The recent article by Eiser and Morse was an excellent
review of studies in this area.[1] We agree that emphasising the outcome
of the child as a whole, rather than using raw clinical indicators is
important, and that measuring Quality of Life (QoL) should help with this.
The article refers to an instrument which we developed to measure QoL in
children with Crohn’s disease.[2] The initial development actuall...
The recent article by Eiser and Morse was an excellent
review of studies in this area.[1] We agree that emphasising the outcome
of the child as a whole, rather than using raw clinical indicators is
important, and that measuring Quality of Life (QoL) should help with this.
The article refers to an instrument which we developed to measure QoL in
children with Crohn’s disease.[2] The initial development actually took
place in the United Kingdom not the USA, further extensive development has
subsequently been done in Canada and the Netherlands, as well as the UK.
Specific concerns were determined from interviews with 82 Canadian
children with Inflammatory Bowel Disease (IBD) aged between 8 and 16
years. These issues were incorporated into an “item reduction list” which
was administered to a further 117 Canadian children with IBD, who ranked
the issues in terms of importance and frequency. From the 50 highest
ranking concerns a 32-item paediatric IBD QoL instrument (IMPACT) has been
developed. The instrument has shown strong correlation with patient global
assessment of QoL and contains questions encompassing 6 domains: bowel
symptoms; systemic symptoms; social/functional concerns; body image; test/treatment concerns; emotional concerns.[3]
We agree with the authors concerns about cross-cultural adaptation of
QoL instruments. We sent the Canadian “item reduction list” to 53 British
children with IBD and asked them to rank the issues in the same way as the
Canadian children did. In addition they were asked if they had any other
concerns and we also conducted focus groups to identify any additional
concerns. The British children with IBD generally had the same concerns as
their Canadian counterparts but the QoL appeared to be worse in British
children.[4] This encouraged us to believe that IMPACT would also be
valid in the UK, but pilot studies have shown that many UK children, their
parents and health professionals found the questions to be too complicated
and/or upsetting. Similar problems have also been experienced by our Dutch
colleagues who have developed a simplified, child-friendly version of the
questionnaire (called IMPACT-II) incorporating the same concerns.[5] In a
pilot study of 21 UK children with IBD who completed both versions of the
questionnaire 16 preferred IMPACT-II as they felt it was easier to
understand and quicker to complete.[6]
We also share the authors concerns that questionnaires can be time
consuming and difficult to complete. We have therefore developed a
portable, touch-screen computer version of IMPACT-II which can be used in
the outpatient clinic. In a further pilot study of 19 UK children with
IBD who completed the paper and computer versions, 17 preferred the
computer version.[7] This is currently undergoing further validation and
we hope that it will be a major step towards providing information about
QoL in children with IBD in the clinical setting.
S MAITY
AG THOMAS Booth Hall Childrens Hospital
Manchester, UK
References
(1) Eiger C, Morse R. A review of measures of quality of life for
children with chronic illness. Arch Dis Child 2001;84:205-11.
(2) Rabbett H, Elbadri A, Thwaites R et al. Quality of life in
children with Crohn’s disease. J Pediatr Gastroenterol Nutr 1996;23:528-33.
(3) Griffiths AM, Nicholas D, Smith C et al. Development of a quality
of life index for pediatric inflammatory bowel disease: dealing with
differences related to age and IBD type. J Pediatr Gastroenterol Nutr
1999;28:S46-52.
(4) Richardson G, Griffiths AM, Miller V, Thomas AG. Concerns of
children with inflammatory bowel disease and quality of life; a cross-
cultural comparison. J Pediatr Gastroenterol Nutr [In press]
(5) Loonen HJ, Derkx HHF, Last RF, Grootenhuis MAM. Development and
validation of a disease specific quality of life instrument for paediatric
inflammatory bowel disease:the Dutch modified questionnaire. J Pediatr
Gastroenterol Nutr 2000;31:S158.
(6) Sage L, Loonen H, Derkx HH, Thomas AG. Development of an
instrument to measure quality of life in UK children with inflammatory
bowel disease. Presented at the annual meeting of the British Society of
Paediatric Gastroenterology, Hepatology & Nutrition, Leeds, January
2001.
