We read with interest your article on follow up of children with
community acquired pneumonia and also your eletter response on the
subject. I t is interesting to note that children with pre-existing asthma
are at significant risk of persistent cough after admission to hospital
for community acquired pneumonia. However the risk of subsequent asthma is
increased only in children of non-atopic parents.
In routine clinical pr...
We read with interest your article on follow up of children with
community acquired pneumonia and also your eletter response on the
subject. I t is interesting to note that children with pre-existing asthma
are at significant risk of persistent cough after admission to hospital
for community acquired pneumonia. However the risk of subsequent asthma is
increased only in children of non-atopic parents.
In routine clinical practice the children with pneumonia are not normally
followed up in the clinic and at the most seen once in the clinic to
ensure resolution of consolidation. The current British thoracic society
guidelines make no recommendation for long term follow up (2). We would
like to note the following issues in your study.
1. Due to the retrospective nature of your study it was not possible
to assess premorbid lung functions. Castro-Rodriguez et al found those
with a diagnosis of pneumonia had lower levels of maximal flows at FRC at
mean age of 2 mo (albeit not significantly) and at age 6 yr and lower
levels of FEV1 and FEF25–75 at age 11 yr. They conclude that children with
x-ray confirmed pneumonia have diminished airway function that is probably
present shortly after birth. These deficits are at least in part due to
alterations in the regulation of airway muscle tone (1).
Therefore the question of whether preexisting abnormal lung function
predisposes to pneumonia or of pneumonia resulting in lung function
abnormality remains unanswered.
2. Bronchial hyperactivity was not determined in your study.
Bronchial hyperactivity is far more common than asthma in children with
pneumonia. In a study by korppi et al (3) bronchial hyperactivity
indicated by methacholine inhalation challenge was present in 45% of the
pneumonia group. All 10 asthmatic patients had bronchial hyperactivity,
but only 20% of hyperactive children had asthma. In another study (4)
bronchial hyperactivity was present in 42% of children with pneumonia at
less than 2 years age when followed to a median age of 19 years.
It is possible that certain percentage of children in the bronchial
hyperactivity group develop asthma over a period of time. It is not very
clear which factors predispose to the development of asthma.
3. Does the outcome of the study suggest that we should be following
up all children with pneumonia? At present we do not have sufficient
evidence to support a change of practice.
References
1. Castro-Rodriguez JA, Holberg CJ, Wright AL, et al. Association of
radiologically
ascertained pneumonia before age 3 yr with asthmalike symptoms and
pulmonary
function during childhood. Am J Respir Crit Care Med 1999;159:1891–7.
2.British Thoracic Society Standards of Care Committee. British
Thoracic Society
Guidelines for the Management of Community Acquired Pneumonia in
Childhood.
Thorax 2002;57(Suppl 1):i1–24.
3. Korppi ML, Kuikka T, Reijonen, et al. Bronchial asthma and
hyperreactivity after early childhood bronchoilitis or pneumonia. Arch
Paediatr Adolesc Med 1994;148:1079–84.
4. Eija Piippo-Savolainen et al Asthma and Lung Function 20 Years after
Wheezing in Infancy: Results From a Prospective Follow-up Study Arch
Pediatr Adolesc Med. 2004;158:1070-1076
Dr Rowland and colleagues have recently reported a prospective audit
on the use of rectal paraldehyde in children with prolonged seizures (1).
On the basis of their data they conclude that “This would appear to
confirm that paraldehyde should remain a treatment for the management of
prolonged tonic-clonic convulsions, including convulsive status
epilepticus”. Unfortunately there are several issues that req...
Dr Rowland and colleagues have recently reported a prospective audit
on the use of rectal paraldehyde in children with prolonged seizures (1).
On the basis of their data they conclude that “This would appear to
confirm that paraldehyde should remain a treatment for the management of
prolonged tonic-clonic convulsions, including convulsive status
epilepticus”. Unfortunately there are several issues that require
discussion before that conclusion can be justified.
There seems to be little doubt that rectal paraldehyde has some
anticonvulsant activity, a feature in common with a multitude of other
drugs ranging from the older drugs (phenytoin, phenobarbitone, lidocaine,
chlormethiazole, diazepam, clonazepam etc) through to the newer agents
(midazolam, sodium valproate, levetiracetam, lacosamide). The issue is not
whether rectal paraldehyde is an anticonvulsant drug but whether it is
justifiably in a national guideline as a second line agent in preference
to any of the above agents.
