Many thanks for an excellent update on Appendicitis. Only comment I
would like to make is about the bottom line.
A review by a paediatric surgeon for all suspected Appendicitis to
decide on further management is almost impossible in the existing NHS. I
have worked in 5 different DGH's and one Children's hospital A&E. In DGH,
its hard to get a paediatric surgeons review even for pro...
Many thanks for an excellent update on Appendicitis. Only comment I
would like to make is about the bottom line.
A review by a paediatric surgeon for all suspected Appendicitis to
decide on further management is almost impossible in the existing NHS. I
have worked in 5 different DGH's and one Children's hospital A&E. In DGH,
its hard to get a paediatric surgeons review even for probable
Appendicitis, leave alone suspected Appendicitis due to logistic reasons.
As the child need to be transferred to a different hospital and they
should have an in patient bed available. It doesn't work simple and
straightforward most of the time
The scenario in the children's hospital A&E where we had onsite
paediatric surgical team, most of the paediatric surgical registrar are
not very keen to deal with this clinical problem. Not sure why but they
really get annoyed.
For this clinical problem (Acute abdominal pain) which is extremely
common
May be, the bottom line should be: An experienced Paediatrician
should assess a patient with suspected appendicitis rather than a
paediatric surgeon
Dr.Ganesh Sambandamoorthy Specialty Registrar Paediatrics London
Deanery
in the interesting paper “Is it my calcium, Doctor?” (1), the authors
concluded that “Amy’s hypercalcaemia” is due to a “primary
hyperparathyroidism” and they don’t cite celiac disease (CD) as a specific
cause of hyperparathyroidism (HPT), although they first wrote that “she
had a previous history of celiac disease for which she was on a gluten
free diet” (GFD).
in the interesting paper “Is it my calcium, Doctor?” (1), the authors
concluded that “Amy’s hypercalcaemia” is due to a “primary
hyperparathyroidism” and they don’t cite celiac disease (CD) as a specific
cause of hyperparathyroidism (HPT), although they first wrote that “she
had a previous history of celiac disease for which she was on a gluten
free diet” (GFD).
CD is frequently associated with abnormal bone metabolism involving
both mineralization, leading to osteomalacia, and bone mass reduction,
resulting in osteoporosis. Recent studies describe an elevated prevalence
of secondary HPT not only among adults (27%), but also among children
(53%) with CD (2).
The pathogenesis of bone metabolism in CD is not completely
understood, but at least two mechanisms must be considered, one relating
to malabsorption and the other to presence of systemic or local
inflammation (2).
In undiagnosed celiac subjects, malabsorption of calcium and/or
vitamin D leads to a secondary HPT. Although prompt introduction of a
strict GFD in paediatric patients can bring to normalized bone metabolism,
including parathyroid hormone (PTH) levels, in adolescents and in adults
with protracted exposure to gluten before CD diagnosis, GFD may not bring
rapid improvement in bone metabolism abnormalities (3). Long-term exposure
to gluten (for late diagnosis or bad compliance to GFD) and abnormal bone
metabolism produce chronic stimulation of the parathyroid, which in turn
causes parathyroid hyperplasia not responsive to GFD1.
The association between asymptomatic CD and normocalcemic or mildly
hypercalcemic HPT, like as in Amy’s case, is reported in literature (4):
some patients developed a parathyroid adenoma with hypercalcemic HPT which
improved after surgery, but in longstanding undiagnosed CD patients a
tertiary HPT characterised by autonomous hypersecretion of PTH causing
hypercalcemia may arise (4,5).
In conclusion we believe that CD must be considered also in “Amy’s
case” as possible cause of secondary HPT and that the compliance to GFD
should be evaluated.
References
1. Stanley S, Shaw NJ. Is it my calcium, Doctor? Arch Dis Ed Pract
2009;94:169-76
2. Zanchi C, Di Leo G, Ronfani L et al. Bone metabolism in celiac
disease. J Pediatr. 2008;153(2):262-5.
3. Kalayci AG, Kansu A, Girgin N, et al. Bone mineral density and
importance of a gluten free diet in patients with celiac disease in
childhood. Pediatrics 2001;108;89-91
4. Maida MJ, Praveen E, Crimmins SR. Coeliac disease and primary
hyperparathyroidism: an association? Postgrad Med J 2006;82:833-5
5. Alzahrani AS, Al Sheef M. Severe primary hyperparathyroidism
masked by asymptomatic celiac disease. Endocr Pract 2008;14(3):347-5
Blair and colleagues mentioned CHILD2015 in their article and I would
like to invite all ADC readers with an interest in this subject to join.
Please see invitation below. To join, please go to:
www.hifa2015.org/child2015-forum and click on 'Join CHILD2015'.
With thanks,
Dr Neil Pakenham-Walsh MB,BS
Co-moderator, CHILD2015
Coordinator, HIFA2015
Global Healthcare Information Network
16 Woodfield Drive
C...
Blair and colleagues mentioned CHILD2015 in their article and I would
like to invite all ADC readers with an interest in this subject to join.
Please see invitation below. To join, please go to:
www.hifa2015.org/child2015-forum and click on 'Join CHILD2015'.
