We read with interest the article by Rodríguez-Morán et al who
undertook a community-based cross-sectional study of 488 apparently
healthy children aged 10–13 years to assess the hypothesis that magnesium
deficiency is associated with elevated high-sensitivity C reactive protein
(hsCRP) levels (1).
The headline of the article is ‘’Serum magnesium and C-reactive protein
levels’’ whereas in their study the authors wrote th...
We read with interest the article by Rodríguez-Morán et al who
undertook a community-based cross-sectional study of 488 apparently
healthy children aged 10–13 years to assess the hypothesis that magnesium
deficiency is associated with elevated high-sensitivity C reactive protein
(hsCRP) levels (1).
The headline of the article is ‘’Serum magnesium and C-reactive protein
levels’’ whereas in their study the authors wrote that objective was to
assess interaction between hsCRP levels and magnesium levels. CRP is
different from hsCRP.
In their study, eligible children have been allocated to three groups
according to their body mass index (BMI): (a) normal weight; (b)
overweight and (c) obese and definitions in methods were given as ‘’obese
was defined as a BMI equal or greater than the 95th percentile, overweight
by a BMI between the 85th and 95th percentiles, and normal weight by a BMI
lower than the 85th percentile’’. However, obese children have been also
included in their study. In our opinion, obese children are not healthy
children because they have metabolic disturbance.
Clinically important electrolyte disturbances such as hypokalemia and
hypocalcemia have been well described in patients with hypomagnesemia of
various causes (2). Tsau et al concluded that analyses of PTH levels in 13
children suggested that inhibition of PTH synthesis or secretion was
responsible for hypomagnesemic hypocalcemia in most patients (3). On the
other hand, in their study Rodríguez-Morán et al measured only serum
magnesium and hsCRP levels, lipid profile, glucose and insulin levels.
Whereas serum magnesium levels together calcium levels could be also
measured. All serum magnesium, calcium and PTH levels should be measured
concomitantly.
Obesity in children appears to be associated with increased risk of
cardiovascular and metabolic diseases later in life. Early development of
insulin resistance and impaired oxidant-antioxidant status may lead to
endothelial dysfunction and increased carotid intima media thickness (IMT)
even in childhood. In their study Giannini et al aimed to measure IMT and
the relationship between IMT, insulin resistance and oxidant status in
obese pre-pubertal children. In 53 obese pre-pubertal children,
anthropometric measurements and inflammatory markers (hs-CRP and PGF-2
alpha), have been evaluated compared with 41 healthy pre-pubertal
subjects. OGTT have been performed and insulin resistance (IR) indices
have been calculated in all patients. In their study, obese children had
higher levels of PGF-2 alpha and hs-CRP compared to healthy subjects.
Furthermore, fasting insulin levels and HOMA-IR were higher in obese
children than in controls (4).
On the other hand, in their study, Rodríguez-Morán et al included only
children at Tanner stage 1 or 2 because of accompanied with probably
insulin resistance. Table 2 showed characteristics of children according
to hs-CRP and serum magnesium levels but the authors included also obese
group in this study in any case it is expected that obese children have
high insulin levels and insulin resistance. So, control group should have
been composed of subjects with normal weight by a BMI lower than the 85th
percentile and obese group should have been extracted from control group.
We think that early changes in glucose metabolism and an alteration of
oxidant-antioxidant status may be present in obese pre-pubertal children;
this could lead to increase early cardiovascular disease. Furthermore
studies are needed before any conclusion can be drawn.
References
1. Rodríguez-Morán M and Guerrero-Romero F. Serum magnesium and C-reactive
protein levels. Arch Dis Child 2008;93;676-680.
2. Elisaf M, Milionis H, Siamopoulos KC. Hypomagnesemic hypokalemia and
hypocalcemia: clinical and laboratory characteristics. Miner Electrolyte
Metab 1997;23(2):105-12.
3. Tsau YK, Tsai WY, Lu FL, Tsai WS, Chen CH. Symptomatic hypomagnesemia
in children. Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi 1998;39(6):393-
7.
4. Giannini C, de Giorgis T, Scarinci A, Ciampani M, Marcovecchio ML,
Chiarelli F,Mohn A. Obese related effects of inflammatory markers and
insulin resistance on increased carotid intima media thickness in pre-
pubertal children. Atherosclerosis 2008;197(1):448-56.