There are several reasons why the positioning of rectal paraldehyde
in the APLS guideline is difficult to justify. A major consideration is
the recommendation that the intravenous access used for administration of
the first line agent (lorazepam in the APLS guideline) is ignored whilst
rectal paraldehyde is administered, a position not adopted in other
developed countries (2). The treating physician will have far more control
of the situation if a second intravenous agent is administered. Rectal
administrations do not have precisely predictable bioavailability even if
intrafaecal injections and rectal expulsions do not occur. A potential
difficulty with the administration of intravenous phenytoin is the length
of time the infusion takes. However, in our large population based study
it was clear that seizure termination with phenytoin usually occurred
before the end of the infusion (3). In addition, that study revealed that
phenytoin was approximately 9 times more likely to result in seizure
termination within ten minutes of administration than rectal paraldehyde
further supporting the view that intravenous therapy is to be preferred to
rectal therapy, at the time that rectal paraldehyde is currently
recommended. Our study also showed 5% of those treated with rectal
paraldehyde had recurrence of seizures within 4 hours compared to no
children treated successfully with intravenous phenytoin.
The evaluation of the efficacy of rectal paraldehyde in the study by
Rowland et al did not only assess the efficacy when it was administered at
the time that is suggested in the APLS guideline. Approximately 30% of
children received it as a first line agent because of previous failures or
side effects with benzodiazepines. This is very likely to introduce a bias
to the sample. Another potential source of bias is that the sample
recruited is not representative of the population at large. The majority
of patients had pre-existing epilepsy (compared to approximately 12% in
our population based cohort4), was older (mean age 6.12 years, range 5
months to 16 years compared to mean age 3.24 years, range 2 months to 15
years), and it is not obvious that any had febrile convulsions, which is
the most common aetiology in the population (4). In addition, few children
contributed many of the episodes (e.g. four patients were treated 13 times
because a benzodiazepine had previously failed. Recurrent administration
of rectal paraldehyde is likely to have been successful as the families
clearly persisted with the strategy). Our population based study is much
less likely to be biased and evaluated the effect of paraldehyde at the
time suggested by APLS and does not support its use (3). The reason
proposed for the difference in efficacies reported in these 2 studies is
that dosing was more appropriate in the study by Rowland et al. Although
this is possible it seems to be unlikely as Rowland et al did not show a
dose dependent effect in their study, we adjusted for dose administered in
our analyses and consistent with the Rowland study we also did not show
dose dependence. Therefore, the most likely reasons for the differences
observed between the 2 studies are selection bias and use of the drug
outside of the current guidance.
Another potential role for rectal paraldehyde is in children in whom
it has not been possible to establish intravenous access. However,
intravenous therapy is more effective in the Accident and Emergency
setting, even for first line therapy in that setting, and therefore the
imperative for appropriate treatment for convulsive status epilepticus
should be to establish intravenous access and rectal treatment should be
seen as a last resort (3).
For the reasons above the study by Rowland et al has not provided
information that is material to the development of a generic national
guideline, nor have they provided evidence that the current APLS guidance
is appropriate. Their data may however suggest that rectal paraldehyde
could have benefit in selected patients with epilepsy and can be
considered for individualised protocols for children with recurrent
prolonged seizures.
Rod C Scott
Richard FM Chin
Brian GR Neville
References
Reference List
1. Rowland AG, Gill AM, Stewart AB et al. Review of the efficacy of
rectal paraldehyde in the management of acute and prolonged tonic-clonic
convulsions. Arch Dis Child 2009.
2. Yoong M, Chin RF, Scott RC. Management of convulsive status
epilepticus in children. Arch Dis Child Educ Pract Ed 2009;94:1-9.
3. Chin RF, Neville BG, Peckham C, Wade A, Bedford H, Scott RC.
Treatment of community-onset, childhood convulsive status epilepticus: a
prospective, population-based study. Lancet Neurol 2008;7:696-703.
4. Chin RF, Neville BG, Peckham C, Bedford H, Wade A, Scott RC.
Incidence, cause, and short-term outcome of convulsive status epilepticus
in childhood: prospective population-based study. Lancet 2006;368:222-229.
The leading article on child protection by Ben Matthews et al (1)
starts with a promising review of the difficulties experienced by UK
Paediatricians with child protection work. However, their argument that
low substantiated cases of abuse and neglect in UK represent the
reluctance of paediatricians in England to engage in the business of child
protection is not supported by their statistics. Also, their approach of
comp...
The leading article on child protection by Ben Matthews et al (1)
starts with a promising review of the difficulties experienced by UK
Paediatricians with child protection work. However, their argument that
low substantiated cases of abuse and neglect in UK represent the
reluctance of paediatricians in England to engage in the business of child
protection is not supported by their statistics. Also, their approach of
comparing substantiation rates across different child protection systems
and processes is flawed. The authors introduce the concept of mandatory
reporting laws for child abuse. These have a limited evidence base for
truly improving outcomes for children, but have a potential for personal
penalties for professionals who may not have reported child abuse for any
reason and also introduce a risk of complacency about child protection
work in the future.
