We read with interest the study and recommendations by Brogan and
colleagues (Arch Dis Child 2000;83:506-507). We agree with them on a
number of issues and wish to draw attention to the following points.
(1) Previous international studies do not support a temperature of
>37.4oC as an inclusion criteria of significant fever for significant bacterial sepsis (SBS).[1][2] A minimum tempe...
We read with interest the study and recommendations by Brogan and
colleagues (Arch Dis Child 2000;83:506-507). We agree with them on a
number of issues and wish to draw attention to the following points.
(1) Previous international studies do not support a temperature of
>37.4oC as an inclusion criteria of significant fever for significant bacterial sepsis (SBS).[1][2] A minimum temperature of
38oC for 0 to 2 month old and 39oC for 3-36 month old children is recognised as an indicator of SBS. Hypothermia may also be significant. In children older than 3 years, the highest recorded temperature of 40oC or more in association with other
parameters may be more significant. Interestingly, in their own series, 4/5 with SBS had temperatures of 38.9 to 40.4oC. We propose
that a temperature of at least 38oC should be considered as significant fever.
(2) Lethargy has been mentioned as one of the diagnostic criteria of SBS.
As a diagnostic criterion, it should be defined more objectively rather
than as proposed by the authors. It may be defined as "a
level of consciousness characterised by poor or absent eye contact or as
the failure of a child to recognise parents or caregivers or to interact
with persons or objects in the environment."[3]
(3) Although we fully agree with the cautious interpretation of total WBC
count in relation to serious sepsis, we would like to mention the
importance of absolute neutrophil count (ANC) more than 10000/microlitre, especially in pneumococcal and to some extent in meningococcal sepsis. ANC
of more than 10000 has 76% sensitivity, 78% specificity and 99.2% negative
predictive value in pneumococcal sepsis.[4]
(4) The term toxic needs to be defined as a clinical picture consistent
with a varied constellation of lethargy, poor perfusion or marked
hypo/hyperventilation.[3]
We therefore suggest that the aide-memoir of significant bacterial sepsis
should be modified from ILL to ILLNESS: Irritability, Lethargy, Low capillary refill, Neutrophilia/Neutropenia, Elevated (or low) temperature suggests Significant Sepsis.
Dr S Mukherjee
Senior House Officer
Dr L Patel
Senior Lecturer and Honorary Consultant
References
(1) Baker MD. Evaluation and management of infants with fever. Pediatr Clin North Am 1999;46:1061-72.
(2) McCarthy PL, Lembo RM, Fink HD, Baron MA, Cicchetti DV. Observation, history and physical examination in diagnosis of serious illness in febrile children of less than or equal to 24 months. J Pediatr 1987;110:26-30.
(3) Baraff Lj, BassJW, Fleisher RF, Klein JD, McCracken GH, Powel KR, Schringer DL. Practice guideline for management of infants & children 0-36 months of age with fever without focus. Pediatrics 1993;92:1-12.
(4) Kuppermann N, Fleisher GR, Jaffe DM. Predictor of occult pneumococcal bacteremia in young febrile children. Ann Emerg Med 1998;31:679-87.
In reply to the comments by Yim Yee Chan and R Lakshman in which they
ask if all patients truely suffered from appendicitis in our study group.
The answer is that histopathological investigation confirmed the diagnosis
appendicitis in all cases.
Yours sincerely,
VC Cappendijk, MD and FWJ Hazebroek, MD, PhD
Department of Paediatric Surgery, Sophia Children's Hospital...
In reply to the comments by Yim Yee Chan and R Lakshman in which they
ask if all patients truely suffered from appendicitis in our study group.
The answer is that histopathological investigation confirmed the diagnosis
appendicitis in all cases.
Yours sincerely,
VC Cappendijk, MD and FWJ Hazebroek, MD, PhD
Department of Paediatric Surgery, Sophia Children's Hospital University
Hospital Rotterdam The Netherlands
The treatment of childhood asthma is controversial: although
oral glucocorticoid treatment in children with asthma was
associated with clinical improvement.[1] There are concerns
about corticosteroids, since stopping drug treatment in
children with asthma results in clinical deterioration,[2]
or in the return of bronchial hyperresponsiveness within two
weeks,[3] with the obvious conclusion that the nat...
