We noted with interest the recent study reported by Murray
et al[1] in which the characteristics of a cohort of 46 children with
reflex sympathetic dystrophy (RSD) were reported. In a similar fashion in
our paediatric rheumatology unit, chronic idiopathic musculoskeletal pain
syndromes including RSD form a significant proportion of referrals. A
retrospective review of 23 children referred to us in...
We noted with interest the recent study reported by Murray
et al[1] in which the characteristics of a cohort of 46 children with
reflex sympathetic dystrophy (RSD) were reported. In a similar fashion in
our paediatric rheumatology unit, chronic idiopathic musculoskeletal pain
syndromes including RSD form a significant proportion of referrals. A
retrospective review of 23 children referred to us in whom a diagnosis of
RSD was made between April 1993 and November, revealed many similarities
with the population described by Murray et al. This is illustrated in the table below:
Clinical characterisitics
of 23 children with RSD compared with 46 described by Murray et al
In a similar manner many of our patients had seen multiple medical
and health practitioners prior to referral and diagnosis. Five patients
had pre-existing medical conditions (2 inactive juvenile idiopathic
arthritis, 2 recurrent transient synovitis of the hip, one mild cerebral
palsy,and one patient with asthma). A high level of pre-exisiting
conditions with psychological components was seen in our cohort with 4
patients reporting a history of chronic recurrent headaches, 1 of chronic
abdominal pain, 5 of sleep disorders, 2 of anxiety and 2 of depression.
Three patients had a history of conversion disorders: and one recurrent
hyperventilation. In addition 11 (48%) had one or more close relatives
with a chronic or debilitating illness, and in seven of these it was of
musculoskleletal origin. Five patients had a total of 7 first degree
relatives with a diagnosed psychiatric condition.
Presenting symptoms were similar to the reported study with all
patients reporting severe pain in the affected limb(s) in addition to
restriction of joint range of motion (91%); sensory symptoms (55%);
swelling (50%); colour change (55%), and abnormal sweating (14%).
Seventeen patients (77%) had used crutches at some point during their
illness and 7 (32%) had used a wheelchair.
Investigation prior to diagnosis was similar to the reported study.
Eighteen patients (82%) had had plain radiographs of which 4 showed
osteopenia. Eight patients (36%) underwent a bone scan of which 3
demonstrated reduced uptake in the affected limb. No other investigations,
which included MRI, EMG, thermography and nerve conduction studies were
felt to be contributory to diagnosis or management.
Six of 19 patients were admitted to another hospital prior to
referral to our unit of which only 2 of these were reported to have
received in-patient physiotherapy. Ten patients (53%) had outpatient
physiotherapy in some form. In contrast 10 patients (53%), were treated
with a period of limb immobilisation.
Examination findings on presentation to our unit included tenderness
in 100%, hyperalgesia 76%, reduced temperature 71%; discolouration 67%;
muscle wasting 48%; swelling 38%; abnormal sweating 24%, hair loss14%,
and skin atrophy in 9%. Fifteen patients required admission to hospital,
and all received physiotherapy, in addition to simple analgesics and non
steroidal anti-inflammatory drugs as required. All patients had a
pscyhological assessment by the paediatric team, received specific
education and were taught self-management strategies. All were given a
tailored home-exercise programme on discharge.
5 patients in whom adverse psychological factors were felt to be severe
were referred for formal clinical psychology assessment and intervention.
Intervention included patient and family counselling, behavioural and pain
management interventions. Of the patients not admitted, information about
RSD was given in the outpatient department, referral made to local
physiotherapy services and specific medical follow-up arranged.
Average follow-up time from diagnosis was 26 months in our group
(range 5 months to 7 years). Current status was determined from the time
of last clinic visit or by telephone interview (if this was more than 6
months previously). Full outcome information is currently available for 19
patients, 11 of whom were completely well (58%), 5 were clinically
improved but still symptomatic (26%), and 3 patients had not improved
since diagnosis (15%). Of those who had recovered fully the median time to
definite improvement was 4 weeks (range 2-10 weeks) and the mean time to
full recovery 25 weeks (range 4 weeks to 15 months). As with the reported
study by Murray et al, a high rate of reccurence or relapse in our
patient group was seen with 11/19 (58%) having further episodes, of which
4 patients relapsed more than once, and in 2 patients the recurrence
developed in different limb.