At face value, the substantiation rates of child abuse and neglect in
USA (12.1 per thousand children) appear significantly more than England (3
per thousand children). An analysis of the data from the Child
Maltreatment Report (USA, 2007) (2) confirms that the national rate of
referral was 43 per 1000 children. Comparing this with 538,500 child
protection referrals made in England (3) and a child population of
approximately 11.66 million (4), shows that the referral figures for
England are in fact slightly more than USA. Hence it cannot be concluded
that lack of reporting laws in England contributes to the lower
substantiation rates.
Also, child protection procedures in England (5) may not be directly
comparable to other societies with similar child welfare standards.
Initial assessments by children’s social care in England (319,900 in 2008)
could result in a ‘child in need’ conclusion with a plan for service
provision for supporting the child and family. A proportion of the initial
assessments require core assessments (105,100 in 2008) for a more in-depth
assessment of the child’s needs and parental capacity to respond to these
needs. There may be substantiated concerns that a child has suffered
significant harm, but a plan for ensuring the child’s future safety and
welfare can be developed and implemented without having a child protection
conference or a child protection plan. Hence substantiation rate
comparison across countries may have less meaning unless similar
procedures are followed everywhere.
Legislative immunity for reporting professionals is an attractive
concept. However, it is unlikely to exist in isolation of mandatory
reporting laws. Such mandatory reporting laws bring up a whole range of
problems which the authors touch upon in one paragraph towards the end of
their report. A significant majority of paediatricians would agree that
child protection services in some parts of England appear overwhelmed by
the volume of work they face to safeguard children within the current
processes. Overburdening these systems with many more unsubstantiated
notifications (as would arise from mandatory reporting) would not only be
time consuming and costly, but also risk diverting attention and resources
from those children at real risk of abuse.
Mandatory reporting does carry a sting in its tail for professionals
too; failure to report carries a range of personal penalties for non-
reporting (6). The default position of being ‘safe than sorry’ will have
implications for service efficiency and cost. More importantly, if future
generations of professionals have a sense of ‘legislative security’, there
remains a real risk that knowledge, skills and training in child
protection could be adversely affected.
There is no doubt about the fact that paediatricians’ confidence in
child protection work needs to be urgently restored in the UK. The article
by Matthews et al takes a bold first step towards addressing some of the
barriers to this. There is, however, unlikely to be a single solution to a
complex problem like this.
References
1. Mathews B, Payne H, Bonnet C, Chadwick D. A way to restore British
paediatricians’ engagement with child protection. Arch Dis Child 2009; 94:
329-331
2. Administration for Children and Families. Child Maltreatment 2007.
Reports. Chapter 2
http://www.acf.hhs.gov/programs/cb/pubs/cm07/chapter2.htm#screen
3. Department for Children, Schools and Families. Referrals,
Assessments and Children and Young People who are the subject of a Child
Protection Plan, England- year ending 31 Mar 2008
http://www.dcsf.gov.uk/rsgateway/DB/SFR/s000811/index.shtml
4. Office of National Statistics
http://www.statistics.gov.uk/statbase/Product.asp?vlnk=15106
5. Working Together to Safeguard Children. 2006. London
6. Mandatory Reporting of Child Abuse and Neglect: State Statutes and
Professional Ethics
http://www.ndaa.org/pdf/mandatory_reporting_state_statutes.pdf
Samuel and colleagues(1) aim to review the clinical and
epidemiological evidence relevant to the use of pre-implantation diagnosis
(PGD) to create a “saviour sibling.” A thorough literature review
regarding the use of this method should include consideration of the
medical problems that may occur in the child born following assisted
reproduction technology (ART), but this was not addressed in this...
Samuel and colleagues(1) aim to review the clinical and
epidemiological evidence relevant to the use of pre-implantation diagnosis
(PGD) to create a “saviour sibling.” A thorough literature review
regarding the use of this method should include consideration of the
medical problems that may occur in the child born following assisted
reproduction technology (ART), but this was not addressed in this article.
There is a large (and still growing) body of literature reporting the
association of imprinting disorders with ART, which has prompted a call
for large-scale investigation of the incidence of birth defects, cancer,
and other health problems in children born following ART. (2-4) This
information would surely be of interest to the parents of this future
child as they would be responsible for caring for him/her and all his/her
medical (not to mention psychological) burdens.