(7) Sage L, Loonen H, Derkx HH et al. Development of a computerised
touch-screen version of a questionnaire to measure quality of life in
children with inflammatory bowel disease. Presented at the annual meeting
of the Royal College of Paediatrics & Child Health, York, April 2001.
Partsch and colleagues speculate that a rise in
testicular temperature in infants and young children
consequent to the wearing of modern plastic lined disposable
nappies [diapers] may have contributed to both the fall in sperm
counts and the increase in testicular cancer which have been
reported in some countries.[1] In support of this hypothesis
Partsche et al refer to reports of rising incidence ra...
Partsch and colleagues speculate that a rise in
testicular temperature in infants and young children
consequent to the wearing of modern plastic lined disposable
nappies [diapers] may have contributed to both the fall in sperm
counts and the increase in testicular cancer which have been
reported in some countries.[1] In support of this hypothesis
Partsche et al refer to reports of rising incidence rates in
testicular cancer.[2-6] These studies report increased
cancer risk in men born from before 1900 to 1988 diagnosed
up to 1988, from 1916 to 1978, before 1970, from 1907 to 1981,
and from 1865 to 1975, respectively. None reports incidence
of testicular cancer in men who have had the opportunity to
wear modern disposable nappies which have only been widely
available since the late 1970s. There is some suggestion
that the rise in testicular cancer may not be continuing.[7]
There are no data on testicular cancer incidence in men who
are likely to have worn modern disposable nappies as the
peak age for this disease is the late 20s and the men are
simply too young. Similarly, the reports of a declining
sperm count do not include any men born after 1975,[8-11] and even the most recent study from Denmark
includes men born only before 1978.[12]
There is no way that
modern disposable nappies could have contributed to the
changes in male gonadal health reported in men observed to
date since all studies are of men who were born before they
were available.
Partsch et al[1] claim that the scrotal cooling mechanism
was often completely abolished in boys wearing modern
disposable nappies. This would appear to be
over-interpretation of the data they had available, for two
reasons. Firstly, they compared 24-hour mean scrotal
temperature with spot rectal temperature and were unable to
take into account the considerable circadian variation in
core temperature in infants.[13] Secondly, they used
measurement techniques validated in adults but not in
nappy-wearing infants. They have not demonstrated that their
methods, which included covering a considerable portion of
the scrotal surface with adhesive tape, did not interfere
with two aspects of scrotal cooling, ie, evaporation from the
skin surface and contraction and relaxation of the scrotal
sac. There is the very real possibility that the measurement
process itself increased scrotal temperatures in all
children.
There are several inconsistencies in the results table (table 1 in the paper by Partsch et al)[1]; for example, the
mean temperatures and the calculated difference between
temperatures measured with modern plastic lined disposable
nappies and cotton nappies can not be reconciled, which the
authors may wish to clarify.[1]
Further scientific research is clearly needed to establish
the normal range of temperatures in infant testes and
the extent to which they may be affected by different types
of nappies and also the extent to which any changes may
affect testicular health. However, it is clear that modern
plastic lined disposable nappies can have played no role in
the changes in male gonadal health reported worldwide to
date.
References
1. Partsch C-J, Aukamp M and Sippell WG. Scrotal
temperature is increased in disposable plastic lined
nappies. Arch Dis Child 2000;83:364-8.
2. Adami H, Bergström R, Möhner M, et al. Testicular cancer
in nine northern European countries. Int J Cancer
1994;59:33-8.
3. Forman D, Möller H. Testicular cancer. Cancer Surv
1994;19-20:323-41.
4. Hoff Wanderas E, Tretli S, Fossa SD. Trends in incidence
of testicular cancer in Norway 1955-1992. Eur J Cancer
1995;31A:2044-8.
5. Weir HK, Marrett LD, Moravan V. Trends in the incidence
of testicular germ cell cancer in Ontario by histologic
subgroup, 1964-1996. CMAJ 1999;160:201-5.
6. Zheng T, Holford TR, Ma Z, Ward BA, Flannery J, Boyle P.
Continuing increase in incidence of germ-cell testis cancer
in young adults: experience from Connecticut, USA,
1035-1992. Int J Cancer 1996;65:723-9.