With thanks,
Dr Neil Pakenham-Walsh MB,BS
Co-moderator, CHILD2015
Coordinator, HIFA2015
Global Healthcare Information Network
16 Woodfield Drive
Charlbury, Oxfordshire OX7 3SE, UK
Tel: +44 (0)1608 811338
Email: neil.pakenham-walsh@ghi-net.org
HIFA2015: http://www.hifa2015.org
CHILD2015: http://www.hifa2015.org
"Healthcare Information For All by 2015: By 2015, every person
worldwide will have access to an informed healthcare provider"
With thanks to our 2009 Sponsors: British Medical Association,
International Child Health Group, Network for Information and Digital
Access, Royal College of Midwives, Royal College of Nursing, World Health
Organization.
INVITATION TO CHILD2015:
Child Healthcare Information and Learning Discussion group
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information and learning needs of healthcare providers in developing
countries.
CHILD2015 is open to anyone with an interest in improving child
healthcare in developing countries and membership is free. Its goal is
linked with the broader vision of 'Healthcare Information for All by 2015'
(www.hifa2015.org) and the Millennium Development Goals:
“By 2015, every child worldwide will have access to an informed
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The authors of a recent article1 reporting on the management of an
outbreak of tuberculosis in a crèche in Cork had difficulties with the
explanation of what we currently manage as latent M. tuberculosis
infection. In their first paragraph they defined “TB” as active pulmonary
tuberculosis. Where they reported on communication to the parents of the
differences between tuberculosis infection and active disease they menti...
The authors of a recent article1 reporting on the management of an
outbreak of tuberculosis in a crèche in Cork had difficulties with the
explanation of what we currently manage as latent M. tuberculosis
infection. In their first paragraph they defined “TB” as active pulmonary
tuberculosis. Where they reported on communication to the parents of the
differences between tuberculosis infection and active disease they mention
that tuberculosis infection implies the presence of “TB” in the body in
the absence of diseases manifestations, which is a contradiction. On page
111 the authors claimed that the gold standard for diagnosis of
tuberculosis infection is isolation of acid-fast bacilli. Isolation of
acid-fast bacilli however does not only mean infection with mycobacteria
but presence of active disease with a bacterial load high enough to be
detectable.
The majority of people currently labelled as infected with M.
tuberculosis .are labelled as infected on the basis of evidence of an
immunological reaction to M. tuberculosis antigen and not on the basis of
detection of M. tuberculosis itself. Future studies need to explore
markers enabling quantification of extent of the mycobacterial infection.
One which has been explored is quantification of neopterin, which is
generated by macrophages in response to interferon gamma. It can be
measured in urine samples by commercially available assay systems2 .
Another approach would be the radio-immuno-scintigraphic detection of
specific protein antigens produced only by replicating M. tuberculosis
(e.g. Early secretory antigenic target-6 or culture filtrate protein 10)
using radio-labelled monoclonal antibodies visualized 3, 4. Such projects
could be the first steps towards a more precise definition of latent
infection versus active disease and discrimination of latent infection
from immunological memory. This could enable design of a more tailored
treatment regime and monitoring of its impact on elimination of M.
tuberculosis infection.
REFERENCES
1. Gaensbauer JT, Ni Chroinin M. “What we learn in time of
pestilence…”. Arch Dis Child Ed Pract 2009; 94:108-114.
2. Yuksekol I, Ozkan M, Akgul O, et al. Urinary neopterin measurement
as a non-invasive diagnositic method in pulmonary tuberculosis. Int J
Tuberc Lung Dis 2003;7:771-776.
3. Malpani BL, Kadival GV, Samuel AM. Radioimmunoscintigraphic
approach for the in vivo detection of tuberculomas-a preliminary study in
a rabbit model. Nucl Med Biol 1992;19:45-53.
4. Hazra DK, Lahiri VL, Saran S et al. In vivo tuberculoma creation
and its radioimmunoimaging. Nucl Med Communications 1987;8:139-142.
Sir,
Your two recent articles dealing with malrotation of the intestine (1,2),
whilst
being very specific with regard to the colour of
the vomitus (green), were perhaps not specific enough. Yellow vomiting as
a
sign of malrotation has been noted by Millar et
al (3), Walker et al (4) and personal experience some years earlier.
Awareness
of this may aid early diagnosis.
Sir,
Your two recent articles dealing with malrotation of the intestine (1,2),
whilst
being very specific with regard to the colour of
the vomitus (green), were perhaps not specific enough. Yellow vomiting as
a
sign of malrotation has been noted by Millar et
al (3), Walker et al (4) and personal experience some years earlier.
Awareness
of this may aid early diagnosis.
Reflux of yellow bile into the stomach, whether through a
physiological
mechanism or from increased pressure in the
duodenum secondary to complete or partial obstruction, combined with a
prompt gastro-esophageal reflux (as noted in
one case of Millar et al) may not allow for the stasis that presumably
causes
bile to turn green.
That green is for danger is absolute, but lemon-yellow may also be
for
danger in an unidentified, as yet, number of cases.
This requires urgent clarification
1.Kumar JN, Curry JI. Bile stained vomiting in the infant: green is
not good.