The BTS guidelines on the management of asthma clearly state that in
children aged 0-5 years, pressurised metered dose inhaler (pMDI) with
spacer is the preferred method of delivery of inhaled corticosteroids
(ICS); and in children aged 5-12 years and adults, dry powder inhalers
(DPI) are as effective as pMDI with spacer (Grade A evidence).(1) The
cover illustration of the August issue of the Archives shows a young boy...
The BTS guidelines on the management of asthma clearly state that in
children aged 0-5 years, pressurised metered dose inhaler (pMDI) with
spacer is the preferred method of delivery of inhaled corticosteroids
(ICS); and in children aged 5-12 years and adults, dry powder inhalers
(DPI) are as effective as pMDI with spacer (Grade A evidence).(1) The
cover illustration of the August issue of the Archives shows a young boy
with a pMDI with the title “Daily versus as-needed inhaled corticosteroid
for mild persistent asthma”. There are a confusing number of choices of
delivery devices for aerosol therapy and health-care professionals play a
key-role in educating patients and care-givers to optimise inhaled drug
delivery. Efficient delivery with pMDIs is highly technique dependent and
not achieved in most Paediatric patients.(2) The NICE Guidance on asthma
in children states that in England and Wales 60% of all patients (adults
and children) diagnosed with asthma use pMDIs (with or without spacer),
17% use breath-actuated pMDIs, and 23% use DPIs.(3) Children with asthma
and care-givers should be encouraged to use pMDIs with spacer or DPIs
where indicated, for optimal delivery of ICS. The cover illustration as
described above, in a journal endorsed by the RCPCH gives out
wrong/confused signals to health-care professionals that the use of pMDIs
alone, is acceptable practice.
References
(1) British Guideline on the Management of Asthma. Thorax 2008; 63
Suppl 4:iv1-121.
(2) Hagmolen of ten Have, van de Berg NJ, Bindels PJ, van Aalderen
WM, van der PJ. Assessment of inhalation technique in children in general
practice: increased risk of incorrect performance with new device. J
Asthma 2008; 45(1):67-71.
(3) NICE Guidance. Corticosteroids for the treatment of chronic
asthma in children under the age of 12 years. Asthma (in children) -
corticosteroids. TA131. 2007.
Ref Type: Report
The above letter by Haythornthwaite et al. raises a number of
important points. It also highlights how misinterpretation of the
findings, no matter how subtle and easily made, can have an impact on the
way in which the findings could be viewed and possibly used. Each point
raised by the above authors are dealt with below:
1) This paper concludes that PACU model is an effective alternative
to...
The above letter by Haythornthwaite et al. raises a number of
important points. It also highlights how misinterpretation of the
findings, no matter how subtle and easily made, can have an impact on the
way in which the findings could be viewed and possibly used. Each point
raised by the above authors are dealt with below:
1) This paper concludes that PACU model is an effective alternative
to A&E services, suggesting that it could work in isolation, so that the
emergency department would be relieved of seeing children.
Response: The paper clearly does not conclude this. It clearly states
that the study suggests the PACU model is “…perceived to be an effective
alternative to standard A&E services for the assessment and early
management of acutely ill children…”. Two key words here are “perceived”
and “standard”. The survey comparison was with a standard A&E service
(i.e. at the time of the study), NOT with an A&E service that also had a
children’s A&E – this is all clear in the article.
Nor do the authors claim that “it IS an effective alternative”, even
to standard A&E, but report that it was “perceived” to be so. The
discussion also states that “…parents and staff prefer the PACU model to
traditional A&E services”. Again the words “prefer” and “traditional” are
key. In this context, traditional/standard A&E simply means where there is
no dedicated children’s A&E.
The findings and conclusions drawn come directly from the responses
provided by staff and parents. These suggest parents prefer the
ambulatory, family-centred approach (indeed this may still be in the form
of an ED unit) to traditional A&E services. This is what the research was
about – not about assessing where the PACU (or ambulatory approach) should
be situated.
