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
I read this article with great interest. It has been a long time
since a PICU data from England and Wales has been published in the
Archives of Diseases in Childhood.
Interestingly, I noted that although the admission in 1-4 yr age
group was lesser (7.54 & 7.22%) than other age groups (more than 10%)
amongst male and female South Asians respectively, the 0–4 yr standardised
admission (incident) rate amongst...
I read this article with great interest. It has been a long time
since a PICU data from England and Wales has been published in the
Archives of Diseases in Childhood.
Interestingly, I noted that although the admission in 1-4 yr age
group was lesser (7.54 & 7.22%) than other age groups (more than 10%)
amongst male and female South Asians respectively, the 0–4 yr standardised
admission (incident) rate amongst South Asian males [351 (336 to 367
95%CI)] and females [264 (250 to 278 95% CI)] is significantly more than
non-South Asian males and females [252 (248 to 256 95% CI)] and [195 (192
to 199 95% CI)] respectively. This presumably reflects that less South
Asian babies are born per 100,000 South Asian population in the U.K.
compared to non-South Asian babies per 100,000 non-South Asians. But is
that really so?
Secondly, I wonder what the standardised incidence rate is for South
Asian and non-South Asian infants less than 1 years of age; and moreover
what proportion of this figure comprises of congenital heart defects,
chromosomal abnormalities, respiratory tract infections and NAIs
(suspected or proven).
Since 95% CI of Odds Ratio of death in all Townsend categories lie on
both sides of 1, the data does not reliably suggest that chance of a
paediatric patient’s death is higher if he/she comes from a less deprived
community, in contrary to author’s statement.
It was also interesting to note that the risk of a paediatric
patient’s death generally increases given that a surgical procedure took
place; irrespective of sex, ethnic origin or Townsend category of the
patient.
I could not locate any data mentioning the impact of PIM index on
admission on the actual standardised (proportional population adjusted)
mortality rates in South Asians and non-South Asians respectively. This
parameter would in my opinion open up the very debatable and controversial
grey area of possibility of any treatment bias which we may have in
treating non-South Asian and South Asian subsets of PICU patients (the
bias originating from their ethnic origins).
This paper clearly states that South Asian children are at greater
risk of dying compared to their non-South Asian counterparts when admitted
in PICU setting in the given geographical area studied: England and Wales.
I believe such a statement would automatically raise issue of quality of
medical service provided to the South Asian children when they are treated
in the PICU. Putting this rather boldly, I mean: Is the PICU staff in
England and Wales really intolerant to racial discrimination while
treating their patients? Will this study lead to a modification in PIM
scoring to a higher mortality prediction score for a South Asian child
admitted in PICU in future?
The Authors have probed into some reasons that could explain this
phenomenon, including higher infant mortality in South Asians in general,
possibility of effect of consanguineous marriages in Pakistani population
leading to chromosomal disorders. They acknowledged that their study could
not identify children with congenital abnormalities in their collected
data. I would be more interested to know if PIM index of South Asian and
non-South Asian children really reflected their actual population adjusted
mortality rates. If it does, then it would reflect PICU staff’s good
medical and ethical (of intolerance to racial discrimination) practice.
However, if it does not, then unfortunately it might open up, I am afraid,
the unwanted floodgate of debate on racial discrimination in paediatric
practice until proven otherwise
I read this article with interest and was pleased by the emphasis
given to Medical Education in this journal(1, 2). There is necessity for
more literature on Medical Education in frontline journals like this.
Reading the RCPCH document for Level 2 competency for Core Highest
Specialist Training in Paediatrics(3), I was disappointed that Best
Evidence Medical Education (BEME)was not included.
I read this article with interest and was pleased by the emphasis
given to Medical Education in this journal(1, 2). There is necessity for
more literature on Medical Education in frontline journals like this.
Reading the RCPCH document for Level 2 competency for Core Highest
Specialist Training in Paediatrics(3), I was disappointed that Best
Evidence Medical Education (BEME)was not included.