Any discussion that left this information out would not in any way
“engender trust” but would take advantage of parents at a time when they
are most vulnerable and, therefore, more prone to dismiss the long-term
implications that a decision such as PGD would have for themselves and for
their future child, whose existence would arise for, and be delimited by,
a specific purpose – that of serving as a “biological insurance” for an
older sibling.
Yours sincerely,
Marjorie Garvey, MB, BCh
Division of Developmental Translational Research, NIMH
Neuroscience Center
6001 Executive Blvd,
Rockville, MD 20852
The views expressed in this letter are the authors’ own opinions and
do not necessarily represent the views of the NIMH. Dr Garvey has no
competing interests.
References
1. Samuel GN, Strong KA, Kerridge I, Jordens CF, Ankeny RA, Shaw PJ.
Establishing the role of pre-implantation genetic diagnosis with human
leucocyte antigen typing: what place do "saviour siblings" have in
paediatric transplantation? Arch Dis Child 2009;94:317-20.
2. Cheung AP. Assisted reproductive technology - Both sides now. J
Reprod Med 2006;51:283-92.
3. Manipalviratn S, DeCherney A, Segars J. Imprinting disorders and
assisted reproductive technology. Fertil Steril 2009;91:305-15.
4. Niemitz EL, Feinberg AP. Epigenetics and assisted reproductive
technology: A call for investigation. Am J Hum Genet 2004;74:599-609.
We read with interest the finding of an unchanged incidence of
microalbuminuria with time in children with type 1 diabetes in the Oxford
Regional Prospective Study cohort. Figure 1 demonstrates no difference in
the cumulative prevalence of developing microalbuminuria in relation to
year of diabetes onset. However we note the small numbers of patients
remaining at 10 years, particularly in group C, and wonder whether a
d...
We read with interest the finding of an unchanged incidence of
microalbuminuria with time in children with type 1 diabetes in the Oxford
Regional Prospective Study cohort. Figure 1 demonstrates no difference in
the cumulative prevalence of developing microalbuminuria in relation to
year of diabetes onset. However we note the small numbers of patients
remaining at 10 years, particularly in group C, and wonder whether a
difference between the groups may be found if the results of group B and C
were combined.
As commented by Amin et al, this finding is different from that
previously reported in our clinic-based cohort which showed a significant
decline in the rates of early elevation of albumin excretion rate (AER
≥7.5µ/min) and microalbuminuria (AER ≥20µ/min) in adolescents
between 1990-2002 (1). It is well recognised that the prevalence of
overweight in children and adolescents is increasing over time (2).
Increased body mass index and waist-hip ratio are independent risk factors
for microalbuminuria in type 1 diabetes (3). We have also shown in a
longitudinal cohort that obesity and insulin dose are independent
predictors for persistent microalbuminuria (4). We speculate that the
increasing BMI in patients with type 1 diabetes over time has offset any
positive effect of improved glycaemic control on the incidence of
microalbuminuria. It would be of interest to investigate the effect of
these measures on the risk of the development of microalbuminuria in this
cohort.
References
1. Mohsin F, Craig ME, Cusumano J, et al. Discordant trends in
microvascular complications in adolescents with type 1 diabetes from 1990
to 2002. Diabetes Care 2005;28:1974-80.
2. Libman IM, Pietropaolo M, Arslanian SA, LaPorte RE, Becker DJ.
Changing prevalence of overweight children and adolescents at onset of
insulin-treated diabetes. Diabetes Care 2003;26:2871-5.
3. Chaturvedi N, Bandinelli S, Mangili R, Penno G, Rottiers RE,
Fuller JH. Microalbuminuria in type 1 diabetes: rates, risk factors and
glycemic threshold. Kidney Int 2001;60:219-27.
4. Stone ML, Craig ME, Chan AK, Lee JW, Verge CF, Donaghue KC.
Natural history and risk factors for microalbuminuria in adolescents with
type 1 diabetes: a longitudinal study. Diabetes Care 2006;29:2072-7.
I read with interest this latest paper questioning the recommendation
from NICE about the management of UTI in children.
While the need for evidence is crucial to informed practice it is not
always the case that in all medical conditions that this level is reached.
Consensus therefore can be arrived at after a thorough review of good
practice by eminent practitioners in the field. I have no doubt that the
respected membe...
I read with interest this latest paper questioning the recommendation
from NICE about the management of UTI in children.
While the need for evidence is crucial to informed practice it is not
always the case that in all medical conditions that this level is reached.
Consensus therefore can be arrived at after a thorough review of good
practice by eminent practitioners in the field. I have no doubt that the
respected members of NICE that came up with the recommendations were
following this age long medical way of doing things.
In my practice as a general paediatrician, I have had the 'piviledge' of
using different guidelines on this subject (Radiologists,College of
Paediatrics,College of Physicians & Nephrologists) to name a few.