2) PACUs need to be associated with an emergency department (ED),
either on the same site or in a near by large hospital; PACUs when ward
based, have problems of immediate access and are rarely designed to
receive and manage ambulance admissions. The PACU described in the survey
conducted by Blair et al found this in their own setting, with only 76% of
parents saying access was easy compared with 95% in the emergency cohort.
Response: Such points are acknowledged and in line with the paper.
3) Another major difference between a PACU and an ED is the
availability of people trained and skilled at triage and re-triage, i.e.
being able to prioritise large numbers of patients safely. It is less of a
problem when the doctors are able to see and treat patients immediately
when the numbers are small. The numbers of patients seen on the PACU
during the study period was 4,190 annually, the emergency department at
the hospital in the study sees 25 000 children per year. There is no
mention of any resuscitation facilities in the ambulatory setting, or
mention of any resuscitation of critical ill patients in the paper, a
concerning omission. Worryingly, there is no mention of critical incidents
or adverse outcomes in the two units over the same period.
Response: We recognise that the volume of patients differed between
the two settings. The focus of our paper was not on critically ill
children but on acute illness requiring diagnostic evaluation over a
period of time. This element is the major component of the PACU approach
which has now been incorporated in the current emergency service provision
at the site.
4) A major limitation of this study is that the data on emergency
patients were collected at night time and the data on PACU patients were
collected from the day. This is a fatal flaw in the study.
Response: This is a limitation as recognised in the paper. It is not
a "fatal flaw" however, for a number of reasons. Firstly, it provides data
on perceptions of parents who attended A&E and therefore allows for a
comparison of perceptions towards the two environments. The groups also
were relatively well-matched (with a few small differences). A&E parents
attended at night which may have biased the results to a certain degree.
This is clearly recognised in the paper. It was not possible to do
anything different because patients would attend PACU during the day and
be dealt with by A&E when PACU was closed. Indeed, our approach reflected
the REALITY of the current services provided at the time. Furthermore,
"night" does not necessarily mean "middle of the night", but could mean
just after when PACU was closed.
We also assess PACU from a number of other angles (e.g. patient
pathway, staff interviews, PACU parental survey in its own right, with a
representative sample of parents, and including a question around
comparison with previous A&E experiences). All "triangulate" to support
the conclusions.
5) The major advantages of the PACU in the study appeared to be a
child friendly environment and paediatric trained staff. It is important
to note that the comparison in this setting was between a PACU and an
emergency department without a separate paediatric area; this has since
changed at the hospital involved in the study, and paediatric emergency
medicine is developing in this context.
Response: The above statement supports our previous statements in
this response letter. The paper clearly states this and the article is in
no way an attack on "paediatric emergency medicine" – indeed it states in
the discussion: "Given that…a recent review found 40% of A&E departments
do not provide specialist paediatric services, these findings suggest the
need to adopt such an approach". This clearly shows we are in agreement in
terms of the general principles. The study merely adds to the evidence
that incorporating a PACU-type approach to emergency paediatric medicine
may be beneficial to meeting the needs of families.
6) The advantages described in this paper of the PACU, in the
assessment of acutely ill children, could be achieved by the creation of a
paediatric ED. This allows the child centred approach to be applied to all
attending paediatric patients, including ill and injured children of all
types. A paediatric ED provides a system with robust triage, resuscitation
facilities and easy access.
The Trust where this study was conducted has realised this and have since
opened a paediatric emergency department which has an integrated PACU
which is functioning well and has taken over the PACU cohort of patients.
The unit described in the paper is now closed.
The paediatric ED now can triage patients (and, if required, resuscitate
them) to a PACU/observation unit when indicated, so avoiding unwarranted
admissions. The creation of PACUs is not to be perceived as an alternative
to paediatric emergency departments, rather it adds another resource in
providing optimal management of unwell children.
Response: The article makes no suggestion (and does not even come
close to suggesting) that PACUs should be perceived as “an alternative to
paediatric emergency departments”. This was not the comparison made in the
methodology, as we have clarified.
Further, we state clearly in the article that, since the study, the
PACU approach has been integrated with A&E at the front end of the
hospital. In addition, at the same point in the article we highlight that
access to PACU was more difficult for parents than A&E - surely this shows
we are implying the recent integration of PACU with A&E is a “move
forward”. However, we could not make any further judgments on this as this
is not what the study was about. Authors must stick to the original
research questions.
