area. Sodium
polyacrylate has been removed from tampons as it was associated with the
development of Toxic Shock Syndrome.[6] The inner liner has previously
been shown to contain nonylphenyl ethoxylate, which acts as an oestrogen
mimic, and dioxins.[3]
In addition the use of 'disposable' nappies has important
environmental consequences which may impact on child health. Manufacture
of 'disposable' nappies uses 3.5 times more energy, 8 times as many non-
renewable resources and 90 times as many renewable resources when compared
to washable nappies. The description of nappies as disposable is
misleading. In this country nappies make up approximately 4% of household
waste (800 000 tonnes per year) and every 'disposable' nappy and its
contents ever used is still present in a landfill site.[2]
There are environmentally friendly and safe alternatives to the
'disposable' nappy. Modern washable nappies are very different to the
traditional idea of buckets of terries. There are now shaped cotton
nappies with velcro fastenings, alternatives to nappy pins, breathable
covers and disposable paper inner liners. Concern that the incidence of
nappy rash is higher with washable nappies is unfounded - it has been
shown that it is the length of contact of urine with the skin that is most
important in the development of nappy rash[7] and it may be that an infant
in a 'disposable' has more chance of developing nappy rash as they are
often changed less frequently than an infant in washable nappies. In
addition there are cost savings both to individuals and organisations
using washable nappies and there have been several successful hospital
projects using washable nappies on post natal wards.[2][3]
As paediatricians committed to the health of children we should be
aware of the issues raised by the use of 'disposable' nappies, the
alternatives that exist and sources of information and support for
parents who are concerned about ensuring a safe and sustainable future for
their children.
Dr Carrie Heal
Dr Chris Cooper
Consultant Paediatricians, Royal Albert Edward Infirmary, Wigan, UK
References
(1) Partsch C-J, Aukamp, Sippell WG. Scrotal temperature is increased in
disposable plastic lined nappies. Arch Dis Child 2000;83:364-8.
(2) Link A. Preventing Nappy Waste Women's Environmental Network 1996.
(3) Sustainable Wales. Dumping the Diaper! Reusable Nappy Report.
(4) Greenpeace. Greenpeace calls on parents to return contaminated nappies
to producers: new tests show that TBT-free nappies are a rarity. Press
Release 19th May 2000 www.greenpeace.org.
(6) Reingold AL Toxic shock syndrome: an update. Am J Obstet Gynecol 1991;165(4pt2):1236-9.
(7) Philipp R, Hughes A, Golding J. Getting to the bottom of nappy rash.
ALSPAC Survey Team. Avon Longitudinal Study of Pregnancy and Childhood. Br
J Gen Pract 1997;47:493-7.
We welcome the debate stimulated by our paper. Indeed, this was our
aim in publishing it.
We agree with Mr Caldwell that a degree of underreporting is likely.
Our system provides a clear definition to all staff of what constitutes a
reportable medication error (listed in the appendix). It does not include
errors that are averted such as mis-prescribed errors corrected by
pharmacists prior to dis...
We welcome the debate stimulated by our paper. Indeed, this was our
aim in publishing it.
We agree with Mr Caldwell that a degree of underreporting is likely.
Our system provides a clear definition to all staff of what constitutes a
reportable medication error (listed in the appendix). It does not include
errors that are averted such as mis-prescribed errors corrected by
pharmacists prior to dispensing. We also noted that error-reporting rates
vary widely in the literature. We discussed some of the reasons advanced
to explain such variations, such as whether the reporting system is
mandatory or voluntary and the intensity of the search for errors.
However, the published evidence about medication error rates in paediatric
settings is very limited especially in the context of a nationally funded,
universal, health care system such as the NHS. There is, therefore, little
firm paediatric evidence to support Mr. Caldwell's opposite view that
errors are "…extremely common, overlooked and often ignored."
In our experience, most reported errors were minor. Serious events
with adverse outcomes were uncommon and, we think, are unlikely not to be
reported. If anything, we would suspect it is minor errors that are most
likely to go unrecorded. This may be of considerable importance if
analysis of minor events highlights system problems whose correction may
help avoid future serious incidents.
Mr Caldwell suggests that voluntary systems may increase error
reporting. It needs to be recognized that voluntary systems are not a
panacea but may also detect only a fraction of overall errors. Again, we
would suspect that minor errors might most likely be missed. The thrust of
the editorial by Cohen[1] appears to relate to errors with serious adverse
outcomes. There are also some potential difficulties with voluntary
systems. For example, how we do we ensure that parents are notified about
error occurrence if reporting is voluntary? What happens about errors of
such seriousness that issues of criminal negligence arise?