I can therefore see the need for NICE to start the process of
bringing in something that could at least simplify the patient journey.
I welcome this information from NewCastle which I believe will go a
long way in providing useful evidence to be used by NICE to review its
recommendation in due course.I wonder if the authors found any
correlation between systemic symptoms/increased inflammatory markers and
renal scarring.
The NICE guide helps to focus minds and opens the debate on the need
by all to provide the neccessary evidence to support ongoing and future
practice.
Reference; M G Coulthard, H J Lambert and M J Keir;
Do systemic symptoms predict the risk of kidney scarring after urinary
tract infection?Arch. Dis. Child. 2009;94;278-281.
Pijpers et al rightly highlight the lack of high quality evidence for
the treatment of constipation. In their conclusion they state
‘Insufficient evidence exists supporting that laxative treatment is better
than placebo in children with constipation’. This paper derives from the
Academic Medical Centre, Amsterdam, where Benninga’s group have
successfully demolished all other treatments for constipation other than
laxative...
Pijpers et al rightly highlight the lack of high quality evidence for
the treatment of constipation. In their conclusion they state
‘Insufficient evidence exists supporting that laxative treatment is better
than placebo in children with constipation’. This paper derives from the
Academic Medical Centre, Amsterdam, where Benninga’s group have
successfully demolished all other treatments for constipation other than
laxatives, and by this statement, they appear to have removed the last
hope for Paediatricians treating this common and distressing condition. If
the statement that laxatives are no more effective than placebo how can
they explain the dose-response obtained by Youssef et al with PEG 3350?(1)
They highlight the lack of placebo studies (although eleven were
included in their review) but, as they suggest, it is perhaps unsurprising
that clinical investigators are reluctant to design placebo-based studies
in children in spite of the clear-cut results which can be obtained by
this design. In their Results section they show the superiority of PEG-
based laxatives over lactulose (based on four studies) but are unable to
make any recommendations.
My major concern is that only the abstract will be read by
Paediatricians, General Practitioners and health care funding bodies who
will interpret their Conclusions statement as meaning laxatives being are
no better than placebo. How can the need for long term treatment for
constipation be defended when the medications prescribed are described in
this way?
1. Youssef NN, Peters JM, Henderson W, et al. Dose response of PEG
3350 for the treatment of childhood fecal impaction. J Pediatr
2002;141:410–14.
Prof David CA Candy MB.BS, MSc, MD, FRCP, FRCPCH, FCU
Consultant Paediatric Gastroenterologist
Research Director
Royal West Sussex NHS Trust
Chichester PO19 6SE
Honorary Paediatric Gastro-Enterologist
Royal Alexandra Children's Hospital
Brighton BN2 5BE
Facsimile 01243 831431
Phone 01243 831441
david.candy@wsht.nhs.uk
Competing Interests: DCAC is external advisor to the NIHCE Clinical
Guidelines Development Group for Paediatric Constipation. He has received
research funding from Norgine Ltd, manufacturers of PEG-based laxatives
and is cited in this article.
Subhi et al have asked when oxygen should be given to children at
high altitude observing that hypoxaemia is the most common fatal
complication in deaths occurring from pneumonia in children in developing
countries (1). Might the answer be never?
Supplementary oxygen appears to be harmful in climbers on Everest
possibly because it eliminates the up-regulation of oxidative
phosphorylation by mass action by hypoc...
Subhi et al have asked when oxygen should be given to children at
high altitude observing that hypoxaemia is the most common fatal
complication in deaths occurring from pneumonia in children in developing
countries (1). Might the answer be never?
Supplementary oxygen appears to be harmful in climbers on Everest
possibly because it eliminates the up-regulation of oxidative
phosphorylation by mass action by hypocarbia (2) but the benefical effects
of this up-regulation could be concealed by the adverse effects of
hypothermia at this altitude. A more relevant question might be should
supplementary oxygen be given to children with pneumonia or even asthma at
low altitude for in these circumstances hypothermia is unlikely to be a
confounding factor.
Supplementary oxygen was not a significant factor in the non-
traumatic deaths that occurred in descent from the summit of Everest.
Nevertheless the putative beneficial effects of hypocarbia on oxidative
phosphorylation can be expected to be far greater at sea level, than on
Everest, for they will not be concealed by the adverse effects of
hypothermia. Asthmatics, for example, might be better off not receiving
oxygen. The same applies to patients with sepsis. In the latter
progressive adjustments to the ventilator settings designed to achieve as
low PaCO2 as safely possible might not only up-regulate oxidative
phosphorylation but also limit the severity of the metabolic acidosis that
can develop in these patients. In so doing the associated development of
cellular apoptosis and necrosis, the local inflammatory response induced
by cellular necrosis, and organ dysfunctions and deaths might also be
prevented.