The treatment of childhood asthma is controversial: although
oral glucocorticoid treatment in children with asthma was
associated with clinical improvement.[1] There are concerns
about corticosteroids, since stopping drug treatment in
children with asthma results in clinical deterioration,[2]
or in the return of bronchial hyperresponsiveness within two
weeks,[3] with the obvious conclusion that the nature of
drug treatment is suppressive rather than curative. More
importantly, despite prednisolone treatment in acute asthma,
reduction of symptoms and normalisation of pulmonary
function there is evidence of continuing airway inflammation .[1]
However such negative results could be greatly reduced
if more and more pediatricians adopted the practice of
prescribing reduced doses.[4,5] Using the lowest possible
dose and/or alternate-day dosing appears to be safer,[4]
and growth rates[4] and endocrine and lung function return
to normal.[5]
To reduce the risk of systemic effects, it
has been suggested to prefer long acting drugs and start
treatment at 3 PM, since there are no differences compared
to qid dosing, nor influences on 24-h cortisolemia and
cortisoluria.[6]
Completely ignored[1] or disregarded[7] is the issue of
specific immunotherapy (SIT) in children. We have recently
demonstrated that 27/29 (93,1%) controlled studies in 2.042
children and as many controls have shown the effectiveness
of SIT in pediatric age in the treatment of asthma due to
pollens, house dust mites (Der p), epidermal derivatives,
and moulds (p<_0.0001.8 in="in" all="all" studies="studies" the="the" children="children" of="of" control="control" groups="groups" were="were" treated="treated" with="with" available="available" drugs="drugs" and="and" cared="cared" for="for" by="by" their="their" doctors="doctors" as="as" study="study" group.="group." therefore="therefore" _931="_931" have="have" confirmed="confirmed" sit="sit" positive="positive" influence="influence" on="on" natural="natural" history="history" a="a" total="total" remission="remission" asthmatic="asthmatic" symptoms="symptoms" who="who" regularly="regularly" completed="completed" cycle.8="cycle.8" addition="addition" severe="severe" adverse="adverse" reactions="reactions" during="during" are="are" almost="almost" non="non" existent="existent" children.9p="children.9p"/>
From an immunological point of view, oral glucocorticoid
treatment in the children with asthma was associated with
significant reductions in serum concentrations of IL-5,
sCD25, and ECP. However, serum concentrations of IL-5,
sCD25, and ECP remained significantly higher than in
controls, even after treatment with oral glucocorticoids
(p=0.03).[1] Regarding SIT, allergen-induced, in vitro
production of certain cytokines such as IL-4 and IL-10
decreased after SIT; IL-13 (which can induce IgG4 and IgE
antibody production by B cells) increased after SIT.[10]
Therefore IL-13 might play an important role in the
generation of IgG4-blocking antibody during SIT.[10] More
consistent with the reversal of Th2 T cells and associated
cytokines (IL-4 and IL-5) into TH1 T cells and Th1-like
cytokines (IL-2 and IFN-gamma) is the production of IL-12.[11] Thus, the potential ability to shift the Th1/Th2
balance of immune response to allergens creates a favourable
cytokine microenvironment to suppress the allergic reaction
in the asthmatic airway.[12] Accordingly, the production of
IL-5 in asthmatic children treated with corticosteroids[1]
does not appear to be a positive effect.
Arnaldo Cantani, MD, PhD
Professor of Pediatrics
Allergy and Clinical Immunology Division
Monica Micera, MD
University of Roma "La Sapienza"
Viale Regina Elena 324, I 00161 Roma
References
(1) El-Radhi AS, Hogg CL, Bungre JK, Bush A, Corrigan CJ.
Effect of oral glucocorticoid treatment on serum
inflammatory markers in acute asthma. Arch Dis Child 2000;83:158-62.
(2) Waalkens HJ, Van Essen-Zandvliet EE, Hughes MD, et al.
Cessation of long-term treatment with inhaled corticosteroid
(budesonide) in children with asthma results in
deterioration. Am Rev Respir Dis 1993;148:1252-7.
(3) Simons FER, Dolovic J, Moothe DW, et al. A comparison of
beclomethasone, salmeterol, and placebo in children with
asthma. N Engl J Med 1997;337:1659-65.
(4) Kamada AK, Szefler SJ. Glucocorticoids and growth in
asthmatic children. Pediatr Allergy Immunol 1995;6:145-54.
(5) Nicolaizik WH, Marchart JL, Pearce MA, Warner JO.
Endocrine and lung function in asthmatic children on inhaled
corticosteroids. Am J Respir Crit Care Med 1994;150:624-8.
(6) Pincus DJ, Szefler SJ, Ackerson LM, Martin RJ.
