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 paper by Cappendijk and Hazebroek[1] successfully demonstrates
the problems with diagnosis of appendicitis in the young child.
It makes the important point that diarrhoea may be a feature of
appendicitis and lead to misdiagnosis. In addition, children can have
coexisting pathologies leading to delayed diagnosis. We have seen a cystic
fibrosis child with DIOS (distal intestinal obstruction...
The paper by Cappendijk and Hazebroek[1] successfully demonstrates
the problems with diagnosis of appendicitis in the young child.
It makes the important point that diarrhoea may be a feature of
appendicitis and lead to misdiagnosis. In addition, children can have
coexisting pathologies leading to delayed diagnosis. We have seen a cystic
fibrosis child with DIOS (distal intestinal obstruction syndrome) and
appendicitis. Urinary tract infection and appendicitis can also occur
together.
Children with communication problems and learning difficulties are
another high risk group for delay in diagnosis.
The differential diagnosis of appendicitis is large[2] and a child
who presented with abdominal pain and subsequently had appendectomy need
not necessarily have suffered from appendicitis. We would be interested to
know whether the histopathological results were in agreement with clinical
diagnosis.
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. Hutson JM, Woodward AA and Beasley SW. Jones' Clinical Paediatric
Surgery - Diagnosis and management. Blackwell Science Asia publications.
Fifth Edition. 1999;Chapter 20:page 142.
Poor postnatal weight gain was a significant factor in the
multivariate analysis despite controlling for low birthweight,
prematurity, neonatal problems, poor socio-economic status and many other
potential confounding factors and remained significant when further highly
predictive covariates of SIDS such as infants put down prone, infants
found with head covered and tobacco exposure were added...
Poor postnatal weight gain was a significant factor in the
multivariate analysis despite controlling for low birthweight,
prematurity, neonatal problems, poor socio-economic status and many other
potential confounding factors and remained significant when further highly
predictive covariates of SIDS such as infants put down prone, infants
found with head covered and tobacco exposure were added to the model. In
this sense postnatal weight gain was independently associated with an
increased risk of SIDS. We also found the difference in weight gain
between the two groups measured from birthweight to the last known weight
was equally apparent if measured from birth to the 6 week assessment. We
therefore stand by our conclusion in the abstract that poor postnatal
weight gain ‘was independently associated with an increased risk of SIDS’
and also that poor postnatal weight gain ‘could be identified at the
routine six week assessment’.
We find it difficult to understand how this conclusion advocates an
intervention campaign on the basis of these two statements and disagree
with Logan and colleagues that our discussion on this matter was
circumspect. We point out clearly that poor weight gain itself is not a
sensitive marker and that it ‘should be seen as a thread in a web of
factors that render an infant vulnerable to SIDS and is both a consequence
of adverse health and social conditions’.
We agree that absolute risks must be used for targeted prevention
campaigns but do not advocate such a campaign based on our solitary
finding. Preliminary analysis of risk scoring on the first two years of
our dataset, tested on the third year show that 42% of SIDS families can
be identified from 8% of the population using just a few prenatal factors.
Incorporating postnatal factors such as weight gain may improve the
specificity and sensitivity of such a scoring system.
To our knowledge the “Back to Sleep” campaign initiated in October
1991 has not been evaluated in an appropriately controlled study yet the
SIDS rate in England & Wales more than halved from 1.7 deaths per 1000
livebirths in 1990 to 0.77 deaths in 1992.[1] Findings from our study have
helped build upon the advice regarding safe sleeping practices, parents
are now advised not only to avoid placing infants in the prone position
but also the side position, bed-sharing under certain circumstances,
sharing a sofa to sleep and to avoid head covering by placing the feet of
the infant at the foot of the cot. In 1998 the SIDS rate fell a further
25% in England & Wales to 0.45 deaths per 1000 livebirths.[2] There is
no direct evidence that these recommendations and fall in SIDS rates are
linked although the dramatic fall in the prevalence of parents placing
their infant in the prone position to sleep (57% before the campaign[3] to
3% after the campaign[4]) suggest many parents take up such
recommendations.
A targeted population intervention would perhaps be inappropriate
given the reduced number of SIDS deaths in this country but risk scoring
systems could be used to identify and study ‘high risk’ families to both
increase our understanding of the risks associated with the infant
sleeping environment and improve the advice we give parents in the hope
that the number of SIDS deaths reduces still further.