Two variables would seem to be particular important in the regulation
of oxidative phosphorylation: the PaCO2 and the pH, the protonmotive force
increasing as the extracellular, or more specifically the
extramitochondrial, pH falls. The effects appear to be independent of one
another. In the first place "the mammalian central chemoreceptor for
respiratory control is responsive independently to H+ and CO2 and that H+
and CO2 exert differential effects on the respiratory centre in terms of
frequency and magnitude" (3). Secondly lactate is a linear function of
tissue PCO2 in rats (4). Thirdly in patients with sepsis those with a high
lactate paradoxically appear to have a higher tissue pH than those with a
low lactate (5) presumably because up-regulation of oxidative
phosphorylation decreases the likelihood of developing a "lactic
acidosis".
Hypoxia exerts its effects upon respiration through peripheral
chemoreceptors. In our study of ventilated dogs progressive decreases in
FiO2 failed to induce oxygen supply-dependency before death from cardiac
arrest (6). In retrospect this demonstrated the remarkable capacity to
deliver adequate amounts of oxygen to tissues in the face of hypoxic
stress, a finding confirmed by the studies on Everest. There was another
study, conducted by Canadian investigators, that followed DO2 and VO2 in
dying patients and found that oxygen supply-dependency failed to develop
until the DO2 was so abnormally low that the findings were difficult to
believe at the time. Regretably I have been unable to locate the
reference. If, however, my recollection is accurate these studies add to
the weight of evidence demonstrating that DO2 may not be the limiting
factor in the acutely ill. More importantly, perhaps, is the hypothetical
risk of ischaemia/ reperfusion or hyopoxia/reoxygenation injury if acute
hypoxia is reversed with oxygen.
To prevent reprfusion/reoxygenation injury, which must be a primary
objective during resuscitation, it would seem desirable to withold
supplementary oxygen in all circumstances and possibly even to reduce FiO2
to abnormally low levels or give supplementary carbon monoxide during the
initial phases of resuscitation. To optimize ATP resynthesis in a child
who is critically ill it might be best to reduce the PaCO2 as low as
possible, and that might be as low as 10 mmHg, and/or to reduce the
arterial bicarbonate concentration so that the pH is clamped at normal or
slightly lower (7,8). Clamping of the pH at the derisred level could in
theory be achieved using the pH-stat technique using two auto-burettes,
one filled with a suitable acid and the other a suitable alkali (9).
Giving supplementary oxygen to children with acute respiratory
infections and even asthma might never be advisable. If oxygen is to be
given it might be better to give it intraperitoneally for giving it into
the lumen of the gut appears to be cardioprotective in hypoxaemia. There
are good grounds for doing so (10, 11,12). The risk/benefit of such an
approach has, however, not been established except in the case of ECMO.
1. Rami Subhi, Katherine Smith, Trevor Duke When should oxygen be
given to children at high altitude? A systematic review to define altitude
-specific hypoxaemia. Archives of Disease in Childhood 2009;94:6-10
2. Dexamethasone and hepatic energetics in climbers attempting
Everest. Richard G Fiddian-Green (17 January 2009). eLetter re: Matiram
Pun. Important points in analysing deaths on Mount Everest
BMJ 2009; 338: b41.
3. Y Harada, M Kuno, and Y Z Wang. Differential effects of carbon
dioxide and pH on central chemoreceptors in the rat in vitro. J Physiol.
1985 November; 368: 679–693
4. Nakagawa Y, Weil MH, Tang W, Sun S, Yamaguchi H, Jin X, Bisera J.
Sublingual capnometry for diagnosis and quantitation of circulatory shock.
Am J Respir Crit Care Med. 1998 Jun;157(6 Pt 1):1838-43.
5. Effect of dobutamine on oxygen consumption and gastric mucosal pH
in septic patients. Gutierrez G, Clark C, Brown SD, Price K, Ortiz L,
Nelson C. Am J Respir Crit Care Med. 1994 Aug;150(2):324-9.
6. Grum CM, Fiddian-Green RG, Pittenger GL, Grant BJ, Rothman ED,
Dantzker DR. Adequacy of tissue oxygenation in intact dog intestine. J
Appl Physiol. 1984 Apr;56(4):1065-9.
8. Monitoring of tissue pH: the critical measurement. Fiddian-Green
RG. Chest. 1999 Dec;116(6):1839-41.
9. Mechanisms of disposal of acid and alkali in rabbit duodenum.
Fiddian-Green RG, Silen W.
Am J Physiol. 1975 Dec;229(6):1641-8.