Research would now need to be undertaken to further evaluate the key
areas raised around ED services, and Haythornthwaite et al have provided a
worthy addition to possible future topics for further research and debate
in this area.
Thank you for sharing this interesting study. Do such staggering
results in this core area of physician activity, however, not also beg the
question of system failure? A number of reasons come to mind, eg. time
pressures, the frequent need to re-chart, wide variations in chart design
etc.
It may seem enticing to include navigating this system in the ST
interviews but would it then not just add yet another bell-c...
Thank you for sharing this interesting study. Do such staggering
results in this core area of physician activity, however, not also beg the
question of system failure? A number of reasons come to mind, eg. time
pressures, the frequent need to re-chart, wide variations in chart design
etc.
It may seem enticing to include navigating this system in the ST
interviews but would it then not just add yet another bell-curve test to
an already generic selection process? Looking for excellence and critical
thought, how about presenting your findings to the candidates and asking
for their suggestions on how to solve the problem?
We read with interest the review of TB services for children in the
UK by
Adalat et al. Although the survey was conducted several years ago and
prior
to the publication of the recent NICE guidelines, several key issues
mentioned in the article continue to impair the care for children with TB
in
the UK:
- Tuberculosis in children remains an under-appreciated condition and is
not sufficiently prioritized in public healt...
We read with interest the review of TB services for children in the
UK by
Adalat et al. Although the survey was conducted several years ago and
prior
to the publication of the recent NICE guidelines, several key issues
mentioned in the article continue to impair the care for children with TB
in
the UK:
- Tuberculosis in children remains an under-appreciated condition and is
not sufficiently prioritized in public health planning.
- unified approaches to diagnosis and management of latent infection in
children are still lacking.
- few hospitals can provide negative-pressure cubicles required for
isolation
of children with active disease (who's carers might also be infected).
This shortage will become more and more pressing, as MDR TB cases
continue to rise in adults and have started to affect children.
- management of TB as a family disease requires good communication
between chest physicians and designated paediatricians, and in our own
experience, TB nurses with paediatric experience often provide that
crucial
link.
- development of clinical and research networks will be important
particularly in assessing the diagnosis and management of children
supposedly latently infected with TB, as practice continues to vary widely
both within the UK and in Europe. Networks will also be important for the
management of more complex cases of TB or those with MDR TB which will
need involvement from those with greater experience, such as adult
physicians or designated paediatricians.
We acknowledge Dr Nichols's point that the 2006 WHO charts still (and
indeed fortunately) show that a small proportion of infants will
demonstrate weight faltering and these infants may well need assessment
for underlying pathology and/or nutritional support. Indeed the
application of these WHO charts to UK practise is the subject of an
ongoing DoH-funded RCPCH expert working group and implementatio...
We acknowledge Dr Nichols's point that the 2006 WHO charts still (and
indeed fortunately) show that a small proportion of infants will
demonstrate weight faltering and these infants may well need assessment
for underlying pathology and/or nutritional support. Indeed the
application of these WHO charts to UK practise is the subject of an
ongoing DoH-funded RCPCH expert working group and implementation study,
which we agree is a necessity before these charts can be safely launched
in the UK, currently scheduled for March 2009
(http://www.rcpch.ac.uk/Research).
We consider that the adequacy of exclusive breast-feeding is a
different issue, which has been subject to much study and review (1) and
also continuing debate (2).
Yours sincerely
C Wright, R Lakshman, P Emmett and K Ong
1) Kramer MS & Kakuma R. Optimal duration of exclusive
breastfeeding.
Cochrane Database Syst Rev. 2002;(1):CD003517).
2) Fewtrell et al. Optimal duration of exclusive breastfeeding: what
is the evidence to support current recommendations? Am J Clin Nutr. 2007
Feb;85(2):635S-638S.
Whilst I am pleased to see that Drs Khashu and Balasubramaniam have
agreed to retract their previous statement that "Weak evidence suggests an
increased risk of necrotising enterocolitis with the use of Gelofusine in
neonates" it is clear from the second paragraph of Dr Khashu’s letter [1]
that they still have not grasped the point of logic that Dr Evans and I
have separately tried to get across. As a very similar error t...