7. Andersen AG, Jensen TK, Carlsen E, et al. High frequency of sub-optimal semen quality in an unselected
population of young men Hum Reprod 2000;15:366-72.
8. Auger J, Kunstmann JM, Czyglik F, Jouannet P. Decline in
semen quality among fertile men in Paris during the past 20
years. N Engl J Med 1995;332:281-5.
9. Benshushan A, Shoshani O, Paltiel O, Schenker JG, Lewin
A. Is there really a decrease in sperm parameters among
healthy young men? A survey of sperm donations during 15
years. J Assist Reprod Genet 1997;14:347-53.
10. Carlsen E, Giwercman A, Keiding N, Skakkebaek NE.
Evidence for decreasing quality of semen during past 50
years. BMJ 1992;305:609-13.
11. Irvine S, Cawood E, Richardson D, MacDonald E, Aitken J.
Evidence of deteriorating semen quality in the United
Kingdom: birth cohort study in 577 men in Scotland over 11
years. BMJ 1996;312:467-71.
12. Pharris-Ciurej ND. Cook LS. Weiss NS. Incidence of
testicular cancer in the United States: has the epidemic
begun to abate?. Am J Epidemiol 1999;150:45-6.
13. Wailoo MP. Petersen SA. Whittaker H. Goodenough P.
Sleeping body temperatures in 3-4 month old infants.
Arch Dis Child 1989;64:596-9.
Conflict of Interest
I have provided advice on scientific and epidemiological aspects of this
study to 2 trade associations which act on behalf of modern plastic lined
disposable nappy manufacturers EDANA and AHPMA.
We thank David Strauss for his interest in our work but he fails to
substantiate
his claims that there are 'substantial problems' with it.
First, we wish to correct an error on page 470 (Arch. Dis. Child. 2000; 83: 470), column 2, line 11,
`dying
before' should read 'surviving until'.
With regard to Strauss's remarks on LAS, both the abstract and the
results
section include the phrase 'survived to age 5', so Strauss has not
explained our
result, but
merely repeated this information. Even the brief precis of the
LAS in the paper makes it clear that it would be difficult, if not
impossible,
as well as unwise, to attempt to complete it for a 2 year old.
That some-one might misquote our work is true, but not our responsibility.
With regard to mobility and mental ability, we have reported exactly
what is
measured, and have referenced other work which includes measures different
from
ours. It appears that Strauss wishes we had speculated about information
we do
not have. Note that IQ was constructed to have a mean of 100, and
standard
deviation of 15. On this scale, fewer than 4 in 10,000 people would have
an IQ
less than 50, our definition of severe cognitive disability.
Fewer than 5 in 10 million people would have an IQ of less than 20, the
number
mentioned by Dr Rosenbloom.
It seems obvious that persistent vegetative state or indeed leukaemia
or need
for ventilation twice a year are clearly additional and largely
independent risk factors for death which any court would take in to
account.
With regard to hazard or odds ratios, our discussion does comment on
multivariate versus univariate models (Arch. Dis. Child. 2000; 83: 472).
Whether univariate or multivariate, one still has a relative statistic, so
that any lack of similarity in the baseline categories will be relevant.
Strauss claims that `The real reason is simpl(y)' the difference between
multivariate and univariate analyses: he gives hazard ratios for tube
feeding,
and states that the univariate ratio of 23.6 is 'about as large as any in
Hutton
et al's Table 5'. However, Strauss fails to quote a factor - hand use -
which,
unlike tube feeding, can be
easily compared with our work, and that of South East Thames. In
correspondence
with
Hutton, Strauss stated "Re. hand use: our multivariate OR was 1.52 and
our
univariate OR was 5.69": a value which is substantially less than 23.6,
and than
our results.
Further, Strauss states that this lower ratio is for a more disabled
group: "But
our
definitions are very different from yours. Our 'bad' group is 'no
functional use
of hand' ... while your 'severe manual disability' group is much more
inclusive'
...". Thus the `reason' Strauss gives fails to explain the difference in
results
for manual disability.