10. The intestinal factor in irreversible hemorrhagic shock. LILLEHEI
RC. Surgery. 1957 Dec;42(6):1043-54.
11. The intestinal factor in irreversible endotoxin shock.
LILLEHEI RC, MACLEAN LD. Ann Surg. 1958 Oct;148(4):513-24
12. Supplemental systemic oxygen support using an intestinal
intraluminal membrane oxygenator.
Gross BD, Sacristán E, Peura RA, Shahnarian A, Devereaux D, Wang HL,
Fiddian-Green R. Artif Organs. 2000 Nov;24(11):864-9.
Olaciregui et al. reported an interesting article and concluded that
the diagnostic value of procalcitonin (PCT) is greater than C reactive
protein (CRP) in predicting infants with more invasive bacterial diseases
(sepsis, bacteraemia). However, due to the following reasons, the
conclusion should be more conservative.
First, the authors claimed that the area under curve (AUC) is greater...
Olaciregui et al. reported an interesting article and concluded that
the diagnostic value of procalcitonin (PCT) is greater than C reactive
protein (CRP) in predicting infants with more invasive bacterial diseases
(sepsis, bacteraemia). However, due to the following reasons, the
conclusion should be more conservative.
First, the authors claimed that the area under curve (AUC) is greater
when comparing PCT using a cut-off point of 0.5 ng/ml and CRP using a cut-
off point of 30 mg/l (Table 2). I think it is a misuse of receiver
operating characteristic (ROC) curves. Because ROC curves are plotted by
sensitivity and 1-specificity using different cut-off points, AUC will not
change when shifting cut-off points.(1) Obviously, it is not sufficient to
support any specific cut-off point by comparing AUC of ROC curves.
Second, the authors strengthened the conclusion by larger odds ratio
of PCT in the multivariate logistic regression model in subgroup analysis
(Table 3 and Table 4). However, because CRP and PCT are both good
predictors of serious bacterial infections, they must be highly correlated
with each other. It brings a very serious problem of collinearity.(2)
Thus, I am afraid that the model is an unstable model and the result might
greatly change when adding some more cases. It should be very conservative
when explaining the results of this model.
Finally, because CRP is almost routinely performed for febrile
infants under 3 months of age in clinical practice, it is meaningless to
argue PCT is better than CRP or not. It will be more interesting to see
how much the increment in AUC is between CRP alone and PCT plus CRP. Some
new methods of measuring quantify the improvement such as net
reclassification improvement and integrated discrimination improvement can
be applied for this purpose.(3)
References:
1.Bewick V, Cheek L, Ball J. Statistics review 13: receiver operating
characteristic curves. Crit Care 2004;8(6):508-12.
2.Nathanson BH, Higgins TL. An introduction to statistical methods
used in binary outcome modeling. Semin Cardiothorac Vasc Anesth
2008;12(3):153-66.
3.Pencina MJ, D'Agostino RB, Sr., D'Agostino RB, Jr., Vasan RS.
Evaluating the added predictive ability of a new marker: from area under
the ROC curve to reclassification and beyond. Stat Med 2008;27(2):157-72;
discussion 207-12.
Dear Sir
I absolutely agree with your conclusions about demand feeding being
something “we might all be able to live with”, but we should really
respect the children’s “demand”. I also agree that there is no strong
evidence to support exclusive breast feeding for six months, but there is
neither strong evidence about the optimal complementary diet and there is
not any certainty that the child introduced to solid foods wi...
Dear Sir
I absolutely agree with your conclusions about demand feeding being
something “we might all be able to live with”, but we should really
respect the children’s “demand”. I also agree that there is no strong
evidence to support exclusive breast feeding for six months, but there is
neither strong evidence about the optimal complementary diet and there is
not any certainty that the child introduced to solid foods will accept
them assuming the pediatrician's "scientifically" prescribed doses. On the
contrary this is the least likely event, in the sense that children will -
- in general -- eat more or less of that which was prescribed. Moreover
offering solid foods to a child who is not interested at all to them, one
is just looking for feeding problems. Man proposes, Child disposes.
It is about eight years since a considerable group of family
paediatricians, throughout Italy, started practicing what we today define
“Demand Complementary Feeding”, i.e. “Baby led introduction of
complementary foods in the context of family meals whenever and wherever
they take place.” The proposal was first published in 2002 (1), and then
reaffirmed in 2006 (2).