It is necessary to move from opinion-based education to evidence-
based education. Since its introduction, the implementation of BEME has
been slow due to lack of awareness. We hardly read literature on
education, or more appropriately, are not even aware that such literature
exists(4).
Whereas it was once assumed that a competent basic or clinical
scientist would naturally be an effective teacher, it is now acknowledged
that preparation for teaching is essential. In a review of this topic,
authors conclude that the very nature of being professional in today's
social and fiscal context demands that medical educators provide evidence
of effectiveness and efficiency of their programs(5).
Fortunately we live in a time where ubiquitous acceptance of Evidence
Based Medicine (EBM) has made the concept of Evidence- based practise
irrefutable. All that is needed now is to lead Trainees into applying the
equivalent principles of seeking evidence and implementing appropriate
change based on the best available evidence to engender the thought
process of Evidence –based education.
Specialist Trainee curriculum should therefore encompass guidance on
how BEME can be applied. This may include:
1.encouraging reflection on teaching methods allowing the trainees to
identify the gaps in their teaching practice
2.encouragement to seek feedback from students and the opportunity to
discuss the feedback with experienced teachers to decide on the required
strategy for improvement
3.facilitating the process by providing information about database
such as the Campbell Collaboration (www.campbell.gse.upenn.edu) and Best
Evidence Medical Education collaboration (www.bemecollaboration.org)
These are suggestions for creating a paradigm shift to encourage
young doctors to look at teaching activities in the light of exsisting
best evidence. Emphasis given to Medical Education in high impact journals
will aid in achieving this goal.
Reference:
1.McGraw ME. Delivery of the paediatric curriculum of the Royal College of
Paediatrics and Child Health (RCPCH). Arch Dis Child2009;94(4):254-7.
2.Bindal T, Wall D, Goodyear HM. Specialist registrars’ views on their
teaching role. Arch Dis Child2009;94(4):311-3.
3.A Framework for Competences for Level 2 Training in Paediatrics, 2005
Royal College of Paediatrics and Child Health
4.BEME Guide No. 1: Best Evidence Medical Education. Medical Teacher, 1999
;21 (6): 553 – 562
5.Dauphinee WD, Wood-Dauphinee S.The need for evidence in medical
education: the development of best evidence medical education as an
opportunity to inform, guide, and sustain medical education research. Acad
Med. 2004;79(10):925-30.
Dear Sir,
I appreciate the review of mtDNA depletion provided by Drs Rahman &
Poulton,
and whole-heartedly agree with there opinion that oligo-arrayCGH is not a
first line test for single gene disorders but rather is a follow on test
when sequencing fails to detect 2 causal alleles.
However, in their perspective, they state: “a molecular diagnosis of
dGK deficiency may be regarded as a useful prognostic ind...
Dear Sir,
I appreciate the review of mtDNA depletion provided by Drs Rahman &
Poulton,
and whole-heartedly agree with there opinion that oligo-arrayCGH is not a
first line test for single gene disorders but rather is a follow on test
when sequencing fails to detect 2 causal alleles.
However, in their perspective, they state: “a molecular diagnosis of
dGK deficiency may be regarded as a useful prognostic indicator in
patients in whom liver transplantation is being considered…. molecular
diagnosis of dGK mutation may lead to a decision not to transplant,
particularly if there is evidence of neurological involvement.”
This statement is problematic as in DGUOK deficiency, possibly in
contrast to other disorders such as POLG and MPV17 related depletion,
liver transplantation may be associated with very good long term outcome
and the absence of significant neurological disease. (Dimmock et al Liver
Transplantation 2008 Oct;14(10):1480-5) Since outcome does not correlate
directly with genotype, it is my opinion that molecular diagnosis in
isolation should not be used to make decisions regarding transplantation.
Packman et al. responded to Howell et al.’s article (doi
10.1136/adc.2007.134114) on bilingualism and stuttering. We showed that
speaking two languages in the preschool years increased the chances of
children starting to stutter and decreased the likelihood of recovery from
stuttering relative to speakers who learned English when they started
school.