Peter S Blair*
Peter J Fleming*
Martin Ward Platt#
*FSID Research Unit, Dept Child Health,
Royal Hospital for Children, St Michael’s Hill, Bristol BS2 8BJ, UK
# Newcastle Neonatal Service, Ward 35,
Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP, UK
2. ONS Health Statistics Quarterly 05 Spring 2000. The Stationery Office: 10.
3. Fleming PJ, Gilbert R, Azaz Y et al. Interaction between bedding and sleeping position in the sudden infant death syndrome: a population based case-control study. BMJ 1990;301:85-9.
4. Fleming PJ, Blair PS, Bacon C et al. Environment of infants during sleep and risk of the sudden infant death syndrome: results from 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy BMJ 1996;313:191-5.
I thank doctors Lakshman and Finn for their kind reply, and
recognise that my use of the word "hospital" has given rise
to a misunderstanding. My letter was based on the analysis
the authors have made, not in the ADC article,[1] but in
their eLetter to BMJ.[2]
They wrote:
(1) immunisation with any vaccine in any child
always carries a risk of potentially fatal anaphylaxis...
I thank doctors Lakshman and Finn for their kind reply, and
recognise that my use of the word "hospital" has given rise
to a misunderstanding. My letter was based on the analysis
the authors have made, not in the ADC article,[1] but in
their eLetter to BMJ.[2]
They wrote:
(1) immunisation with any vaccine in any child
always carries a risk of potentially fatal anaphylaxis
(2)
and must always be carried out in settings where personnel
equipped to recognise and manage it are present (3) annual
updates in recognition and management of anaphylaxis for
personnel involved in immunisation are desirable (4)
essential equipment - adrenaline, airway, Ambu bag with
masks and a telephone to call for emergency help should
always be to hand and regularly checked (5) infants and
children must be observed for at least 30 minutes after the
injection to confirm that they are completely well before
they leave the premises".
According to my interpretation, all these prerequisites are
rarely to be found in the offices of paediatricians.
(1) I do not know how many paediatricians are equipped to
recognise and manage anaphylaxis, considering that they
usually operate not in "settings", but in their offices
(2) How many paediatricians are expert in the treatment of
such reactions, and have adrenaline ready in the same tray
as the vaccine?
(3) annual updates for paediatricians are helpful, however
the authors prefer annual updates for personnel involved in
immunisation, but I do not know in which specific place they
are to be held, according to the authors
(4) paediatricians' offices are rarely equipped with Ambu
masks, they are not reanimators or expert in resuscitation
manoeuvres, in addition, adrenaline should also be kept in a
refrigerator, and is no longer valid after 24-36 months;
from an economical point of view, it is not convenient to
store drugs used perhaps once in a year
(5) observation of vaccinated infants and children for at
least 30 minutes is the easiest procedure to follow in a
paediatrician's office.
Can the "settings where personnel equipped, etc",
be paediatricians' offices? or can the "settings" be
interpreted as "hospital-like premises", where annual
discussions are to be held, where adrenaline is used
continuously, and personnel with Ambu masks are operating?
No such precautions were applied during MMR vaccinations in
egg-allergic children made by us, and as far as I know, in
the rest of about 1800 children previously cited by me.[3]
I repeat, such precautions are valid only with children with
severe reactions to egg documented with challenge tests.
However to extend these recommendations[2] to all children
subjected to MMR vaccine appears to be not practical as it
would eliminate all programs in which vaccination is performed by nurses without doctors in attendance, as occurs in most Developing World countries and in almost all public
health clinics First World countries.[3]
References
1. Lakshman R, Finn A. MMR vaccine and allergy. Arch Dis
Child 2000;82:93-5
2. Lakshman R, Finn A. MMR Vaccine and Egg Allergy. BMJ
[eLetter] 31 March 2000
3. Cantani A, Serra A, Arcese G, Lucenti P. Allergic
reactions to MMR vaccines in egg- and not-egg-sensitive
children: a continuing controversy. Pediatr
Asthma Allergy Immunol 1995;9:7-14
Masters et al describe how a modified endotracheal tube can
be used as a nasopharyngeal airway in infants with Pierre Robin syndrome.[1]
We describe further modifications made to overcome some problems which we
encountered in using the technique in one of our patients.
In the original description the protruding part of the airway is cut
into four strands and the upper one cut off. We found t...
Masters et al describe how a modified endotracheal tube can
be used as a nasopharyngeal airway in infants with Pierre Robin syndrome.[1]
We describe further modifications made to overcome some problems which we
encountered in using the technique in one of our patients.