We thank Dr Grigg for his interest in our work.[1] We agree that the asthma attacks may have resolved spontaneously in some cases, which was
precisely why we stated that the markers fell in association with steroid
therapy, and nowhere implied causality. Nevertheless, the statistical
analysis suggests that the chances this occurred at random are extremely
low.
We thank Dr Grigg for his interest in our work.[1] We agree that the asthma attacks may have resolved spontaneously in some cases, which was
precisely why we stated that the markers fell in association with steroid
therapy, and nowhere implied causality. Nevertheless, the statistical
analysis suggests that the chances this occurred at random are extremely
low.
We agree that corticosteroids do not inhibit, except at very high
concentrations, degranulation of the eosinophils induced by incubation
with opsonised particles, such as Sepharose beads in vitro.[2] However,
there is overwhelming evidence that cytokines such as IL-5 prime
eosinophils for increased release of granule proteins in this situation,[3,4] and that they inhibit cytokine-mediated prolongation of eosinophil
survival.[5] These observations, coupled with the abundant evidence that
corticosteroids reduce the expression of eosinophil-active cytokines, such
as IL-5, provide a convincing chain of evidence linking the clinical use
of corticosteroids with reduced release of eosinophil granule proteins in
vivo.
With regard to the controls in this study the ratio of atopic to non-
atopic asthmatics was 4:1 and of atopic to non-atopic controls was 3:1.
These differences are not significant by chi-squared testing. Whilst we
agree that more controls might have strengthened our conclusions,
nonetheless the evidence of unresolved inflammation after an apparently
clinically adequate course of prednisolone, as shown by the elevated
levels of IL-5 and sCD25, remains strong.
ANDREW BUSH
Reader and Honorary Consultant Royal Brompton Hospital
Sydney Street, London SW3 6NP, UK
Email: a.bush@rbh.nthames.nhs.uk
CLAIRE HOGG
Specialist Registrar, Paediatrics Royal Brompton Hospital
Email: c.hogg@rbh.nthames.nhs.uk
CHRIS J CORRIGAN
Senior Lecturer, Dept Resp Med & Allergy
Thomas Guy House, Guy’s Hospital, London SE1 9RT, UK
Email: chris.corrigan@kcl.ac.uk
References
(1) Grigg J. Oral steroids and inflammatory markers in asthma. Arch Dis Child [Rapid Response] 16 August 2000.
(2) Kita H, Abu-Ghazaleh R, Sanderson CJ, et al. Effect of steroids
on immunoglobulin-induced eosinophil degranulation. J Allergy Clin Immunol
1991;87:70-7.
(3) Kita H, Weiler DA, Abu-Ghazaleh RI, et al. Release of granule
proteins from eosinophils cultured with IL-5. J Immunol 1992;149:629-35
(4) Fujisawa T, Abu-Ghazaleh RI, Kita M, Sanderson CJ, Gleich GJ.
Regulatory effect of cytokines on eosinophil degranulation. J Immunol
1990;144:642-6.
(5) Wallen N, Kita H, Weiler D, Gleich GJ. Glucocorticoids inhibit
cytokine-mediated eosinophil survival. J Immunol 1991;147:3490-5.
Professor Salazar-De-Sousa,[1] commenting on the recent paper by Høst et al,[2] maintains that recent prospective and randomised clinical studies have shown that
soy protein (SP) is as allergenic as cow's milk (CM) protein citing a review paper[3]; however, the author failed to detail which are these studies.
In 1990 we demonstrated[4] that Eastham et al[5] have shown an antibody response to SPs in...
Professor Salazar-De-Sousa,[1] commenting on the recent paper by Høst et al,[2] maintains that recent prospective and randomised clinical studies have shown that
soy protein (SP) is as allergenic as cow's milk (CM) protein citing a review paper[3]; however, the author failed to detail which are these studies.