A full recovery from the original episode was achieved in 80% of
patients. We found that although there was no reduction in the time
reported to definite improvement in symptoms, patients admitted had a
significantly reduced time interval between diagnosis and full recovery
being 3.25 months, (range 1-7 months) compared with 6 months, (range 2-12)
months in those not admitted. In our cohort a higher proportion of
patients in whom the diagnosis was made within 4 months of onset of RSD
made a full recovery (88% compared to 67%).
We agree with Murray et al[1] that RSD in children is an important cause
of morbidity and suggest that earlier recognition and treatment is likely
to result in improved outcome. It is clear that psychological issues are
common and perhaps under recognised, and we believe it is mandatory that
these be actively sought and addressed in all patients, as has been
suggested by previous authors.[2,3] Although formal psychological
intervention or psychiatric referral may only be required in some
patients, we believe psychological assessment and teaching of coping
skills and pain management strategies is essential in the management of
all patients with chronic pain syndromes including RSD. If intensive
outpatient physiotherapy support is not available, admission for a period
of intensive physiotherapy should always be considered. We also strongly
agree that there is a very limited role for sympathetic nerve blocks, or
narcotic analgesia in the management of RSD in children, and that limb
immobilisation in this condition is inappropriate and contraindicated.
Karen Davies
Specialist Registrar in Paediatric Rheumatology
R Khubchandani
Consultant Paediatrician
Kevin J Murray
Consultant Paediatric Rheumatologist
Institute of child Health Great Ormond Street Hospital
London WC1N 3JH, UK
Kevin.Murray@gos-tr.nthames.nhs.uk
References
(1) Murray CS, Cohen A, Perkins T, Davidson JE, Sills JA. Morbidity
in reflex sympathetic dystrophy. Arch Dis child 2000;82:231-3.
(2) Sherry DD, McGuire T, Mellins E, Salmonson K, Wallace CA, Nepom
B. Psychomatic musculoskeletal pain in childhood: clinical and
psychological analysis of 100 children. Pediatrics 1991;88:1093-9.
(3) Sherry DD, Wallace CA, Kelley C, Kidder M, Sapp L. Short- and
long-term outcomes of children with complex regional pain syndrome type I
treated with exercise therapy. Clin J Pain 1999;15:218-23.
We thank Dr Briars for his comments and are aware of his opinions
regarding the potential source of the intestinal cytokines which we have
discussed in the paper including reference to his previous paper.[1] We do not agree that our data is dependant upon IL-8 alone. We have
shown statistically significant differences for a whole range of proteins
and types of assays.
We thank Dr Briars for his comments and are aware of his opinions
regarding the potential source of the intestinal cytokines which we have
discussed in the paper including reference to his previous paper.[1] We do not agree that our data is dependant upon IL-8 alone. We have
shown statistically significant differences for a whole range of proteins
and types of assays.
Due to the large number of proteins and types of assays that we have
performed we have not the performed the extensive experiments as reported
by Dr Briars for IL-8. We do know that the polyethylene glycol, a key
constituent of the lavage fluid, does not affect the IL-8 assay. There
are two reasons why variable recovery is unlikely to be a major factor in
our results. First by collecting whole gut lavage (WGL) any intestinal
secretions present, including bile, are extremely dilute. Substances found
in faeces such as stercobilin are effectively absent. Secondly WGL is a
perfusion system found to be equivalent to balloon perfusion systems.[2,3]
Thus the dilution of any interfering factors would be very similar between
the subjects and controls. Using WGL minimises any interference from
intestinal material as much as feasible in vivo.