Whilst I am pleased to see that Drs Khashu and Balasubramaniam have
agreed to retract their previous statement that "Weak evidence suggests an
increased risk of necrotising enterocolitis with the use of Gelofusine in
neonates" it is clear from the second paragraph of Dr Khashu’s letter [1]
that they still have not grasped the point of logic that Dr Evans and I
have separately tried to get across. As a very similar error to that in Dr
Kashu's letter occurs in the formal correction I must assume that the
editors of the Archives of Disease in Childhood are experiencing a similar
difficulty.[2]
Let me try again. Yes, it is true that the Cochrane Review [3] (table
6.11) calculated from published data that Gelofusine when compared with
Fresh Frozen Plasma (FFP), was associated with a statistically significant
increased incidence of necrotising enterocolitis (NEC). It is also true
that the same Cochrane Review found that when Gelofusine was compared with
placebo there was no difference in respect of NEC (Table 5.11). Finally,
when FFP was compared with the same placebo, the placebo was associated
with a statistically significant increased incidence of NEC (Table 4.14).
Setting aside all of the caveats that one should be considering before
trying to conclude anything of substance from this data then the ONLY
logical conclusion from this is that this data suggests that FFP is
PROTECTIVE against NEC.
The interpretation put on this evidence by Drs Khashu and Balasubramaniam
is illogical, unsupportable in any context and wrong. To rearrange the
final sentences of their letter and the correction - It is the same as
saying that “a doubt has been raised by analysis 4.14 regarding a
potential link (between the placebo - maintenance 10% dextrose infusion –
and NEC) and this warrants further research. Pending such safety studies
maintenance dextrose should only be used with caution in preterm infants.”
A statement that is clearly illogical nonsense but yet no more illogical
than what they actually say in the final sentences of their letter and
their correction.1,2
Sam Richmond
Sunderland Royal Hospital
8th March 2008
1. Khashu M. In neonates requiring intravascular volume resuscitation
in the use of gelofusine safe and efficacious? – author’s reply. Arch Dis
Child 2008; 93: 264.
3. Osborn DA, Evans N. Early volume expansion for prevention of
morbidity and mortality in very preterm infants. Cochrane Database of
Systematic Reviews 2004, Issue 2. Art. No.: CD002055
Coulthard proposes that 0.18% saline should be the maintenance fluid
of choice in children and that an intravenous fluid with a sodium
composition of 0.45% saline or higher will lead to an increased number of
cases of hypernatremia. His arguments are based primarily on two false
premises: 1) that SIADH is extremely rare and 2) that renal concentrating
defects are common. In 2003, we proposed the use of 0.9% saline as a...
Coulthard proposes that 0.18% saline should be the maintenance fluid
of choice in children and that an intravenous fluid with a sodium
composition of 0.45% saline or higher will lead to an increased number of
cases of hypernatremia. His arguments are based primarily on two false
premises: 1) that SIADH is extremely rare and 2) that renal concentrating
defects are common. In 2003, we proposed the use of 0.9% saline as a
maintenance parenteral fluid for the prevention of hospital-acquired
hyponatremia, as hypotonic fluids were associated with multiple cases of
death and neurological injury from hyponatremic encephalopathy in
children.[1] Hospitalized children have multiple non-osmotic stimuli for
AVP production that put them at risk for hyponatremia, such as nausea,
vomiting, pain, stress, pulmonary disorders, CNS disorders, malignancies,
narcotics, NSAIDS, dehydration, hypotension, sepsis, adrenal insufficiency
and hypoalbuminemia. These children are all at risk for hospital-acquired
hyponatremia and would benefit from 0.9% saline. Dr. Coulthard’s criteria
for the diagnosis of SIADH, a urine osmolality > 600 mOsm/kg and a FeNa
> 3%, are incorrect. The definition of SIADH, as originally put forth
by Bartter and Schwartz, is that in the absence of a hemodyamic stimulus
for AVP production, renal disease or endocrine disorder, that the urine is
less than maximally dilute (> 100 mOsm/kg) and that urinary sodium
excretion increases in response to fluid volume or sodium intake.[2]
Under most circumstances patients with SIADH have a urine osmolality less
than 600 mOsm/kg.[3] SIADH is one of the most common causes of hospital-
acquired hyponatremia and has been associated with almost every disease
state.