In 1990 we demonstrated[4] that Eastham et al[5] have shown an antibody response to SPs in all SP-fed infants that was comparable to that found to CM in CM-fed infants. However, only soy antigenicity was studied,[4] since the authors measured not IgE antibodies but hemagglutinins to soy and to CM, which mainly belong to IgG antibodies.[5] As the
matter remained controversial, I have published a paper with 142 references and 7 tables, encompassing all diverse aspects of SPs.[6]
If Professor Salazar-De-Sousa reads attentively the data shown in the tables of the paper, he shall convince himself that SFs are recommended for the treatment and/or
prevention of food allergy, also following a recent document of the American Academy of Pediatrics.[7] However, we were distressed about the news "against soy formulas" that we read on the literature, such as "soy formulas should not
prescribed to allergic infants, due to the high incidence of
crossreactions with cow milk proteins".[8]
Professor Salazar, however, appears to be really interested in hydrolysate formulas (HFs). We have documented 202 reactions to HFs in a paper, and 41 case-reports in
another. In total 17 cases of shock-anaphylaxis (one every 3.3 years) versus one/22.3 years provoked by SPFs, with a difference of 676%.
ARNALDO CANTANI
University Professor of Pediatrics Professor of Pediatric Allergy and Immunology University of Roma "La Sapienza"
MONICA MICERA University of Roma "La Sapienza"
References
(1) Salazar-De-Sousa J. Dietary products used in infants for treatment and prevention of food allergy [letter]. Arch Dis Child 2000;83:88.
(2) Høst A, Koletzko B, Dreborg S, et al Dietary products used in infants for treatment and prevention of food allergy. Joint Statement of the European Society for Paediatric Allergology and Clinical Immunology Committee on Hypoallergenic Formulas and the European Society for Paediatric Gastroenterology, Hepatology and Nutrition
Committee on Nutrition. Arch Dis Child 1999;81:80-4.
(3) Kerner JA. Use of infant formulas in preventing or postponing atopic manifestations. J Pediatr Gastroenterol Nutr 1997;24:442-6.
(4) Cantani A, Ferrara M, Ragno W, Businco L. Efficacy and safety of a soy-protein-formula for feeding
babies with atopic dermatitis and cow's milk hypersensitivity. Eur Rev Med Pharmacol Sci 1990;12:311-18.
(5) Eastham EJ, Lichauco T, Grady MI, Walker WA. Antigenicity of infant formulas: role of immature intestine on protein permeability. J Pediatr 1978;93:561-4.
(6) Cantani A, Lucenti P. Natural history of soy allergy and/or intolerance in children, and clinical use of soy-protein formulas. Pediatr Allergy Immunol 1997;8:59-74.
(7) American Academy of Pediatrics. Committee on Nutrition. Soy protein-based formulas: recommendations for use in infant feeding. Pediatrics 1998;101:148-53.
(8) Guarino A. Commento ai testi. In La allergia alimentare. Milano: Plada, 2000.
I read with great interest a manuscript reported by Hodson et al in
the journal (2000;83:45-51. The authors discussed various corticosteroid
treatment protocols in patients with nephrotic syndrome (NS). They
suggested that children in their first episode of NS should be treated
with prednisone for at least three months with an increase in benefit being
shown for up to seven months of treatment.
I read with great interest a manuscript reported by Hodson et al in
the journal (2000;83:45-51. The authors discussed various corticosteroid
treatment protocols in patients with nephrotic syndrome (NS). They
suggested that children in their first episode of NS should be treated
with prednisone for at least three months with an increase in benefit being
shown for up to seven months of treatment.
We used prednisone (daily 60 mg/m2 for 4 weeks, 45, 30, 20, 5 mg/m2 on
alternate days for 4 weeks, respectively) in the treatment of 7 patients
with NS (Group I) and compared its effect with the high dose
methylprednisolone (HDMP) in a dosage of 30 mg/kg/d for 3 days, 20 mg/kg/d for 4 days, 10 mg/kg/d for a week, perorally, before 9 A.M. in the
treatment of 8 patients with NS (Group II).[1]
The patients were followed-up for a duration of 38 ± 5.5 months (24-68
months) in Group I and 42 ± 5.5 moths (16-72 months) in Group II.
No
significant difference was obtained in the duration of remission between
two groups (p>0.05), while HDMP induced early remission than
prednisone (p<_0.05. the="the" mean="mean" relapse="relapse" rates="rates" were="were" _0.8="_0.8" year="year" in="in" both="both" groups.="groups." we="we" think="think" that="that" oral="oral" hdmp="hdmp" treatment="treatment" may="may" be="be" used="used" of="of" ns="ns" and="and" is="is" more="more" effective="effective" inducing="inducing" early="early" remission="remission" than="than" prednisone.p="prednisone.p"/>
Conclusion, it can be recommended that patients with NS can be treated
with the oral HDMP as an alternative treatment to standart oral
prednisone treatment.