Whether a reporting system is mandatory or voluntary probably is less
important than that the system is non-punitive. This is borne out by the
findings of Vincer et al[2] who found approximately a four to six- fold
increase in the reporting of errors by reducing the punitive aspects of
the form by making it an "incident" rather than an "error" form. We have
no doubt that the critical challenge for us all is to make the shift from
assuming "errors" arise from individual negligence to recognising that
"incidents" more usually arise because of systemic organisational
failures. We urgently need to move away from a culture of "fixing the
blame" towards one of recognising and "fixing the problem".
References
(1) Cohen MR. Why error reporting systems should be voluntary. BMJ 2000;320:728-9.
(2) Vincer MJ, Murray JM, Yuill A, Allen AC, Evans JR, Stinson DA. Drug errors and incidents in a neonatal intensive care unit. A quality assurance activity. Am J Dis Child 1989;143:737-40.
Cappendijk and Hazebroek (Arch Dis Child 2000;83:64-6) conclude from
their data that "the major factor in delay is suspected gastroenteritis".
Other studies have not given this factor such prominence and the study
population suggests that the Sophia Hospital was acting as a referral
centre: 32 of 78 children whose admission was delayed for 48 hours had
been seen first by a paediatrician, which may i...
Cappendijk and Hazebroek (Arch Dis Child 2000;83:64-6) conclude from
their data that "the major factor in delay is suspected gastroenteritis".
Other studies have not given this factor such prominence and the study
population suggests that the Sophia Hospital was acting as a referral
centre: 32 of 78 children whose admission was delayed for 48 hours had
been seen first by a paediatrician, which may increase the numbers with
suspected gastroenteritis.
In seeking the chief causes of delayed diagnosis it is helpful to
study all children referred to a district hospital from its catchment
area. Jackson in Newcastle found that parental delay over consulting the
family doctor was important and then, in nearly one-third of 311 home
visits, the practitioner did not decide until a second visit that
admission to hospital for ?acute appendicitis was needed.[1] Jackson, a
paediatrician, did not identify gastroenteritis as a factor. Other work
confirms these findings.[2]
In Aberdeen over 300 children are admitted annually from our region
with acute abdominal pain, and have been studied prospectively since 1965.[3, 4] This soon revealed that about one-third had acute appendicitis, one-third progressively settled without treatment (acute non-specific
abdominal pain, or NSAP) and others had medical and surgical conditions.
Among one year's admissions we found that 20 (18%) of 114 children with
proven acute appendicitis complained of diarrhoea compared with 9% of 119
children with NSAP. Of the 20, 15 had rectal tenderness and proved to have
pelvic appendicitis or peritonitis: we emphasised the importance of
identifying, among the many children with gastroenteritis seen by family
doctors, the few who also complain of abdominal pain, who require careful
abdominal and rectal examination.[3] The practice of "Active Observation"
encourages this.[4]
Occasionally delay in diagnosis of appendicitis is seen by the
surgeon on a call to the
isolation ward, where a child has been mistakenly sent in with suspected
gastroenteritis, but this has not, over the years, been a major problem.
Peter F Jones Emeritus Clinical Professor of Surgery University of Aberdeen, UK
References
(1) Jackson RH. Parents, family doctors and acute appendicitis in childhood. BMJ 1963;ii:277- 81.
(2) Moss JG, Barrie JL, Gunn AA. Delay in surgery for acute appendicitis. J R Coll Surg Edin 1985;30:290-3.
(3) Winsey HS, Jones PF. Acute abdominal pain in childhood: analysis of a year's admissions. BMJ 1967;i:653-5.
(4) Driver CP, Youngson GG. Acute abdominal pain in children: a 25-year comparison. Health Bulletin 1995;53:167-72.
The recent study by Hutton, Colver, and Mackie[1] is in some
respects a useful addition to our knowledge of survival in cerebral palsy.
Unfortunately there some are substantial problems with the paper; we note
three of them below.
In Figure 1A it appears that in the most seriously affected group,
LAS >70%, there is 100% survival to age 9. This scarcely seems
plausible when, as the graph indicate...