Assuming the worst case scenario from Dr Briars' data (i.e. a two fold
overestimate of IL-8 in the cystic fibrosis (CF) patients which is not
found in the controls) still shows very significantly increased IL-8
output in the CF patients (p<_0.0001 and="and" unfeasible="unfeasible" volumes="volumes" of="of" sputum="sputum" would="would" still="still" be="be" required.="required." p="p"/> For these and reasons detailed in our paper and previous
correspondence[4] we do not believe that sputum is the primary cause of the
abnormalities found. Our observations concerning the increase in
intestinal inflammatory markers in the WGL of CF patients have now been
supported by a study which investigates intestinal inflammation within
mucosal biopsy samples.[5] This provides additional support to the
hypothesis that the basic defect of CFTR can be proinflammatory.
Dr Eisenberg correctly points out the potential influence of
pancreatic enzymes and degradation. The results we found for alpha-1-
antitrypsin were unexpected given differences for albumin and IgG. Some
discordance in data has been found previously in WGL from subjects with
active inflammatory bowel disease[6] who are pancreatic sufficient and also
can have raised intestinal permeability.[7]
However our data demonstrating raised albumin and IgG are consistent
with well established data showing raised intestinal permeability in
children with CF.[8] As we discussed, it has been found that protein outputs
from balloon perfusion experiments (which exclude upper intestinal
secretions) are similar to those found in whole gut lavage suggesting that
any potential effect of degradation from pancreatic enzymes is minimal.[2,3] We also showed ECP to be raised in CF children. Like alpha-1-
antitrypsin this is relatively stable in faeces at room temperature
(approx 21%
loss over 24 hours).[10] This loss would be considerably lower during WGL.
Thus degradation would be unlikely to explain this difference.
Nicholas M Croft
Department of Paediatric Gastroenterology
St Bartholomew’s and the Royal London School
of Medicine and Dentistry,
Queen Mary and Westfield College
London, UK
Rosalind L Smyth
Una O’Hea
University Institute of Child Health
Royal Liverpool Children’s Hospital
Liverpool, UK
Tom G Marshall
Royal Hospital for Sick Children
Edinburgh UK
References
(1) Briars GL, Dean TP, Murphy JL, Rolles CJ, Warner JO. Faecal
interleukin-8 and tumour necrosis factor-alpha concentrations in cystic
fibrosis. Arch Dis Child 1995;73:74-6.
(2) Ferguson A, Sallam J, McLintock L, Croft NM, Poxton I. The gut as an
immune organ: intestinal antiendotoxin antibodies. In: Kinney JM, Tucker
HN, eds. Organ Metabolism and Nutrition: Ides for Future Critical Care. New York: Raven Press, Ltd, 1994:231-44.
(3) Croft NM, Ferguson A. High intraluminal fluid flow increases
intestinal IgA output. Scand J Gastroenterol 2000;35:726-31.
(4) Croft NM, Marshall TG, Ferguson A. Gut inflammation in children
with cystic fibrosis on high dose enzyme supplements [letter]. Lancet 1996;347:327.
(5) Raia V, Maiuri L, de Ritis G, et al. Evidence of chronic
inflammation in morphologically normal small intestine of cystic fibrosis
patients. Pediatr Res 2000;47:344-50.
6) Choudari CP, O’Mahony S, Brydon G, Mwantembe O, Ferguson A. Gut
lavage fluid protein concentrations; objective measures of disease
activity in inflammatory bowel disease. Gastroenterology 1993;104:1064-71.
(7) Tibble JA, Sigthorssen G, Bridger S, Fagerhol MK, Bjarnason I.
Surrogate markers of intestinal inflammation are predictive of relapse in
patients with inflammatory bowel disease. Gastroenterology 2000;119:15-22.
(8) Flick JA, Perman JA. Increased intestinal permeability in cystic
fibrosis correlates with the degree of pancreatic exocrine dysfunction.
Pediatr Pulmonol 1990;(suppl):97-8.
(9) Berstad A, Borkje B, Riedel B, Elsayed S. Increased fecal
eosinophilic cationic protein in inflammatory bowel disease. Hepatol Gastroenterol 1993;40:276-8.