Packman et al. responded to Howell et al.’s article (doi
10.1136/adc.2007.134114) on bilingualism and stuttering. We showed that
speaking two languages in the preschool years increased the chances of
children starting to stutter and decreased the likelihood of recovery from
stuttering relative to speakers who learned English when they started
school.
We do not consider, as Packman et al. suggest, that studying the
general population of bilinguals would benefit the study of how speaking a
second language affects stuttering. First, statistically speaking,
demonstrating that bilingualism has no effect on stuttering, as the
authors wish to do, is impossible. Also, investigating the general
population of bilinguals is a flawed approach as bilingualism is massively
heterogeneous within and between societies (including the US, Australia
and Canada, where the authors work). Consequently, stringent controls (not
biased sampling) have to be imposed in studies on bilingualism and
stuttering. The controls we imposed excluded children who were brought up
bilingual for social, educational or financial advantage. This reduced the
heterogeneity in the bilingual sample. We compared bilinguals who had to
use an additional language in the home with a matched sample who only
spoke a language other than English in the home. The two groups of
children selected for our study were directly comparable with respect to
socio-economic status etc., and provided an appropriate sample on which to
test the hypothesis of whether deferring learning English as a second
language affected onset of stuttering and whether stuttering recovered.
The same controls are appropriate for selecting similar groups for study
across countries (unlike a sample from the general population of
bilinguals at large).
They go on to state that our cohort is biased, and refer to a
clinical study that followed up children from about age 3 to 8. 1 They say
that the generally accepted age of stuttering onset is 3 years. However,
the authoritative handbook in the area notes that the onset of
developmental stuttering can occur at any age up to 13 years. 2
Consequently, studies that cease examination at age 8 bias estimates of
age of onset to lower ages by excluding cases where onset occurs after age
8. They also incorrectly state that the gender ratio is 1:1 (there was a
higher ratio of males/females in our study). All studies we are aware of
(including the one they cited 1) show more males stutter than females. For
example, the classic study by Andrews and Harris 3 from 2 to teenage
reported a ratio of 2.4:1. A gender ratio of 1:1 suggests they are
including children who do not stutter as stutterers (they have many false
positives) and there is about an equal chance of misdiagnosis for each
gender. The reasons for such misdiagnoses could be because they 4 use
parental nominations for identifying cases and employ symptoms for
diagnosing stuttering (whole word repetitions) that are excluded by
several authorities. 5 6 7 The inclusion of these would lead to fluent
children being classed as stutterers.
Packman et al. suggest that the Lidcombe program of therapy may be
appropriate to treat bilingual children who stutter. However, the study
they cited excluded children who did not have “proficiency in English” and
there is no translation of the procedure into several of the languages
spoken by our participants. In addition to the fact that they may be
treating children who do not stutter, the statistical treatment in the
study they cite has been faulted and long-term follow-up indicates that
some “children [treated by Lidcombe] may start to stutter again”. 8
They state that an epidemiological study is appropriate to determine
whether there is a relationship between stuttering and bilingualism. We
have warned about the problems of grouping together heterogeneous
bilinguals for study, as is necessary in epidemiological work. They
overlook the fact that our work reported on the risk of starting to
stutter and chance of recovery, using longitudinal data through to
teenage. They suggest the onset age is about three years and that most
recovery occurs in the first three years after onset. Conceivably, an
epidemiological study at ages less than 8 could provide information about
risk factors for onset of stuttering. However, it would not be informative
about recovery since 50% of cases still stuttering at age 8 will recover 9
10, and recovery is not resolved until teenage. 3 9 10 Although
epidemiological work does not require a longitudinal dimension, this is
necessary when studying recovery, where results on the same speakers are
needed in order to avoid biases. As in our study, they will need to use
standardized instruments to establish persistence and recovery at teenage.
If they intend to asses the impact bilingualism has on school performance,
they will again need to extend examination to teenage.