Dr. Coulthard’s concern that 0.45% saline should be avoided for fear
of developing hypernatremia is unfounded. Severe renal concentrating
defects are extremely rare. Congenital nephrogenic diabetes insipidus has
an estimated prevalence of only 1 in 250,000 males. Most of these
children will present with hypernatremia. Patients with renal disease do
have partial renal concentrating defects, but it would be unusual, if not
unheard of, for a child with normal renal function to be hyposthenuric (
unable to concentrate the urine to an osmolality similar to plasma). An
otherwise healthy child will not develop hypernatremia from the use of
0.9% saline as the kidney will excrete a hypertonic urine and generate
free water. We have previously demonstrated that the majority of
otherwise healthy ambulatory children excrete a hypertonic urine on a
regular basis.[4] On the other hand, virtually every hospitalized child
has a potential stimulus for AVP production, and the risk of developing
hyponatremia from the administration 0.18% saline is real. A recent
prospective study has revealed that hypotonic fluids result in a fall in
serum sodium, while isotonic fluids do not produce hypernatremia.[5]
Coulthard himself has reported that 0.18% saline and near isotonic
Hartman’s solution do produce a fall in serum sodium post-operatively and
do not produce hypernatremia.[6] There can be no justification for the
routine administration of 0.18% saline, and there is neither physiological
basis nor empirical evidence to support the idea that isotonic fluids will
produce hypernatremia.
1. Moritz ML, Ayus JC. Prevention of hospital-acquired hyponatremia:
a case for using isotonic saline. Pediatrics 2003;111:227-30.
2. Bartter FC, Schwartz WB. The syndrome of inappropriate secretion
of antidiuretic hormone. Am J Med 1967;42:790-806.
3. Musch W, Decaux G. Treating the syndrome of inappropriate ADH
secretion with isotonic saline. Qjm 1998;91:749-53.
4. Moritz ML. Urine sodium composition in ambulatory healthy
children: hypotonic or isotonic? Pediatr Nephrol 2008. Epub ahead of
print
5. Yung M, Keeley S. Randomised controlled trial of intravenous
maintenance fluids. J Paediatr Child Health 2007;0:0.
6. Coulthard MG, Cheater LS, Long DA. Perioperative fluid therapy in
children. Br J Anaesth 2007;98:146-7.
We were interested to read Dr Coulthard’s opinions on maintenance
intravenous fluids(1) in the context of NPSA patient safety alert 22.(2)
As highlighted by Stewart et al in their response to Dr. Coulthard’s
article(3) there is no default fluid designated by the NPSA however when
we examined all of the NPSA recommendations, with regard to our patient
population, we decided to opt for the isotonic fluid 0.9% Saline with...
We were interested to read Dr Coulthard’s opinions on maintenance
intravenous fluids(1) in the context of NPSA patient safety alert 22.(2)
As highlighted by Stewart et al in their response to Dr. Coulthard’s
article(3) there is no default fluid designated by the NPSA however when
we examined all of the NPSA recommendations, with regard to our patient
population, we decided to opt for the isotonic fluid 0.9% Saline with 5%
Dextrose as a single “default fluid”. We believe that this is logical,
safe and simple.
Firstly it is a logical fluid. The majority of children in whom
intravenous fluids are required on a general paediatric medical and
surgical ward are likely to have excess ADH secretion, and therefore 0.9%
Saline with 5% Dextrose is appropriate. In this circumstance we also
decrease the fluid volume to two-thirds of the volume traditionally cited
as “maintenance”, except in the dehydrated child.
Secondly it is safer than a hypotonic fluid. In children with excess
ADH secretion, there is a tendency to develop hyponatraemia. This is not
prevented by use of an isotonic fluid but it would take longer to develop
than with infusion of a hypotonic fluid, giving opportunity for detection
before serious sequelae occur. Rigorous monitoring of electrolytes is an
essential part of fluid prescription, again as emphasised in the NPSA
recommendation, and the algorithm described in Coulthard’s article is a
useful one in the children in whom hyponatraemia develops.