I was interested by the report of Smyth et al regarding the
finding of markers of intestinal inflammation in whole gut
lavage in patients with cystic fibrosis.[1] As the alpha 1
antitrypsin levels were not increased compared to
controls, perhaps another hypothesis needs to be considered.
Conceivably the inflammatory markers are not actually
increased within the bowel, but rather, they are...
I was interested by the report of Smyth et al regarding the
finding of markers of intestinal inflammation in whole gut
lavage in patients with cystic fibrosis.[1] As the alpha 1
antitrypsin levels were not increased compared to
controls, perhaps another hypothesis needs to be considered.
Conceivably the inflammatory markers are not actually
increased within the bowel, but rather, they are not
degraded due to the lack of intestinal enzymes. Alpha 1
antitrypsin, which is resistent to proteolytic enzyme
activity, would not be affected by such a phenomenon and
therefore, would be the same in patients with cystic
fibrosis and controls. Perhaps the authors would need to
resort to the somewhat dated technique of radiolabeled
albumin to definitively answer this question.
Larry Eisenberg
Reference
(1) Smyth RL, Croft NM, O'Hea U, Marshall TG, Ferguson A. Intestinal inflammation in cystic fibrosis. Arch Dis Child 2000;82:394-9.
Our study[1] was done on a selected group of children who were at an
increased risk of having urinary tract infection (UTI). The inclusion
criteria were the presence of any of the following
1. Clinical suspicion of UTI
2. History of previous UTI or renal anomalies
3. Children requiring antibiotics (urine culture was send prior to
starting antibiotics)...
Our study[1] was done on a selected group of children who were at an
increased risk of having urinary tract infection (UTI). The inclusion
criteria were the presence of any of the following
1. Clinical suspicion of UTI
2. History of previous UTI or renal anomalies
3. Children requiring antibiotics (urine culture was send prior to
starting antibiotics)
4. Any of the dipstick tests (nitrites, protein, leukocyte esterase or
blood) being abnormal.
Out of the 500 children admitted to the hospital during the study period,
only 312 who met above criteria were included in the study and
urine culture was done on all them. This reflected the local practice at
our hospital of sending urine for culture. We wanted to see if a change in
practice where urine culture is undertaken only if nitrites or leukocyte
esterase was positive would be effective in reducing the number of urine
cultures. The inclusion criteria for Sherif et al's study[2] was a clinical
suspicion of UTI, when urine cultures were send and dipstick testing was
done.
We found that UTI could be easily missed if urine culture is
undertaken only if nitrites or leukocyte esterase is positive. Quite
surprisingly the results of our study and Sherif et al's study seems to be
similar. Sensitivity was 34.4% vs 20.0% and specificity was 90.7% vs 99.2%
in our study and Sherif et al's study respectively. Negative predictive value was
92.4% in our study and 96.7% in Sherif et al's study. Only the interpretation of
these results seems to be different.
A test with such a low sensitivity reported in both these studies
cannot be recommended as screening test to exclude UTI. Urinary tract
infection is supposed to produce maximum damage in infants and therefore
one would not like to miss any UTI in this age group. Unfortunately this
is the age group where sensitivity of dipstick testing is the least (20%).
I agree with Sherif et al[3] that because of its high negative predictive
value, it may have some role as a screening test for UTI in situations
where the incidence of UTI is very low.
Positive nitrites had a very high specificity for UTI, which was the basis
of my suggestion that if nitrites are positive, especially in a febrile
infant, empirical treatment with antibiotics may be considered till the
result of urine culture is obtained. But it should not be the whole
criterion for diagnosing UTI.
Dr Sudhin Thayyil-Sudhan
Dr Santosh Gupta
University Hospital of Leicester
55 Hospital Close
Leicester LE5 4WQ, UK
References
(1) Thayyil-Sudhan S, Gupta S. Dipstick examination for urinary tract infections [letter]. Arch Dis Child 2000;82:271.
(2) Sharief N, Hameed M, Petts D. Use of rapid dipstick tests to exlude urinary tract
infection in children. Br J Biomed Sci 1998;55:242-6.