In the original description the protruding part of the airway is cut
into four strands and the upper one cut off. We found the remaining
strands rather thick, so cut them to half the width. We found that
leucoplast tape was the only tape that held the stands in place with no
additional benefit resulting from the use of Tinc Benz. The strands
rubbed badly where they curved over the edge of the nostril. To overcome
this a piece of suction catheter (8F) of just sufficient length to extend
over the lateral and medial walls of the nostril is tied transversely
across the tube with a 3/O silk tie, figure. This lifts the three stands
off the edge of the nostril and prevents any rubbing.
In our patient blockage of the airway occurred after formula but not
breast milk feeds. It is therefore advisable to suction the airway after
each feed. We used a suction catheter with graduation marks enabling
insertion no further than the tip of the airway. If inserted further the
pharyngeal stimulation usually caused vomiting.
If a nasogastric tube is also required this can be taped to one of
the strands rather than the face. The airway was changed every 4-6 days,
immediately before a feed and alternating between nostrils. Using 1%
lignocaine drops and smearing the tube with lignocaine jelly reduced
crying time after insertion.
Compared to the use of an unmodified tube with a large connector
attached to the end, we feel that the technique described by Masters et al
is far superior as it enables the child to lie prone and is less liable to
get knocked or blocked through kinking. We suggest that the modifications
we have described will further improve the acceptability of the technique.
Maria Galogavrou, Keith Foote
Department Paediatrics, Royal Hampshire County Hospital
Winchester, Hampshire SO22 5DG, UK
Reference
1. Masters IB, Chang A B, Harris M, O’Neil M C. Modified
nasopharyngeal tube for upper airway obstruction. Arch Dis Child 1999;186-7.
Maria Galogavrou
Keith Foote
Department Paediatrics,
Royal Hampshire County Hospital,
Winchester, Hampshire, SO22 5DG
Professor Cantani's[1] experience is very similar to what we found
in our review[2] - that egg allergic children do not appear to be at any
greater risk to severe allergic reactions with MMR vaccine.
In our review, we do not advocate hospitalisation of children with
egg allergy for MMR immunisation; on the contrary we suggest that all
children (including
children with egg allergy) can be immu...
Professor Cantani's[1] experience is very similar to what we found
in our review[2] - that egg allergic children do not appear to be at any
greater risk to severe allergic reactions with MMR vaccine.
In our review, we do not advocate hospitalisation of children with
egg allergy for MMR immunisation; on the contrary we suggest that all
children (including
children with egg allergy) can be immunised with MMR vaccine in the
community.
Since anaphylaxis is an extremely rare and unpredictable
consequence of any vaccination, we suggested in our review that all
children (not just children with egg allergy) must receive all
vaccinations (not just MMR) in a place which is equipped to deal with
anaphylaxis- by this we did not mean a hospital - and they must be
observed for sufficient time after the injection to make sure they are
well.
As Professor Cantani mentions, many of the reactions to the MMR may be
due to the gelatin or neomycin. It is generally agreed that MMR vaccine
is contraindicated
in children who have had severe systemic reactions to either gelatin or
neomycin.
References
1. Cantani A, Serra A, Arcese G, Lucenti P. Allergic reactions to MMR
vaccines in egg- and not-egg-sensitive children: a continuing
controversy. Pediatr Asthma Allergy Immunol 1995;9:7-14.
2 Lakshman R, Finn A. MMR vaccine and allergy. Arch Dis Child
2000;82:93-5
Zar et al[1] found that lung deposition of aerolised
technetium-99DTPA inhaled via modified 500 ml plastic bottle was higher
compared to a Babyhaler in both young and other children. There was no
difference in lung deposition when a mask was used. Though other workers[2] have recommended the attachment of facemasks to treat patients of all
ages.
In another study[3] children aged 5 to 13 years...
Zar et al[1] found that lung deposition of aerolised
technetium-99DTPA inhaled via modified 500 ml plastic bottle was higher
compared to a Babyhaler in both young and other children. There was no
difference in lung deposition when a mask was used. Though other workers[2] have recommended the attachment of facemasks to treat patients of all
ages.
In another study[3] children aged 5 to 13 years
with acute asthma were studied and it was concluded that a conventional spacer and sealed
500 ml plastic bottle produced similar bronchodilatation, an unsealed
bottle gave intermediate improvement in lung function, and a polystyrene
cup was least effective as a spacer for children with moderate to severe
airways obstruction.