The recent study by Hutton, Colver, and Mackie[1] is in some
respects a useful addition to our knowledge of survival in cerebral palsy.
Unfortunately there some are substantial problems with the paper; we note
three of them below.
In Figure 1A it appears that in the most seriously affected group,
LAS >70%, there is 100% survival to age 9. This scarcely seems
plausible when, as the graph indicates, 20% of these survivors die in the
next 9 years. The explanation is that the most severely disabled children,
with LAS 70% or more, have to survive to age 5 to be assessed by LAS. Thus
the severely disabled children who die before 5 have no LAS, and are
excluded (actually, it appears from the graph that some children are
evaluated even later than age 5).
The resulting bias could have serious consequences. For example, in a
lawsuit involving a neurologically devastated 2-year old child a plaintiff
may cite Hutton et al to argue for 100% survival over the next seven years.
Hutton et al's results show that, as is well known, low IQ and/or poor
mobility correlate with reduced life expectancy. In his commentary, Dr Rosenbloom usefully asks whether extreme immobility or mental impairment
would give an even greater reduction. The answer is clearly yes, as
indicated by our own work[2][3] and is also acknowledged by other workers in
the area (Evans et al[4] Crichton et al[5]). Indeed it must be so because
an extensive literature shows a much shortened survival in the persistent
vegetative state,[6] which may be regarded as the extreme case of
disability.
In neither Hutton et al's nor in Hutton's previous study of the Merseyside area[7] is this possibility mentioned. As a result, the latter study has
frequently lead plaintiffs to overestimate survival of children with the
most severe disabilities.
In their Table 5, Hutton et al state that in our California study[2] the odds
ratios for various hazards were lower than in several other studies. For
example, in Table 2 of our article we gave a hazard ratio of 3.8 for two
year-olds who were tube fed, compared to those who were not. Hutton et al then
proceeded to speculate at some length on what accounts for the
transatlantic difference.
The real reason is simple: the California data base has many more
variables other data bases, so the marginal effect of any one of them -- ie, when the others are held constant -- is smaller. For example, our
Table 1 showed that if no other factors are taken into account the hazard
ratio for tube feeding (compared to children who could self-feed) was 23.6
-- a much larger ratio than the above 3.8, and in fact about as large as
any in Hutton et al's Table 5. In addition, the definitions of mobility etc. in the
various studies are very different.
David Strauss, PhD, FASA
Emeritus Professor of Statistics
Robert Shavelle, PhD
University of California Life Expectancy Project
References
(1) Hutton JL, Colver AF, Mackie PC. Effect of severity of
disability on survival in north east England cerebral palsy cohort. Arch
Dis Child 2000;83:468-74.
(2) Strauss DJ, Shavelle RM, Anderson TW. Life expectancy of
children with cerebral palsy. Pediatr Neurol 1998;18:143-9.
(3) Strauss DJ, Shavelle RM. Life expectancy of adults with
cerebral palsy. Dev Med Child Neurol 1998;40:369-75.
(4) Evans PM, Evans SJW, Alberman E. Cerebral palsy: Why we must plan for survival. Arch Dis Child 1990;65:1329-33.
(5) Crichton, JU. Response to Letter from Professor Hall. Dev
Med Child Neurol 1995;37:1031-3.
(6) Multi-society task force on PVS. Medical Aspects of the
Persistent Vegetative State, Part I. N Engl J Med 1994;330:499-1508.
(7) Hutton JL, Cooke T, Pharoah POD. Life expectancy in
children with cerebral palsy. BMJ 1994;309:431-5.
Poustie et al state that there is no computer package available in the United Kingdom
for calculating percentage weight for height (%WFH). This is incorrect
and for many years there has been available just such a package entitled
W4H under the copyright of Great Ormond Street Hospital for Children NHS
Trust. The program can be used on any version of Windows from 3.1
onwards, Excel, and on Psion's. This p...
Poustie et al state that there is no computer package available in the United Kingdom
for calculating percentage weight for height (%WFH). This is incorrect
and for many years there has been available just such a package entitled
W4H under the copyright of Great Ormond Street Hospital for Children NHS
Trust. The program can be used on any version of Windows from 3.1
onwards, Excel, and on Psion's. This program was produced by the Eating
Disorders Research Team at Great Ormond Street but can be purchased from
the address below:
Dr Bryan Lask
Child and Adolescent Eating Disorders Research Team
Department of Psychiatry
Jenner Wing, St George's Hospital Medical School
London SW17 0RE, UK
The accurate diagnosis of meningococcal disease is important, not
only for the welfare of the patient, but also for the implementation of
appropriate public health measures. Brogan and Raffles have made a useful
contribution to more reliable diagnosis.[1]
However I feel that their finding of 9% could represent a falsely low
proportion of children with serious bacteraemia because of potential
recru...