Reference
(1) Mocan H, Erduran E, Karagüzel G. High dose methylprednisolone therapy in nephrotic syndrome. Indian J Pediatr 1999;66:171-4.
Liz Donovan's fascinating article certainly suggests that the big
finger is pointing at her. However, although her calculation is numerically
correct (and how nice to find someone using non-US billions) the reasoning
is a little suspect.
First multiplying the probabilities gives the odds against these
seven rare conditions presenting in the order indicated; her final figure
should be divided by 7...
Liz Donovan's fascinating article certainly suggests that the big
finger is pointing at her. However, although her calculation is numerically
correct (and how nice to find someone using non-US billions) the reasoning
is a little suspect.
First multiplying the probabilities gives the odds against these
seven rare conditions presenting in the order indicated; her final figure
should be divided by 7 (5040) to provide the odds against this specific
selection presenting to her in one year.
Second she has calculated the a priori possibility for events that
have already occurred. Just think of the odds against finding someone with
the name Liz Donovan working as a consultant paediatrician in Portsmouth
in the year 2000 having an article accepted by Archives of Disease in
Childhood!
The report of Hacking et al,[1] of a series of infants with very
early onset interstitial lung disease (ILD) with good prognosis, is of
great clinical interest but sadly represents a lost investigative
opportunity.
Firstly, their statement that percutaneous open lung biopsy
has fewer side effects than open lung biopsy (OLB) is not supported by any
direct comparative trial, and cannot be allow...
The report of Hacking et al,[1] of a series of infants with very
early onset interstitial lung disease (ILD) with good prognosis, is of
great clinical interest but sadly represents a lost investigative
opportunity.
Firstly, their statement that percutaneous open lung biopsy
has fewer side effects than open lung biopsy (OLB) is not supported by any
direct comparative trial, and cannot be allowed to stand. Indeed, the
largest published series using this technique[2] was heavily criticized
both for the number of complications and the often non-diagnostic samples
obtained.[3,4] In contrast OLB is safe,[5] permits direct inspection of
the site of biopsy, and allows the acquisition of specimens large enough
to determine the lung architecture in order more precisely to classify the
different types of paediatric ILD. OLB thus allows appreciation of the
distribution of disease involvement within the acinus, allowing more
precise identification of different histopathological patterns. There is
thus no reason to favour percutaneous biopsy over OLB in skilled hands;
indeed the weight of evidence is in favour of OLB.
Secondly, their
selected nomenclature of paediatric ILD is open to criticism. It is
questionable whether the use of term "idiopathic pulmonary fibrosis" (IPF)
is still appropriate in children. IPF is generally used synonymously with
lone cryptogenic fibrosing alveolitis, which in adults is most often
represented histopathologically by the pattern of "usual interstitial
pneumonia" (UIP). However UIP is rarely if ever seen in children; much
more common are lymphocytic interstitial pneumonia (LIP), desquamative
interstitial pneumonia (DIP), non-specific interstitial pneumonia (NSIP)
and chronic pneumonitis of infancy.[6] Identifying these histological
patterns may point towards specific investigations with regard to
aetiology, and may also provide prognostic and treatment data, and we
consider that it is a pity that this or a similar histopathological
classification was not used in this report.
We suggest that more will be
learned about these rare conditions if diagnostic precision is maximized
by comparison of pre-biopsy computed tomography with properly classified
histological findings.[7] Inter-disciplinary collaboration is needed to
achieve this; and it is unfortunate that more details of imaging and an up
to date classification of histology were not included in an otherwise
informative paper.[1]
Dr Andrew G Nicholson MRCPath DM
Consultant Histopathologist
Dr Andrew Bush MD FRCP FRCPCH
Reader and Honorary Consultant in Paediatric Respirology
References
(1) Hacking D, Smyth R, Shaw N, Kokia G, Carty H, Heaf D. Idiopathic pulmonary fibrosis in infants: good prognosis with conservative management. Arch Dis Child 2000;83:152-7.