A metered-dose inhaler (MDI) with spacer is the best way to deliver
inhalation therapy for the treatment of acute asthma. In India,
commercially produced spacers are available but most of the patients find
it too costly and are thus unable to purchase. These patients, then take
the prescribed inhalers directly without any attachment. We know that
inhalers if taken directly are generally ineffective as medicine fails to
reach the lungs. Thus, use of bottle spacers should be incorporated into
the guidelines for asthma management in developing countries. However,
owing to their size, the bottle spacers are inconvenient to carry and in
these patients dry powder inhalers should be recommended as the next best
thing.
Children with asthma can lead relatively normal lives, just like
their non-asthmatic friends. Diligent monitoring and adherence to a
management plan can make all the difference.
References
1. Zar HJ, Weinberg EG, Binns HJ, Gallie F, Mann MD. Lung deposition of aerosol - a comparison of different spacers. Arch Dis Child 2000;82:495-8.
2. O’Callighan C, Milner AD, Swarbrick. Spacer device with facemask attachment for giving bronchodilators to infants with asthma. BMJ 1989;298:160-1.
3. Zar HJ, Brown G, Donson H, Brathwarte N, Manna MD, Weinberg EG. Home-made spacers for bronchodilator therapy in children with acute asthma: a randomised trial. Lancet 1999;354:979-82.
Following their studies of whole gut lavage fluid Smyth
et al have suggested that a non-idiopathic intestinal
inflammation occurs constituitively in CF patients, as a
consequence of a proinflammatory effect of the
patient's CFTR mutations.[1] They reported marginally
elevated excretion of IgG, IgM, IL-1 , neutrophil
elastase and eosinophil cationic protein, and much more
significant increase in excreti...
Following their studies of whole gut lavage fluid Smyth
et al have suggested that a non-idiopathic intestinal
inflammation occurs constituitively in CF patients, as a
consequence of a proinflammatory effect of the
patient's CFTR mutations.[1] They reported marginally
elevated excretion of IgG, IgM, IL-1 , neutrophil
elastase and eosinophil cationic protein, and much more
significant increase in excretion of IL-8 and albumin,
but no increase in excretion of alpha 1-antitrypsin or IgA.
In this study where lavage fluid was administered
continuously, and intestinal effluent was collected in
discrete samples, pooling of the effluent before
analysis would have allowed small differences in
calculated inflammatory marker outputs to be
interpreted as representative of gastroentestinal
output. Of all the inflammatory markers presented only
interleukin-8 shows a range of cytokine outputs in CF
patients with or without fibrosing colonopathy that
does not extend into the range seen in controls, in
these non parametric datasets. The author's evidence
for intestinal inflammation therefore relies heavily on
the validity of their IL-8 Quantikine assay (R&D
Minneapolis) protocol.
I have explored the validity of this assay for use in
supernatants of faecal homogenates in children with
cystic fibrosis and found it wanting. Recovery of a
500 pg/ml spike of IL-8 progressively increased from 41%
in samples which were a 12-fold dilution of faeces to
189% in samples which were a 120,000-fold dilution of
faeces, when used according to manufacturers
instructions. Pre-diluting the samples 50:50 in newborn
calf serum, and using calf serum for further dilutions
gave this assay (R&D catalogue no D8000) mean (sd)
spike recovery of 92.1 (12.5)% and coefficients of
variation of 3.46% (intra assay) and 6.85% (inter
assay).[2]
Without knowledge of Smyth et al's IL-8 ELISA
validation data, I assume that this assay returns
similarly spuriously high IL-8 concentrations in
polyethylene glycol based wholegut lavage fluid to my
120,000-fold dilution faecal supernatant. The absence
of a significant difference between CF patients and
controls in their alpha 1-antitrypsin outputs suggests that
intestinal inflammation was not presentin the CF
patients. Overestimation of the WGLF IL-8 concentration
would explain the apparently implausably large volumes
of swallowed sputum that the authors estimate would be
required to account for their results. In this study
which could not turn off the mucociliary escalator, but
did dramatically increase the rate of intestinal
transit and exclude exogenous pancreatic enzymes,
swallowed sputum is the most likely explanation for the results.
References
1. Smyth RL, Croft NM, O'Hea U, Marshall T G,
Ferguson A. Intestinal inflammation in cystic fibrosis. Arch Dis Child
2000;82:394-9.