(3) Sharief N, Petts D. Dipstick testing of urine [rapid response]. Arch Dis Child 10th August 2000.
Although the paper of El-Radhi et al[1] presents
interesting data about decreases in inflammatory markers during the
resolution of acute asthma, some of their conclusions are not valid.
First, acute asthma has a tendency to resolve without corticosteroid
therapy.[2] Since all of the children with acute asthma (quite rightly)
received steroids, the observed effect may equally reflect processes
associated wit...
Although the paper of El-Radhi et al[1] presents
interesting data about decreases in inflammatory markers during the
resolution of acute asthma, some of their conclusions are not valid.
First, acute asthma has a tendency to resolve without corticosteroid
therapy.[2] Since all of the children with acute asthma (quite rightly)
received steroids, the observed effect may equally reflect processes
associated with spontaneous resolution. Indeed, corticosteroids do not
inhibit the release of eosinophil cationic protein (ECP) from eosinophils.[3] Second, the normal controls are inadequate. Atopy per se is
associated with increased serum levels of ECP,[4] and it is therefore to
be expected that the asymptomatic atopic asthmatics will have higher ECP
levels than the mostly non-atopic controls.
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.
(3) Venge P, Bystrom J, Carlson M, et al. Eosinophil cationic protein
(ECP): molecular and biological properties and the use of ECP as a marker
of eosinophil activation in disease. Clin Exp Allergy 1999;29:1172-86.
(4) Marks GB, Kjellerby J, Luczynska CM, Burney PG. Serum eosinophil
cationic protein: distribution and reproducibility in a randomly selected
sample of men living in rural Norfolk, UK. Clin Exp Allergy 1998;28:1345-
50.
We read with interest the letter by Thayyil-Sudhan and Gupta[1]
reporting their study on the role of dipsticks in the detection of urinary
tract infection in children. We believe that this is a very important
subject and wish to comment on the report and their conclusions in the
light of our published study.[2]
We note that 188 urines were not sent for culture, it is not therefore
possible to d...
We read with interest the letter by Thayyil-Sudhan and Gupta[1]
reporting their study on the role of dipsticks in the detection of urinary
tract infection in children. We believe that this is a very important
subject and wish to comment on the report and their conclusions in the
light of our published study.[2]
We note that 188 urines were not sent for culture, it is not therefore
possible to determine the number of true and false negative dipstick tests
(if any). Without these data, calculation of sensitivity and specificity
of dipstick testing becomes impossible.[3] Because of the above we
believe that the data presented are skewed secondary to a flawed
experimental design. As a consequence of this, the statement of the
authors that "UTI in children cannot be excluded by a negative nitrite or
leukocyte esterase reaction" is difficult to justify.
There is no information to indicate whether children who were on
antibiotic therapy at or immediately prior to admission were included in
the study. If this is the case the possibility of false negative culture
results cannot be excluded and this will add further bias to the results.
No data are provided about the number of infants included in the study.
It has been reported that negative dipstick tests has a higher false
negative rate in infants or in cases of urinary frequency because
decreased bladder incubation time diminishes in-vivo bacterial
multiplication.[4] We are not told about the percentage of the samples,
which were collected by pads compared to mid-stream specimens as this may
further add to the inaccuracy of the culture results.
In our prospective study[2] on 325 children in whom UTI was a possibility
on clinical grounds all urines were sent for laboratory examination. The
laboratory was unaware of the results of the dipstick tests until the end
of the study. Analysis of our data showed that the combination of
negative dipstick tests for nitrite and leucocyte esterase gave a negative
predictive value for UTI of 96.9%, with a specificity of 98.7%. The
figures for infants were 96.7% and 99.2% respectively. A positive nitrite
and/or leucocyte esterase had a positive predictive value of 60.0% and a
sensitivity of 54.6%, compared to 50.0% and 20.0% respectively in
infants. In our series we found that there were four false negative and
six false positive nitrite tests.