In their last paragraph, they state that 4% stutter-like dysfluencies
suggests our children would still be stuttering. Frequencies around this
value have been used to differentiate young children who stutter from
normally fluent speaking peers for English 1 and Dutch. 11 As discussed
earlier, relatively high rates of supposed stuttering events may be due to
inclusion of monosyllabic whole word repetitions, which are a common
feature in fluent children’s and adults’ speech. 12
In summary, we consider our conclusions to be valid. Our experimental
groups were matched appropriately and thoroughly documented with respect
to language background and assessment for stuttering. The authors of the
letter make statements that are contradicted in the literature. There are
major faults in the way the authors of the letter propose to study the
relationship between bilingualism and stuttering.
Acknowledgement
This work was supported by grant 072639 from the Wellcome Trust to Peter
Howell. Address Correspondence to: Peter Howell, Division of Psychology
and Language Sciences, University College London, Gower Street, London
WC1E 6BT, England. Email: p.howell@ucl.ac.uk
References
1Yairi E., Ambrose NG. Early childhood stuttering. Austin, TX: Pro-
Ed, 2005.
2Bloodstein O., Bernstein Ratner N. A handbook on stuttering, 6th ed.
Clifton Park, NY: Thomson, 2007.
3Andrews G., Harris M. The syndrome of stuttering. Clinics in
Developmental medicine (No 17). London: Heinemann, 1964.
4Reilly S., et al. Predicting stuttering onset by the age of 3 years.
Pediatrics, 2009;123:270-277.
6Ryan B. A longitudinal study of articulation, language, rate, and
fluency of 22 preschool children who stutter. Journal of Fluency
Disorders, 2001;26:107-127.
7Wingate ME. Foundations of stuttering. San Diego: Academic; 2002.
8Packman A., Kuhn L. Looking at stuttering through the lens of
complexity. International Journal of Speech-Language Pathology,
2009;11:77– 82.
9Fritzell B. The prognosis of stuttering in schoolchildren: A 10-year
longitudinal study. In Proceedings of the XVI Congress of the
International Society of Logopedics and Phoniatrics, 186-187. Basel:
Karger, 1976.
10Howell P, Davis S, Williams R. Late childhood stuttering. Journal
of Speech Language and Hearing Research, 2008;51:669-687.
11 Boey et al., Characteristics of stuttering-like disfluencies in
Dutch speaking older children, adolescents and adults. Journal of Fluency
Disorders, 2007;32:310-329..
12 Levelt W. Speaking: From intention to articulation. Cambridge, MA:
Bradford Books, 1989.
Peter Howell,
Stephen Davis,
Division of Psychology and Language Sciences, University College
London, United Kingdom
Roberta Williams,
Department of Language and Communication Science, City University
London, United Kingdom
In a recent article published in the journal, Taekema et al.
discussed the use of clinical criteria and laboratory tests to
differentiate between septic arthritis and transient synovitis in
children.2 Distinguishing between these two conditions is crucial to avoid
local and systemic complications (if a joint infection is missed) or
unnecessary hospitalization, surgical interventions, and antibiotic
treatment (if transien...
In a recent article published in the journal, Taekema et al.
discussed the use of clinical criteria and laboratory tests to
differentiate between septic arthritis and transient synovitis in
children.2 Distinguishing between these two conditions is crucial to avoid
local and systemic complications (if a joint infection is missed) or
unnecessary hospitalization, surgical interventions, and antibiotic
treatment (if transient synovitis is misclassified as septic arthritis).
After carefully reviewing available data, the authors concluded that the
presence of fever, refusal to bear weight, and elevated acute-phase
reactants should raise the suspicion of septic arthritis, whereas the
likelihood of transient synovitis increases if these predictors are
absent.2
In recent years, increasing use of blood culture vials for culturing
synovial fluid exudates and nucleic acid amplification techniques have
resulted in the recognition of K. kingae as an emerging pediatric pathogen
and the most common etiology of skeletal system infections below the age
of 3 years.3 Involvement of the hip has been observed in 25 of 116 (22%)
patients with K. kingae arthritis, apyrexia or low-grade fever are common,
and the majority of affected children appear to be only mildly or
moderately ill.3 In addition, the blood white cell count (WCC), C-reactive
protein level, and the erythrocyte sedimentation rate are frequently
within normal limits or only slightly elevated3, and a joint fluid
aspirate WCC <50,000/ml-1 has been found in 11 of 30 (37%) patients
with culture-proven K. kingae arthritis detected in southern Israel since
1987.