The accurate diagnosis of meningococcal disease is important, not
only for the welfare of the patient, but also for the implementation of
appropriate public health measures. Brogan and Raffles have made a useful
contribution to more reliable diagnosis.[1]
However I feel that their finding of 9% could represent a falsely low
proportion of children with serious bacteraemia because of potential
recruitment bias and measurement bias. Knowing that children would not be
given antibiotics if entered into the study, unless they met the ILL
criteria or had a raised WCC or CRP, may have led admitting doctors to
exclude some children that they felt uneasy about observing. This could
easily have been achieved by describing the rash as >2mm for instance
(it is not stated whether the rash was measured or judged by eye).
Secondly it is questionable whether they had discovered all the
bacteraemias. Blood culture or remaining well after discharge could miss
bacteraemia in those children treated with antibiotics before admission or
given a short course in hospital. PCR would have been a useful additional
diagnostic test.
This study is a useful first step, but as the authors say, needs to
be followed up with a prospective trial. The recruiters and assessors of
the children to the study are not the managing clinicians and the
diagnosis of bacteraemia is more thoroughly sought. This is important to
validate the diagnostic technique and also the positive predictive value
of the combination of petechiae and fever.
Reference
(1) Brogan PA, Raffles A. The management of fever and petechiae: making sense of rash decisions. Arch Dis Child 2000;83:506-7.
We read with interest the work of Male et al on perception of breathlessness in acute asthma. They studied 27 children with acute asthma, 12 of whom were hypoxic at presentation with SaO2...
We read with interest the work of Male et al on perception of breathlessness in acute asthma. They studied 27 children with acute asthma, 12 of whom were hypoxic at presentation with SaO2 <_92. children="children" presenting="presenting" with="with" significant="significant" hypoxia="hypoxia" sao292="sao292" are="are" considered="considered" as="as" a="a" group="group" who="who" report="report" late="late" to="to" hospital="hospital" and="and" risk="risk" death="death" from="from" asthma="asthma" presenters="presenters" those="those" sao2="sao2"/>92% (early presenters). Perception of breathlessness was measured by what the children reported as the amount of puff they had (HMP score). This was measured on a six-point scale using the concept of blowing up a balloon. Spirometric criteria of respiratory function were measured at admission and at various points during recovery. The authors found lower HMP scores in the hypoxic population, (4 vs 3, p=0.062). They further showed higher HMP/FEV1 ratios in children presenting with hypoxia. They concluded that those with lower SaO2 at presentation perceived breathlessness poorly. This could in some children, contribute to their late presentation and/or death from asthma. At the same value of FEV1 the late presenter reported a higher puff. The result of a high value of HMP/FEV1 in children presenting with significant hypoxia is a remarkable finding from the study.
But the physiological relation of low FEV1 with hypoxia and the possibility of different permutations of FEV1 and HMP score capable of yielding the same ratio preclude the use of this ratio alone as an identifier of the late presenter. The authors acknowledging this handicap went on to examine change in HMP score (from the time of admission to 72 hours), per unit change in FEV1 (deltaHMP/deltaFEV1) per percent of predicted value, against initial SaO2. The hypoxic population was found to have significantly lower dHMP/dFEV1 ratios (median 0.021%-1 vs 0.073%-1 with a p=0.0081).
One child for instance, with SaO2 of 84% at presentation had a dHMP/dFEV1 of 0.04,whereas another with SaO2 of 98% at presentation had a dHMP/dFEV1 of 0.08 (figure 5). The authors conclude, that because the former was reporting a lower improvement than what he had actually undergone, his perception was faulty. This child, they state was at risk of dying because he would stay back home longer, continuing to deteriorate.
There is another way of looking at the data. The child reporting a lower improvement, is essentially a whiner, or the one who genuinely feels so much worse, or, tolerates so little breathlessness. If he were to behave similarly at home as he was in hospital -reporting himself more breathless for his airway obstruction, he would be the one to come so much earlier to medical attention. It is not clear, how the authors assume that the vociferous whiner in improvement, would be a silent sufferer (not perceiving a critical compromise in his lung functions), during worsening.