2. Briars GL, Shepherd RW. Faecal interleukin-8 and TNF ELISA: The
first validated assay protocol. Immunology and Cell Biology
1997;suppl 1:A114
According to our studies 1803 children allergic to egg have
been safely received the MMR vaccine. Systemic reactions
were present only in 0.1% of cases and untoward reactions
only in 1.7% cases (p = 0.0001).[1] No child vaccinated by
us has manifested immediate reactions.[1] According to
Sampson et al[2] the MMR vaccine is safe in such children,
evaluating on the basis of confidence intervals (95%) t...
According to our studies 1803 children allergic to egg have
been safely received the MMR vaccine. Systemic reactions
were present only in 0.1% of cases and untoward reactions
only in 1.7% cases (p = 0.0001).[1] No child vaccinated by
us has manifested immediate reactions.[1] According to
Sampson et al[2] the MMR vaccine is safe in such children,
evaluating on the basis of confidence intervals (95%) that
97.5% of children can be safely vaccinated. The reactions
reported by various authors were provoked by the gelatin
present in plasma-expanders, which provokes reactions in
0.07-0.2% of cases and neomycin of which MMR vaccine
contains 25 mg.[1]
In 47 non egg-allergic children a case
of anaphylactic shock was due to gelatin, while the skin
reactions to neomycin are more frequent, thus explaining the
prevalence of urticarial manifestations in the vaccinated
children. However the risk of untoward reactions in non
egg-allergic children, is almost non existent, being =
0.00005%.[1] Two recent works increase the confusion,
because one[3] suggests to perform MMR vaccinations in all
children under controlled conditions in hospital, and the
other[4] restrict these precautions to children with
cardiorespiratory responses to egg and/or chronic asthma.
No
one gives suggestions about possible reactions to gelatin
and/or neomycin.
We judge these conclusions[3, 4]
allarmistic, and suggest that no guideline should prevent
MMR vaccination in children. Obviously we recommend to
vaccinate in the hospital all the children who have
manifested severe, life-threatening reactions to egg. The
door remains open for children who have had anaphylactic
reactions to gelatin or neomycin: give MMR vaccine in
hospital. Adrenaline at hand could be a useful addition.
References
1. Cantani A, Serra A, Arcese G, Lucenti P. Allergic
reactions to MMR vaccines in egg- and not-egg-sensitive
children: a continuing controversy. Pediatr Asthma Allergy
Immunol 1995;9:7-14.
2. James JM, Burks AW, Roberson PK, Sampson HA. Safe
administration of the measles vaccine to children allergic
to eggs. N Engl J Med 1995;332:1262-6.
3. Lakshman R, Finn A. MMR vaccine and allergy. Arch Dis
Child 2000;82:93-5
4. Khakoo GA, Lack G. Recommendations for using MMR vaccine
in children allergic to eggs. BMJ 2000;320:929-32.
The demonstration by Blair et al[1] of an association between poor postnatal
growth and an increased risk of SIDS, is a useful addition to our
understanding of the aetiology of this condition. It is unfortunate that
the conclusion in the abstract that "Poor postnatal weight gain was
independently associated with an increased risk of SIDS and could be
identified at the routine six week assessment" (italics added...
The demonstration by Blair et al[1] of an association between poor postnatal
growth and an increased risk of SIDS, is a useful addition to our
understanding of the aetiology of this condition. It is unfortunate that
the conclusion in the abstract that "Poor postnatal weight gain was
independently associated with an increased risk of SIDS and could be
identified at the routine six week assessment" (italics added) goes beyond
the data presented.
It can be estimated from the data in this study that the overall risk
of SIDS was 0.77/1000 livebirths. The risk in babies with birthweights
>15th centile, the group in whom the relationship with postnatal growth
was detected, was 0.68/1000. Given the reported odds ratio of 1.75
associated with being in the slowest growing 16% who might be identified
at by six weeks, the data suggest that the absolute risk of SIDS among
this group would be about 1.1/1000. Even a programme targeted at infants
below the 2nd centile for growth at six weeks, would identify a group
whose absolute risk of SIDS was about 4.2/1000, i.e. for every infant who
might benefit from the intervention, there would be 240 who wouldn't. Even
if it were accepted that this level of risk was sufficient to trigger an
intervention, the nature of the intervention remains unclear.
To the best
of our knowledge, with the exception of the 'Back to Sleep' campaign,
there is no convincing evidence of the effectiveness of any intervention
aimed at preventing SIDS. None of the intervention programmes described
in the accompanying commentary[2] have been evaluated in appropriately
controlled studies.