The dipstick tests are most likely to be useful as a screening test to
exclude UTI in children but may be less suitable for infants. It should
not be used to diagnose urinary tract infection. We therefore disagree
with Thayyil-Sudan and Gupta in their view that “if nitrites are positive
empirical treatment or UTI seems to be reasonable until cultures are
positive”.
References
(1) Thayyil-Sudhan S, Gupta S. Dipstick examination for urinary tract
infections [letter]. Arch Dis Child 2000;82:271-2.
(2) Sharief N, Hameed M, Petts D. Use of rapid dipstick tests to exlude
urinary tract infection in children. Br J Biomed Sci 1998;55:242-6.
(3) Lohr JA. Use of routine urinalysis in making a presumptive diagnosis
of urinary tract in children. Pediatr Infect Dis J 1991;10: 646–50.
(4) Hellerstein SL. Urinary tract infections: Old and new concepts. Ped Clin N Am 1995;42:1433–57.
How many times do general practitioners here parents say "I do not want my baby vaccinated"? Quite often, I guess. As vaccine uptake rates are
maintained at high levels, notifications of the diseases prevented by them
have fallen. As the incidence of these diseases have fallen from the
public consciousness, public attention has deviated from these nasty
diseases to its side effects. The paper from Go...
How many times do general practitioners here parents say "I do not want my baby vaccinated"? Quite often, I guess. As vaccine uptake rates are
maintained at high levels, notifications of the diseases prevented by them
have fallen. As the incidence of these diseases have fallen from the
public consciousness, public attention has deviated from these nasty
diseases to its side effects. The paper from Gold M et al[1] is a reminder
to health professionals that vaccination schedules can be safely carried
on in spite of most adverse reactions.
Some districts, including ours, run immunisation helplines for
primary healthcare teams.[2] The most common query we get is from the practice
nurse when a mother presents with the child for the next dose of DPT, Hib, and
meningitis C vaccine and reports a severe local reaction or prolonged crying
after the previous dose. What we find time and time again is that parents
seldom go to their general practitioner immediately. An opportunity
to check the reaction out and make clear and careful decisions about the
future is lost. It is debatable how reliable or vivid parental accounts of
a swelling or length and quality of crying could be a month later. We did
not find any reference as to how well the yellow card system of reporting
adverse immunisation reactions is used in the UK.
A report from the US[3]
does suggest that their counterpart to the yellow card (VAERS) may not be
reliable. In light of the paper by Gold et al[1] and our experience we have the following
suggestions to make:
1. Practice nurses and general practioners should encourage parents to bring the
child back if they are worried about side effects
2. The yellow card system of reporting adverse drug reactions should
be used appropriately
3. Health professionals should seek expert advice before not
recommending any vaccine
4. There are very few true vaccine side effects. The Green Book[4] in
the UK should reflect the increasing evidence of vaccine safety. This can
help boost professional and parental confidence in vaccination programmes.
Dr Ashok Nathwani
Consultant Paediatrician
Portsmouth, UK
References
(1) Gold M, Goodwin H, Botham S, Burgess M, Nash, Kempe A. Re-vaccination of 421 children with past history of an adverse vaccine reaction in a special immunisation service. Arch Dis Child 2000;83:128-31.
(2) Finlay F, McKechnie L, Pearce A, Lenton S. Immunisation telephone hotline audit. Ambulatory Child Health 1999;5:295-302.
(3) Braun MM, et al. Report of a US Public Service workshop on Hypotonic Hyporesponsive Episode (HHE) after pertussis immunisation. Pediatrics 1998;102:e52.
(4) Immunisation against Infectious Disease. London: HMSO, 1996.
I read with interest the article on Imaging the Less Seriously Head
Injured Child.[1]
The authors state that bruising with a yellow hue suggests that
injury occurred at least 48 hours earlier. Unfortunately this statement
is not referenced and the main articles I am aware of on the age and
colour of bruising are those of Stevenson and Bialas published in ADC in 1996,[2] Schwartz & Ricci, 1996,...