(2) Spencer DA, Alton HM, Raafat F, Weller PH. Combined percutaneous lung biopsy and high-resolution computed tomography in the diagnosis and management of lung disease in children. Pediatr Pulmonol 1996;22:111-16.
(3) Bush A. Diagnosis of interstitial lung disease. Pediatr Pulmonol 1996;22:81-2.
(4) Flake AW. Is a CT guided needle better than a knife? Pediatr Pulmonol 1996;22:83-4.
(5) Coren ME. Nicholson AG, Goldstraw P, Rosenthal M, Bush A. Open lung biopsy for diffuse interstitial lung disease in children. Eur Respir Dis 1999;14:817-21.
(6) Nicholson AG, Kim H, Corrin B, Bush A, du Bois RM, Rosenthal M, Sheppard MN. The value of classifying interstitial pneumonitis in childhood according to defined histological patterns. Histopathology 1998;33:203-11.
(7) Copley SJ, Coren M, Nicholson AG, Rubens MB, Bush A, Hansell DM. Diagnostic accuracy of thin-section CT and chest radiography of pediatric interstitial lung disease. AJR 2000;174:549-54.
Our group has been evaluating ways[1] of empowering parents to
promote family centred care in the neonatal intensive care unit.[2] We therefore read with
interest the important article showing parental hope to be more strongly
associated with the health related quality of life (HRQL) than neonatal or
current physical deficits.[3]
Hope is prevalent amongst parents and staff in the neonatal in...
Our group has been evaluating ways[1] of empowering parents to
promote family centred care in the neonatal intensive care unit.[2] We therefore read with
interest the important article showing parental hope to be more strongly
associated with the health related quality of life (HRQL) than neonatal or
current physical deficits.[3]
Hope is prevalent amongst parents and staff in the neonatal intensive
care unit[4] and comes in a spectrum ranging from hope for survival to
hope of a normal outcome. We would like the authors to define what hope
is. It is interesting that hope is not listed in the Mosby’s Dictionary
but hopelessness is: "a state in which an individual sees limited or no
alternatives or personal choices available and is unable to mobilize
energy on his or her own behalf."[5]
The incidence of single parent families in the cohort was 17%. This
is lower than the 50% reported in an earlier study with divorce rate for
families having a child with spina bifida being nine times higher than
that for the local population.[6] We also note that 54% of the 13 to 20
year olds responded to the study. There is a risk of ascertainment bias
as it is possible that those who did not cooperate may have a poorer
outcome.[7]
As important as parental hope is the hope of the child with spina
bifida, the attitude of siblings and the health care givers (including
intervention services and respite care services) both in the neonatal and
post discharge period. For the 13 to 20 year olds it would have been
informative to correlate HRQL with the Miller’s Hope Scale (MHS) of the
children themselves. Do we know what is the earliest age that a child is
able to hope? The authors may also like to discuss why they did not
include parental hope in the first 5 years of life considering the
critical period for infant-parent bonding.[8] What is the incidence of
mental retardation amongst the children and how does it impact on MHS and
HRQL? Is there any significant difference for children born in the
periods of aggressive treatment compared with those born during the period
of selective treatment.
It is possible that parental hope does not improve HRQL in the
child; rather improved HRQL of the child allows parental hope. Thus hope
may be the result rather than the cause of better HRQL.
THHG Koh MA FRCPCH FRACP Senior Staff Specialist in Neonatal
Paediatrics
Collie L RN Neonatal Research Nurse
Budge D RN Neonatal Research Nurse
Regional NICU, Kirwan Hospital
Townsville, Great Barrier Reef Queensland 4817, Australia
This is part of the T.A.P.E. project, funded by The Royal Children's
Hospital Foundation, Brisbane.
References
(1) Koh THHG, Jarvis C. Promoting effective communication in NICU by
audiotaping parents-neonatologist conversations. Int J Clin Pract 1998;52:27-9.
(2) Harrison H. The principles of family-centered neonatal care.
Pediatrics 1993;92:643-50.