Finally it is simple – further contributing to safety. Fluids may be
prescribed by colleagues who are not familiar with paediatric patients; we
have minimised fluid prescribing in children by non-paediatric doctors.
They may be commenced at night or at exceptionally busy times, where human
error is more likely. Reducing complexity is a major factor in changing
systems to prevent patient harm.(4)
There are potential complications with this fluid, such as
hypernatraemia, hyperchloraemia, metabolic acidosis, hypertension and
phlebitis, and we are currently auditing this; however we believe the
evidence is that the risk of these are less than the risk of
hyponatraemia. We recognise the risks of adopting a “new standard of care”
without a good evidence base and we support the call by Choong et al,
following their systematic review of hypotonic vs isotonic fluids(5) , for
clinical trials to compare different fluid regimens. In the meantime a
national clinical alert network should be established to report problems
with the administration of isotonic fluids – such a facility may have
identified the problems with hypotonic solutions with which we are only
dealing with now – over 50 years later.
In summary, the use of a single default isotonic fluid such as 0.9%
Saline with 5% Dextrose is logical, safe and simple, when used together
with fluid restriction and close monitoring as recommended by NPSA.
Patient-tailored prescriptions can follow later if required.
References
(1)Coulthard MG. Will changing maintenance intravenous fluid from
0.18% to 0.45% saline do more harm than good? Arch Dis Child 2008
;93(4):335-40.
(2) NPSA Safety Alert 22. Reducing the risk of harm when
administering intravenous fluids to children. National Patient safety
Agency. http://www.npsa.nhs.uk. 2007
(3)Stewart PC, Nutt C, McGrath K. Solutions are less complicated than
theory. Arch Dis Child 2008, e-letter.
(4) Nolan, T. System changes to improve patient safety. BMJ
2000;320:771-773.
(5) Choong K et al. Hypotonic versus isotonic saline in hospitalised
children: a systematic review. Arch. Dis. Child 2006;91:828-835.
Dear Editor,
Cote et al recently reported that a small proportion of infants deaths
that were unexplained after careful examination occur when babies are left
in sitting devices (1). Vaucher suggests that the relative risk of death
may actually be lower in sitting devices since some babies spend prolonged
periods in sitting devices (2). This would be correct if risk was similar
for all devices. In practice though, the majo...
Dear Editor,
Cote et al recently reported that a small proportion of infants deaths
that were unexplained after careful examination occur when babies are left
in sitting devices (1). Vaucher suggests that the relative risk of death
may actually be lower in sitting devices since some babies spend prolonged
periods in sitting devices (2). This would be correct if risk was similar
for all devices. In practice though, the majority of deaths were in car
safety seats, consistent with a recent cohort of apparent life threatening
events (3).
There is increasing direct evidence that restraint in a car safety
seat can compromise young infants’ airways (4,5). Further, we have shown
in both premature and young term infants who were restrained in age
appropriate infant car safety seats that a simple foam plastic insert
placed behind the infant’s back to push the body forward, with a slot to
allow the typically protuberant occiput of young infants to rest behind
the spinal line, prevents head flexion and reduced the frequency of falls
in SpO2 (4, 5). In the premature infants, this intervention prevented
narrowing of the upper airways that otherwise occurred when the infants
fell asleep in their car seat (4). Interestingly, although desaturation
can indeed also occur in a car bed, this was also clinically associated
with head flexion in some of the events in a report from Salhab et al (6),
suggesting that the key common mechanism is forced flexion of the head on
the neck leading to upper airway narrowing.
Although the data from Cote et al suggest that the absolute risk is
very small (1), given the importance of car seats for crash protection,
and the near-universal, and in many countries mandated exposure to travel
in car seats, it is essential to address even small risks.
1. Cote A, Bairam A, Deschesne M, Hatzakis G. Sudden infant deaths in
sitting devices. Arch Dis Child 2008;93:384-9.
2. Vaucher N. Sitting devices could protect against sudden infant death.
Arch Dis Child 2008;93:448.
3. Tonkin SL, Vogel SA, Bennet L, Gunn AJ. Apparent life-threatening
events in infant car safety seats. BMJ 2006;333:1205-6.