I read with interest the article on Imaging the Less Seriously Head
Injured Child.[1]
The authors state that bruising with a yellow hue suggests that
injury occurred at least 48 hours earlier. Unfortunately this statement
is not referenced and the main articles I am aware of on the age and
colour of bruising are those of Stevenson and Bialas published in ADC in 1996,[2] Schwartz & Ricci, 1996,[3] and Langlois and Gresham in 1991.[4]
Langlois and Gresham studied the colour changes of bruises with time
and from their study found it was only possible to conclude that a bruise
with a yellow colour was more than 18 hours old. The significance of the
appearance of other colours in terms of estimating the time of occurrence
was not helpful.
Stevenson and Bialas[2] also found that ageing of bruises was much
less precise than text books imply and found that green or yellow hues
suggested an injury to be at least 24 - 48 hours old. Shwartz & Ricci
concluded that the available literature does not permit the estimation of
a bruise's age with any precision based on colour.[3]
I should be grateful to know if Glasgow and McGovern found any
further research to assist them in ageing bruises as I make a particular
point in my teaching of Child Protection and the writing of medico/legal
reports to urge extreme caution on statements which specify the age of
injuries based on their colouring.
Dr L Light
References
(1) Glasgow JFT, McGovern SJ. Imaging the less seriously
head injured child. Arch Dis Child 2000;82:333-5.
(2) Stevenson T, Bialas Y. Estimation of the age of bruising. Arch Dis Child 1996;74:53-5.
(3) Schwartz AJ, Ricci L. How accurately can bruises be aged
in abused children? Literature review and synthesis. Pediatrics 1996;97:254-7.
(4) Langlois NET, Gresham GA. The ageing of bruises: a
review and study of the colour changes with time. Forensic Sci Int 1991;50:227-38.
Stewart-Brown's paper on the compatibility of medical practice
in community paediatrics with that in public health[1] is a superlative
effort. This is more so as it has come at a time when community paediatrics
is being actively discussed by the RCPCH (UK Royal College of Paediatrics and Child Health) for a variety of reasons but,
perhaps, most importantly because it does not seem to attract enough...
Stewart-Brown's paper on the compatibility of medical practice
in community paediatrics with that in public health[1] is a superlative
effort. This is more so as it has come at a time when community paediatrics
is being actively discussed by the RCPCH (UK Royal College of Paediatrics and Child Health) for a variety of reasons but,
perhaps, most importantly because it does not seem to attract enough
specialist registrars.
It can be argued that all paediatricians (just not
community paediatricians) can and do play an important role in child
advocacy issues at various levels. From the clinical perspective the
community paediatric role in immunisation and child health surveillance is
the most important.
Trainees in paediatrics need to recognize that child public health is
a small (albeit important) role of the community paediatricians. The bulk
of community paediatricians are neurodevelopmental specialists. Many have
an important role in child protection. Some community paediatricians are
developing a behavioural paediatric interest in their clinical practice.
Most districts in the UK need their community paediatricians to look after
families with children with disabilities. Some districts (like ours) need
them to offer outpatient epilepsy services as well. With increasing
prevalence of behavioural problems in children, many community
paediatricians have trained (or retrained) themselves to cater to this
need. Useful links with child psychiatric and psychology colleagues have
been forged. In fact, our counterparts in the US are called developmental
and behavioural paediatricians and their core curriculum reflects the depth
of training offered for both these domains.[2]
There is no doubt, therefore,
that the term “community paediatrics” is a misnomer and may not offer
confidence to the budding specialist registrar who may find being a
neurologist or an oncologist a better bet. There is increasing specialism
within community paediatrics, and the job title needs to reflect that
expertise.
It is very possible that a small minority of (community)
paediatricians may chose to train with a major public health interest. It
may be helpful to know that the American Acdemy of Pediatrics has a
section for paediatricians with this interest.[2] The bulk should continue
(to train and practice) with a major clinical interest and that should be
an important selling point for community paediatrics. Hopefully job titles
in the future will reflect the clinical expertise. This will not only help
trainees but also purchasers, referers and the families we serve.
This letter is not meant to be in any way critical of Dr Stewart-Brown’s paper which, in fact has highlighted the importance of public
health medicine for (community) paediatricians. Health promotion is indeed
a skill that can be applicable easily in clinical practice.