The point is that the change in WHO recommendations about the most
appropriate age of introducing solid foods, gradually sliding towards more
mature stages of child development, allowed us to catch those cues you
talked about, without the confusing confounding factors arising from the
practice of an imposed weaning. So, today, we can not say any more that
babies on an exclusive milk-diet show interest in table-food because they
are hungry or antsy for something different. They do not know yet that
such thing is food. They are, as every baby between five to six month old,
interested in table-food as well as in every other thing parents, or other
trusty caregivers, are doing all day long. Only after parents yield to
their irresistible staring, flustering and reaching, babies taste, often
recognize, appreciate and finally accept happily “that thing”,-- which
they did not know what it was -- as food.
In a cohort study (personal data) in which mothers were followed during
pregnancy, they were instructed through specific courses and interviewed
in the second half of the first year. Nearly all of them had recognised
timely their children's "interest cues" and most of them had carried on
meeting their increasing requests of any food on the table, at the
children’s pace. Obviously, they did not show problems of refusal or of
selected diet, and their mother never worried about insufficient intake or
fights for the last crumb. And, on the other hand, there is a decrease in
useless work for the paediatrician. Sooner or later all children,
gradually, within the end of the first year substituted their midday and
evening milk-meals with solid food.
At last, but not least, all that, obviously and inevitably, entails an
elementary and simple parent’s education about the optimal diet (from now
on) for the whole family, that does not necessarily means a tasteless
diet. Weaning, as well breast feeding, is primarily a family task.
1) Lucio Piermarini. Autosvezzamento. Medico e Bambino 2002;21:468-
471
2) Lucio Piermarini. Complementary feeding at request. Medico e Bambino
2006;25:439-442
We read with interest your article on follow up of children with community acquired pneumonia and also your eletter response on the subject. I t is interesting to note that children with pre-existing asthma are at significant risk of persistent cough after admission to hospital for community acquired pneumonia. However the risk of subsequent asthma is increased only in children of non-atopic parents. In routine clinical pr...
Sir,
Dr Rowland and colleagues have recently reported a prospective audit on the use of rectal paraldehyde in children with prolonged seizures (1). On the basis of their data they conclude that “This would appear to confirm that paraldehyde should remain a treatment for the management of prolonged tonic-clonic convulsions, including convulsive status epilepticus”. Unfortunately there are several issues that req...
The leading article on child protection by Ben Matthews et al (1) starts with a promising review of the difficulties experienced by UK Paediatricians with child protection work. However, their argument that low substantiated cases of abuse and neglect in UK represent the reluctance of paediatricians in England to engage in the business of child protection is not supported by their statistics. Also, their approach of comp...
Dear Editor,
Samuel and colleagues(1) aim to review the clinical and epidemiological evidence relevant to the use of pre-implantation diagnosis (PGD) to create a “saviour sibling.” A thorough literature review regarding the use of this method should include consideration of the medical problems that may occur in the child born following assisted reproduction technology (ART), but this was not addressed in this...
We read with interest the finding of an unchanged incidence of microalbuminuria with time in children with type 1 diabetes in the Oxford Regional Prospective Study cohort. Figure 1 demonstrates no difference in the cumulative prevalence of developing microalbuminuria in relation to year of diabetes onset. However we note the small numbers of patients remaining at 10 years, particularly in group C, and wonder whether a d...
I read with interest this latest paper questioning the recommendation from NICE about the management of UTI in children. While the need for evidence is crucial to informed practice it is not always the case that in all medical conditions that this level is reached. Consensus therefore can be arrived at after a thorough review of good practice by eminent practitioners in the field. I have no doubt that the respected membe...
Pijpers et al rightly highlight the lack of high quality evidence for the treatment of constipation. In their conclusion they state ‘Insufficient evidence exists supporting that laxative treatment is better than placebo in children with constipation’. This paper derives from the Academic Medical Centre, Amsterdam, where Benninga’s group have successfully demolished all other treatments for constipation other than laxative...
Subhi et al have asked when oxygen should be given to children at high altitude observing that hypoxaemia is the most common fatal complication in deaths occurring from pneumonia in children in developing countries (1). Might the answer be never?
Supplementary oxygen appears to be harmful in climbers on Everest possibly because it eliminates the up-regulation of oxidative phosphorylation by mass action by hypoc...
To the editor:
Olaciregui et al. reported an interesting article and concluded that the diagnostic value of procalcitonin (PCT) is greater than C reactive protein (CRP) in predicting infants with more invasive bacterial diseases (sepsis, bacteraemia). However, due to the following reasons, the conclusion should be more conservative.
First, the authors claimed that the area under curve (AUC) is greater...
Dear Sir I absolutely agree with your conclusions about demand feeding being something “we might all be able to live with”, but we should really respect the children’s “demand”. I also agree that there is no strong evidence to support exclusive breast feeding for six months, but there is neither strong evidence about the optimal complementary diet and there is not any certainty that the child introduced to solid foods wi...
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