4. Tonkin SL, McIntosh CG, Hadden W, Dakin C, Rowley S, Gunn AJ. Simple
car seat insert to prevent upper airway narrowing in preterm infants: A
pilot study. Pediatrics 2003;112:907-13.
5. Tonkin SL, McIntosh CG, Nixon G, Rowley S, Gunn AJ. Can we reduce
episodes of haemoglobin desaturation in full-term babies restrained in car
seats? Acta Paediatr 2008;97:105-11.
6. Salhab WA, Khattak A, Tyson JE, Crandell S, Sumner J, Goodman B, et al.
Car seat or car bed for very low birth weight infants at discharge home. J
Pediatr 2007;150:224-8.
We read with interest the article by Rodríguez-Morán et al who undertook a community-based cross-sectional study of 488 apparently healthy children aged 10–13 years to assess the hypothesis that magnesium deficiency is associated with elevated high-sensitivity C reactive protein (hsCRP) levels (1). The headline of the article is ‘’Serum magnesium and C-reactive protein levels’’ whereas in their study the authors wrote th...
The BTS guidelines on the management of asthma clearly state that in children aged 0-5 years, pressurised metered dose inhaler (pMDI) with spacer is the preferred method of delivery of inhaled corticosteroids (ICS); and in children aged 5-12 years and adults, dry powder inhalers (DPI) are as effective as pMDI with spacer (Grade A evidence).(1) The cover illustration of the August issue of the Archives shows a young boy...
RESPONSE
The above letter by Haythornthwaite et al. raises a number of important points. It also highlights how misinterpretation of the findings, no matter how subtle and easily made, can have an impact on the way in which the findings could be viewed and possibly used. Each point raised by the above authors are dealt with below:
1) This paper concludes that PACU model is an effective alternative to...
Thank you for sharing this interesting study. Do such staggering results in this core area of physician activity, however, not also beg the question of system failure? A number of reasons come to mind, eg. time pressures, the frequent need to re-chart, wide variations in chart design etc.
It may seem enticing to include navigating this system in the ST interviews but would it then not just add yet another bell-c...
We read with interest the review of TB services for children in the UK by Adalat et al. Although the survey was conducted several years ago and prior to the publication of the recent NICE guidelines, several key issues mentioned in the article continue to impair the care for children with TB in the UK: - Tuberculosis in children remains an under-appreciated condition and is not sufficiently prioritized in public healt...
Dear Editor,
We acknowledge Dr Nichols's point that the 2006 WHO charts still (and indeed fortunately) show that a small proportion of infants will demonstrate weight faltering and these infants may well need assessment for underlying pathology and/or nutritional support. Indeed the application of these WHO charts to UK practise is the subject of an ongoing DoH-funded RCPCH expert working group and implementatio...
Whilst I am pleased to see that Drs Khashu and Balasubramaniam have agreed to retract their previous statement that "Weak evidence suggests an increased risk of necrotising enterocolitis with the use of Gelofusine in neonates" it is clear from the second paragraph of Dr Khashu’s letter [1] that they still have not grasped the point of logic that Dr Evans and I have separately tried to get across. As a very similar error t...
Coulthard proposes that 0.18% saline should be the maintenance fluid of choice in children and that an intravenous fluid with a sodium composition of 0.45% saline or higher will lead to an increased number of cases of hypernatremia. His arguments are based primarily on two false premises: 1) that SIADH is extremely rare and 2) that renal concentrating defects are common. In 2003, we proposed the use of 0.9% saline as a...
We were interested to read Dr Coulthard’s opinions on maintenance intravenous fluids(1) in the context of NPSA patient safety alert 22.(2) As highlighted by Stewart et al in their response to Dr. Coulthard’s article(3) there is no default fluid designated by the NPSA however when we examined all of the NPSA recommendations, with regard to our patient population, we decided to opt for the isotonic fluid 0.9% Saline with...
Dear Editor, Cote et al recently reported that a small proportion of infants deaths that were unexplained after careful examination occur when babies are left in sitting devices (1). Vaucher suggests that the relative risk of death may actually be lower in sitting devices since some babies spend prolonged periods in sitting devices (2). This would be correct if risk was similar for all devices. In practice though, the majo...
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