(3) Kirpalani HM, Parkin PC, Willan AR, Fehlings DL, Rosenbaum PL,
King D, Van Nie AJ. Quality of life in spina bifida: importance of
parental hope. Arch Dis Child 2000;83:293-7.
(4) Cole FS. Extremely preterm birth--defining the limits of hope.
N Engl J Med 2000;343:429-30.
(5) Mosby’s Dictionary. 3rd Ed, CV Mosby Company St Louis, 1990.
(6) Tew BJ, Laurence KM, Payne H, Rawnsley K. Marital stability
following the birth of a child with spina bifida. Br J Psychiatry 1977;131:79-82.
(7) Tin W, Fritz S, Wariyar U, Hey E. Outcome of very preterm birth:
children reviewed with ease at 2 years differ from those followed up with
difficulty. Arch Dis Child Fetal Neonatal Ed 1998;79:F83-7.
I was dismayed to see your publication of the letter by Dr Sam
regarding the role of lumbar puncture in meningococcal disease.[1]
While fully understanding the need to get as much information as possible,
the benefits of isolating the causative organism need to be weighed
against the risk of causing clinical deterioration in a patient who may
have cardiovascular compromise, and or, raised intracranial pressu...
I was dismayed to see your publication of the letter by Dr Sam
regarding the role of lumbar puncture in meningococcal disease.[1]
While fully understanding the need to get as much information as possible,
the benefits of isolating the causative organism need to be weighed
against the risk of causing clinical deterioration in a patient who may
have cardiovascular compromise, and or, raised intracranial pressure, both
are which are recognised contraindications to lumbar puncture.[2] There
are clear and recognised risks of performing this procedure in such
patients.
The potential benefits of lumbar puncture include making a diagnosis
of meningitis and isolation of the organism for epidemiological and
sensitivity testing.
In the UK the typical haemorrhagic rash of meningococcal infection is
pathognomonic of the disease and should be treated as such prospectively,
until further confirmatory evidence is available. With Polymerase Chain
Reaction (PCR) of meningococcal DNA in blood allowing up to 100%
sensitivity for diagnosis in the first 24 hours of illness,[3] there is
little to be gained from looking for bacteria or cells in the cerebrospinal fluid (CSF).
The antibiotic regimen is no different for either meningococcal
meningitis or septicaemia, with 7 days of a 3rd generation cephalosporin
being the treatment of choice because of improved CSF penetration.[4]
There are no reports of meningococcal resistance to this treatment in the
UK, so performance of a lumbar puncture for bacterial sensitivity testing
appears to be unnecessary.
Prospective therapy while awaiting results of culture or PCR from
blood seems to be a small price to pay in this life-threatening illness.
An analogy could be drawn from the management of epiglottitis. It is
generally accepted that throat swabs should not be taken from children
with epiglottitis until the child’s airway has been protected due to the
risk of clinical deterioration. It is time that textbooks of emergency
paediatrics stated clearly that lumbar punctures on children with a
haemorrhagic rash and clinical signs of meningococcal infection should be
not be carried out until the clinical condition has been stabilised, and
if the procedure will add further valuable information that cannot be
obtained elsewhere.
References
(1) Sam WIC. The role of lumbar puncture in meningococcal disease [letter]. Arch Dis Child 2000;83:370.
(2) Advanced Paediatric life Support, 2nd Edition. The Advanced Life
Support Group. BMJ Publishing Group, London, UK. 1997.
(3) Newcombe J, Cartwright K, Palmer WH, McFadden J. PCR of peripheral
blood for diagnosis of meningococcal disease. J Clin Microbiol
1996;34:1637-40.
(4) Peltola H, Anttila M, Renkonen OV. Randomised comparison of
chloramphenicol, ampicillin, cefotaxime and ceftriaxone for childhood
bacterial meningitis. Finnish Study Group. Lancet 1989;i:1281-7.
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I was dismayed to see your publication of the letter by Dr Sam regarding the role of lumbar puncture in meningococcal disease.[1] While fully understanding the need to get as much information as possible, the benefits of isolating the causative organism need to be weighed against the risk of causing clinical deterioration in a patient who may have cardiovascular compromise, and or, raised intracranial pressu...
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