Dr Ashok Nathwani
Consultant (Community) Paediatrician
Portsmouth, UK
References
(1) Stewart-Brown S. Is the ethos of medical practice in community paediatrics compatible with that in public health? Arch Dis Child 2000;83:101-3.
(2) Section on Community Pediatrics, American Acdemy of Pediatrics, http://www.aap.org/commpeds/ [accessed 3 Aug 2000].
Dr Mitchell is concerned that the methodology used in our study does
not simulate the release of aerosol from a metered dose inhaler (MDI). As
discussed in the article, the method of aerosol delivery in our study
differs from that of a MDI but as the delivery system was kept constant
and the particular spacer varied, a valid comparison of the efficacy of
different spacers could be made.[1] This deli...
Dr Mitchell is concerned that the methodology used in our study does
not simulate the release of aerosol from a metered dose inhaler (MDI). As
discussed in the article, the method of aerosol delivery in our study
differs from that of a MDI but as the delivery system was kept constant
and the particular spacer varied, a valid comparison of the efficacy of
different spacers could be made.[1] This delivery system has been
previously developed and tested in older children.[2] In these studies
aerosol lung deposition was equivalent from a conventional spacer or
sealed modified bottle spacer but a cup performed poorly delivering
significantly less aerosol to the lungs than did the other spacers.
The validity of these findings was borne out by the results of a
clinical study in which a similar response to bronchodilator was obtained
when children with acute asthma were given a beta-2 agonist via an MDI-
bottle or conventional spacer but a poor response occurred in those using
a cup.[3]
We agree with Dr Mitchell that the presence of an inhalation valve
may affect pulmonary deposition of aerosol. However, valveless spacers
may also function efficiently as spacers. When compared to an MDI alone,
increased lung deposition has been reported with a valved Cone Spacer and
a valveless Tube Spacer.[4] These two spacers have also been found to
produce similar increases in bronchodilation compared to a MDI alone.[3]
Moreover, oropharyngeal deposition may be reduced by up to 60% with a
valveless spacer.[4] Recently, valveless spacers have been reported to
enhance the delivery of aerosol to the lungs in infants with chronic lung
disease compared to the same spacer with a valve.[5] The results of our
clinical study suggest that a valveless bottle spacer provided effective
drug delivery to the lungs resulting in similar bronchodilation compared
to that obtained with a valved conventional spacer.[6]
The availability of a spacer device is essential in order to provide
care to children with asthma. For many children particularly those in
developing countries, a low cost spacer is not available. We believe that
our studies have shown that a modified 500ml plastic bottle functions
effectively as a spacer providing equivalent or superior aerosol
deposition to a conventional spacer and producing similar clinical
improvement. Such a bottle-spacer is a first step in providing asthma
care to many children throughout the world.
Heather J Zar
Michael Mann
Eugene Weinberg
Department of Paediatrics and Child Health
Red Cross Children's Hospital
University of Cape Town, South Africa
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) Zar HJ, Liebenberg M, Weinberg E, Binns HJ, Mann MD. The efficacy
of alternative spacer devices for delivery of aerosol therapy to children
with asthma. Ann Trop Paed 1998:18;75-9
(3) Rivlin J, Mindorff C, Reilly PA, Levison H. Pulmonary response
to a bronchodilator delivered from three inhalation devices. J Pediatr
1984;104:470-3
(4) Newman SP, Moren F, Pavia D, et al. Deposition of pressurized
suspension aerosols inhaled through extension devices. Am Rev Respir Dis
1981;124:317-20
(5) Fok TF, Lam K, Chan CK et al. Aerosol delivery to non-ventilated
infants by metered dose inhaler: Should a valved spacer be used? Pediatr
Pulmonol 1997:24;204-212
(6) Zar HJ, Brown G, Donson H, Brathwaite N, Mann MD, Weinberg EG.
Home-made spacers for bronchodilator therapy in children with acute
asthma: a randomised trial. Lancet 1999:354;979-82.
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