Although bacterial arthritis is not considered a self-limited disease,
transient involvement of the joints during an episode of K. kingae
bacteremia has been documented.1, 4 Children with this condition presented
with a body temperature <380C, limping or refusal to walk or bear
weight, but lacked objective signs of osteoarthritis or leukocytosis.
Despite this apparently benign clinical presentation, blood cultures were
obtained, and K. kingae was isolated, usually 3-4 days after collection.
By the time blood cultures became positive, the skeletal complaints had
resolved without antimicrobial therapy, suggesting an abortive joint
infection. Even when no antibiotics were prescribed after the positive
culture results were known, some patients made an uneventful recovery.1
Had blood cultures not been obtained, these children would have been
diagnosed as suffering from transient synovitis, raising the possibility
that patients in which this diagnosis is made have, in fact, hip joint
infections caused by K. kingae. Adding blood cultures to the laboratory
work-up of children with presumptive transient synovitis is strongly
recommended, even in the absence of fever, constitutional symptom, or
elevated acute-phase reactants. If the hip joint is aspirated, the
specimen should be inoculated into a blood culture vial to improve the
recovery of K. kingae.
REFERENCES
1.Lebel E, Rudensky B, Karasik M, Itzchaki M, Schlesinger Y. Kingella
kingae infections in children. J Pediatr Orthop B 2006; 15:289-92.
2.Taekema HC, Landham PR, Maconochie I. Towards evidence based medicine
for paediatricians. Distinguishing between transient synovitis and septic
arthritis in the limping child: how useful are clinical prediction tools?
Arch Dis Child 2009; 94:167-8.
3.Yagupsky P. Kingella kingae: from medical rarity to an emerging
paediatric pathogen. Lancet Infect Dis 2004; 4:358-67.
4.Yagupsky P, Press J. Unsuspected Kingella kingae infections in afebrile
children with mild skeletal symptoms: the importance of blood cultures.
Eur J Pediatr 2004; 163:563-4.
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...
I read this article with great interest. It has been a long time since a PICU data from England and Wales has been published in the Archives of Diseases in Childhood.
Interestingly, I noted that although the admission in 1-4 yr age group was lesser (7.54 & 7.22%) than other age groups (more than 10%) amongst male and female South Asians respectively, the 0–4 yr standardised admission (incident) rate amongst...
I read this article with interest and was pleased by the emphasis given to Medical Education in this journal(1, 2). There is necessity for more literature on Medical Education in frontline journals like this.
Reading the RCPCH document for Level 2 competency for Core Highest Specialist Training in Paediatrics(3), I was disappointed that Best Evidence Medical Education (BEME)was not included.
It is nece...
Dear Sir, I appreciate the review of mtDNA depletion provided by Drs Rahman & Poulton, and whole-heartedly agree with there opinion that oligo-arrayCGH is not a first line test for single gene disorders but rather is a follow on test when sequencing fails to detect 2 causal alleles.
However, in their perspective, they state: “a molecular diagnosis of dGK deficiency may be regarded as a useful prognostic ind...
Dear Editor.
Packman et al. responded to Howell et al.’s article (doi 10.1136/adc.2007.134114) on bilingualism and stuttering. We showed that speaking two languages in the preschool years increased the chances of children starting to stutter and decreased the likelihood of recovery from stuttering relative to speakers who learned English when they started school.
We do not consider, as Packman et al. s...
In a recent article published in the journal, Taekema et al. discussed the use of clinical criteria and laboratory tests to differentiate between septic arthritis and transient synovitis in children.2 Distinguishing between these two conditions is crucial to avoid local and systemic complications (if a joint infection is missed) or unnecessary hospitalization, surgical interventions, and antibiotic treatment (if transien...
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