Chronotherapy of asthma with inhaled steroids: The effect of
dosage timing on drug efficacy. J Allergy Clin Immunol
1995;95:1173-8.
(7) WHO Position Paper Allergen immunotherapy: therapeutic
vaccines for allergic diseases. Allergy 1998;53(suppl 44):1-42.
(8) Cantani A, Arcese G, Lucenti P, Gagliesi D, Bartolucci M.
A three year prospective study of allergen immunotherapy to
inhalant allergens: evidence of safety and efficacy in 300
children with allergic asthma. J Invest Allergol Clin
Immunol 1997;7:90-7.
(9) Cantani A, Gagliesi D. Specific immunotherapy in
children. Allergy 1996;51:265-6.
(10) Lu FM, Chou CC, Chiang BL, Hsieh KH. Immunologic changes
during immunotherapy in asthmatic children: increased IL-13
and allergen-specific IgG4 antibody levels. Ann Allergy
Asthma Immunol 1998;80:419-23.
(11) Durham SR, Till SJ. Immunological changes associated
with allergen immunotherapy. J Allergy Clin Immunol 1998;102:157-64.
(12) Wang CR, Liu ST, Liu MF, Lee GL, Wang GR, Chuang CY. The
effect of allergen immunotherapy on in vitro IL-4 and
IFN-gamma production by peripheral mononuclear cells in
house dust-sensitive Chinese patients with bronchial asthma.
Asian Pac J Allergy Immunol 1999;17:249-54.
This article tells us that over the last 30 years the US youth
has shown a decrease in total energy consumed, as well as the percentage
of energy from fat and in particular saturated fats. So what are the
conclusions of the article? That "these trends .... may compromise the
health of future US populations". In the discussion section worries are
expressed about low iron and fibre intakes: despite the fact th...
This article tells us that over the last 30 years the US youth
has shown a decrease in total energy consumed, as well as the percentage
of energy from fat and in particular saturated fats. So what are the
conclusions of the article? That "these trends .... may compromise the
health of future US populations". In the discussion section worries are
expressed about low iron and fibre intakes: despite the fact that both
have risen steadily in the past 30 years. Concern is also expressed about
falling calcium intake, due to a decrease in consumption of dairy
products. US milk intake has always been exceptionally high, and being
rich in saturated fat a reduction was probably desirable. However, the
current lower intake still supplies levels of calcium much higher than
those for children in other developed countries.
There seems little doubt that US children are growing fatter, but I
am at a loss to see in what way their dietary intake explains this.
Presumably the reduction in energy intake is offset by an even greater
reduction in activity, but the effect is that the diet of today's
adolescents, though supplying more energy than required for current levels
of activity, in composition terms appears to be healthier than it has ever
been.
The old fashioned disciplinarian mother used to shout to her children
in the next room "whatever you're doing: stop it!". This appears to
still be our attitude to young people as a group. It is sad to see a
scientific article falling back onto the accepted paradigm that the youth
of today are decadent and unhealthy. Could they not have had the
imagination to actually explore the meaning of these results and even dare to suggest that some things might be improving instead of getting worse?
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.
We read with interest the study and recommendations by Brogan and colleagues (Arch Dis Child 2000;83:506-507). We agree with them on a number of issues and wish to draw attention to the following points.
(1) Previous international studies do not support a temperature of >37.4oC as an inclusion criteria of significant fever for significant bacterial sepsis (SBS).[1][2] A minimum tempe...
Dear Editor
In reply to the comments by Yim Yee Chan and R Lakshman in which they ask if all patients truely suffered from appendicitis in our study group. The answer is that histopathological investigation confirmed the diagnosis appendicitis in all cases.
Yours sincerely,
VC Cappendijk, MD and FWJ Hazebroek, MD, PhD
Department of Paediatric Surgery, Sophia Children's Hospital...
The treatment of childhood asthma is controversial: although oral glucocorticoid treatment in children with asthma was associated with clinical improvement.[1] There are concerns about corticosteroids, since stopping drug treatment in children with asthma results in clinical deterioration,[2] or in the return of bronchial hyperresponsiveness within two weeks,[3] with the obvious conclusion that the nat...
This article tells us that over the last 30 years the US youth has shown a decrease in total energy consumed, as well as the percentage of energy from fat and in particular saturated fats. So what are the conclusions of the article? That "these trends .... may compromise the health of future US populations". In the discussion section worries are expressed about low iron and fibre intakes: despite the fact th...
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...
Pages