A high HMP/FEV1 at presentation correctly identifies the faulty perceiver, who reports himself better than his pulmonary parameters. It reflects truthfully the changes in perception and worsening obstruction, in the period immediately preceding presentation. But, a low dHMP/dFEV1, measured in the course of improvement, confounded by presumably more aggressive treatment including oxygen administration for lower SaO2, does not seem a logical parameter to identify those at risk of death from late presentation. Further research is required to identify other characteristics of the subpopulation of asthmatics, who are at a greater risk of late presentation and death from asthma, and also, whether faulty perception of improvement, identified by a low dHMP/dFEV1 is, one of their traits.
References
(1) Barnes P. Blunted perception and death from asthma. N Eng J Med 1994;330:1383-4.
(2) Kikuchi Y, Okabe S, Tamura G, et al. Chemosensitivity and perception of dyspnea in patients with a history of near fatal asthma. N Eng J Med 1994;330;1329-34.
(3) Male I, Seddon P. The measurement of breathlessness in children with asthma. Am J Resp Crit Care Med 1996;153:A557.
Dear Editor:
If sleep studeis are worth doing, they are worth doing well. The study of sleep disordered breathing is another area of paediatrics that the UK has stumbled to embrace.[1, 2] Sleep medicine has exponentially increased in adults in recent years, yet in paediatrics many questions remain unanswered.
While, van Someren et al made a valiant attempt to answer an important question,[3] they did...
Dear Editor:
I am grateful to Dr Waterston for his commentary. In order to clarify the issues that he raised, I will confirm the following:
(1) I was suggesting that the practice in all branches of tertiary paediatrics should be considered as a disability service from the perspective of the family and child’s predicament. I was not confining the proposal to traditional neurodisability.
(2)...
Dear Editor
The article from the Netherlands by Cappendijk and Hazebroek[1] has again confirmed what is already known in clinical practice. A recent paper from the Leicester Royal infirmary[2] is almost identical.
As the authors pointed out, the factors determining the diagnostic delay are numerous and often cannot be influenced. However, I agree with their statement that “in a child with abdominal pai...
Partsch, Aukamp and Sippell propose that increased testicular temperature in early childhood might affect later spermatogenesis. They suggest that 'disposable' nappies could contribute to this and demonstrate a significant difference between the scrotal skin temperature recorded in infants using 'disposable' nappies and washable cotton nappies. They mention in their introductory paragraph that other environ...
We welcome the debate stimulated by our paper. Indeed, this was our aim in publishing it.
We agree with Mr Caldwell that a degree of underreporting is likely. Our system provides a clear definition to all staff of what constitutes a reportable medication error (listed in the appendix). It does not include errors that are averted such as mis-prescribed errors corrected by pharmacists prior to dis...
Dear Editor
Cappendijk and Hazebroek (Arch Dis Child 2000;83:64-6) conclude from their data that "the major factor in delay is suspected gastroenteritis". Other studies have not given this factor such prominence and the study population suggests that the Sophia Hospital was acting as a referral centre: 32 of 78 children whose admission was delayed for 48 hours had been seen first by a paediatrician, which may i...
The recent study by Hutton, Colver, and Mackie[1] is in some respects a useful addition to our knowledge of survival in cerebral palsy. Unfortunately there some are substantial problems with the paper; we note three of them below.
In Figure 1A it appears that in the most seriously affected group, LAS >70%, there is 100% survival to age 9. This scarcely seems plausible when, as the graph indicate...
Poustie et al state that there is no computer package available in the United Kingdom for calculating percentage weight for height (%WFH). This is incorrect and for many years there has been available just such a package entitled W4H under the copyright of Great Ormond Street Hospital for Children NHS Trust. The program can be used on any version of Windows from 3.1 onwards, Excel, and on Psion's. This p...
The accurate diagnosis of meningococcal disease is important, not only for the welfare of the patient, but also for the implementation of appropriate public health measures. Brogan and Raffles have made a useful contribution to more reliable diagnosis.[1]
However I feel that their finding of 9% could represent a falsely low proportion of children with serious bacteraemia because of potential recru...
We read with interest the work of Male et al on perception of breathlessness in acute asthma. They studied 27 children with acute asthma, 12 of whom were hypoxic at presentation with SaO2...
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