The discussion in the paper is rather more circumspect than the
conclusion in the abstract, but it is the latter which, reinforced by the
accompanying commentary, is likely to have disproportionate impact on
those readers who do not read the whole paper. In the commentary Dr
Carpenter acknowledges that the low rates of SIDS make such interventions
difficult to justify but then suggests that "Targeting such infants for
weight monitoring at home….. will also identify numerous other problems at
a remedial stage." This is a suggestion for which there is currently
little evidence.
There are clear dangers in recommending population interventions on
the basis of relative risks without taking account of absolute risks or of
the need for interventions to be of proven effectiveness.
Stuart Logan*
Helen Bedford*
David Elliman#
*Department of Paediatric Epidemiology,
Institute of Child Health,
30 Guilford Street, London WC1N 1EH, UK
#St Georges Hospital,
Blackshaw Road, London SW17 0QT, UK
References
1. Blair PS, Nadin P, Cole TJ, Fleming PJ, Smith IJ, Platt MW, Berry PJ, Golding J. Weight gain and the sudden infant death syndrome: change in weight z scores may identify infants at increased risk. Arch
Dis Child 2000;82:462-9.
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...
Dear Editor
The paper by Cappendijk and Hazebroek[1] successfully demonstrates the problems with diagnosis of appendicitis in the young child.
It makes the important point that diarrhoea may be a feature of appendicitis and lead to misdiagnosis. In addition, children can have coexisting pathologies leading to delayed diagnosis. We have seen a cystic fibrosis child with DIOS (distal intestinal obstruction...
Authors response
Poor postnatal weight gain was a significant factor in the multivariate analysis despite controlling for low birthweight, prematurity, neonatal problems, poor socio-economic status and many other potential confounding factors and remained significant when further highly predictive covariates of SIDS such as infants put down prone, infants found with head covered and tobacco exposure were added...
Dear Editor
I thank doctors Lakshman and Finn for their kind reply, and recognise that my use of the word "hospital" has given rise to a misunderstanding. My letter was based on the analysis the authors have made, not in the ADC article,[1] but in their eLetter to BMJ.[2]
They wrote:
(1) immunisation with any vaccine in any child always carries a risk of potentially fatal anaphylaxis...
Dear Editor:
Masters et al describe how a modified endotracheal tube can be used as a nasopharyngeal airway in infants with Pierre Robin syndrome.[1] We describe further modifications made to overcome some problems which we encountered in using the technique in one of our patients.
In the original description the protruding part of the airway is cut into four strands and the upper one cut off. We found t...
Dear Editor
Professor Cantani's[1] experience is very similar to what we found in our review[2] - that egg allergic children do not appear to be at any greater risk to severe allergic reactions with MMR vaccine.
In our review, we do not advocate hospitalisation of children with egg allergy for MMR immunisation; on the contrary we suggest that all children (including children with egg allergy) can be immu...
Dear Editor
Zar et al[1] found that lung deposition of aerolised technetium-99DTPA inhaled via modified 500 ml plastic bottle was higher compared to a Babyhaler in both young and other children. There was no difference in lung deposition when a mask was used. Though other workers[2] have recommended the attachment of facemasks to treat patients of all ages.
In another study[3] children aged 5 to 13 years...
Dear Editor
Following their studies of whole gut lavage fluid Smyth et al have suggested that a non-idiopathic intestinal inflammation occurs constituitively in CF patients, as a consequence of a proinflammatory effect of the patient's CFTR mutations.[1] They reported marginally elevated excretion of IgG, IgM, IL-1 , neutrophil elastase and eosinophil cationic protein, and much more significant increase in excreti...
Dear Editor,
According to our studies 1803 children allergic to egg have been safely received the MMR vaccine. Systemic reactions were present only in 0.1% of cases and untoward reactions only in 1.7% cases (p = 0.0001).[1] No child vaccinated by us has manifested immediate reactions.[1] According to Sampson et al[2] the MMR vaccine is safe in such children, evaluating on the basis of confidence intervals (95%) t...
Sir
The demonstration by Blair et al[1] of an association between poor postnatal growth and an increased risk of SIDS, is a useful addition to our understanding of the aetiology of this condition. It is unfortunate that the conclusion in the abstract that "Poor postnatal weight gain was independently associated with an increased risk of SIDS and could be identified at the routine six week assessment" (italics added...
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