Arch Dis Child Educ Pract Ed 2008;93:84-86
2. Williams H. Green for danger! Intestinal Malrotation and Volvulus.
Arch
Dis Child Educ Pract Ed 2007;92:87-91
3. Millar AJW, Rode H, Cywes S. Malrotation and Volvulus in Infancy and
Childhood. Semin Pediatr Surg 2003;12:229-36
4. Walker GM et al. Colour of bile vomiting in intestinal obstruction in
the
Newborn:questionnaire study. BMJ,
doi:10.1136/bmj.38859.614352.55(published 31 May 2006)
Kempley et al (1) have recommended the length based on the gestation
of the neonates rather than the rule of ‘7-8-9’, which has been being used
traditionally over the years. I have read both articles with great
interest – excellent review by Wylie’s (2) on neonatal resuscitation
published in education and practice of Archives diseases in childhood and
Endotracheal tube length for neonatal intubation...
Kempley et al (1) have recommended the length based on the gestation
of the neonates rather than the rule of ‘7-8-9’, which has been being used
traditionally over the years. I have read both articles with great
interest – excellent review by Wylie’s (2) on neonatal resuscitation
published in education and practice of Archives diseases in childhood and
Endotracheal tube length for neonatal intubation by Kempley et al,
published in resuscitation.
Review article by Wylie is excellent and recommends the length as has
been used traditionally over the years. Work done by Kempsley et al is
based upon evidence. They have clearly demonstrated a better linear
relationship between the gestational age and accurate endotracheal tube
length.
We prefer naso-endotracheal intubation in our unit. There is no clear
evidence or rule regarding the length of the endotracheal tube while using
the naso-endotracheal tube. Wylie has recommended adding one cm to the
oral endotracheal length as determined by ‘7-8-9’ rule. Therefore, again
we should probably add 1 cm in the length of endotracheal recommended by
Kempsley et al while inserting tube nasally. However another useful tip
can be – fix the endotracheal tube with proximal end of the black marking
at the level of cords.
We should use gestation-based guidelines on ETT length for neonatal
oral intubation to minimise a reduction in tube malposition and uneven
lung expansion. For the naso-endotracheal route adding 1cm to the length
recommended by Kempsley et al looks more sensible.
With interest we read the paper by Tighe et al about the use of pH-
monitoring in childhood.(1) However, we believe that the authors
overestimate the role of this technique and their omission of a detailed
discussion of the utility of pH-impedance monitoring renders this review
incomplete.
The term ‘gold standard’ can no longer be applied to 24-hour pH-
monitoring because pH-probes only d...
With interest we read the paper by Tighe et al about the use of pH-
monitoring in childhood.(1) However, we believe that the authors
overestimate the role of this technique and their omission of a detailed
discussion of the utility of pH-impedance monitoring renders this review
incomplete.
The term ‘gold standard’ can no longer be applied to 24-hour pH-
monitoring because pH-probes only detect a minority of gastro-oesophageal
reflux (GOR) episodes.(2) Combined pH-impedance monitoring allows for the
detection of all reflux (liquid, mixed, gas, acidic, weakly acidic, weakly
alkaline). With an increasing body of evidence showing a role for weakly
acidic bolus GOR in symptom generation, the measurement of acidity alone
provides an incomplete picture of the degree of bolus reflux and the
relationship of bolus reflux to symptom episodes. Therefore, symptomatic
reflux cannot always be excluded when a pH-study (acid exposure) is
normal. The ability to detect bolus reflux, independently of acidity,
allows symptomatic reflux to be more accurately detected. Not mentioned in
this article, is that there are statistical measures of association
between GOR episodes and symptoms (e.g. symptom association probability
score). By detecting all bolus reflux, pH-impedance monitoring markedly
increases the yield of positive symptom association in infants and
children.(3)
In addition, infants with GORD present differently from older
children and, as other tests such as upper GI endoscopy are more difficult
to perform in infants, the case for invasive functional testing may be
greater for infants than older children. In infants, conservative
management before any testing or pharmacological therapy is proven
effective(4). However, with PPI therapy recently being shown to be
ineffective in infants who fail such conservative therapy (5), pH-studies
may in fact be justifiable on the basis of establishing acid-related
disease when endoscopy is not possible. A recent study in such infants
shows that the degree of symptom improvement on esomeprazole correlates
with the level of acid exposure off therapy.(6) Nevertheless, the big
issue with pH-monitoring is the cut off value of the reflux index used to
diagnose pathological acid exposure. The fact remains that no outcome
studies testing the value of the reflux index criteria are available.
Until they are, clinicians need to be very conservative in interpreting
these findings.
We contend that pH-impedance monitoring has greater clinical utility
than pH monitoring alone, since it allows for a more complete
investigation of reflux and the association of reflux with symptoms.
Sincerely yours,
Michiel P. van Wijk, Clara M. Loots, Taher I. Omari, and Marc A.
Benninga
1.Tighe M, Cullen M, Beattie R. How to use: a pH study. Arch Dis
Child Educ Pract Ed. 2009 Feb;94(1):18-23.
2.Wenzl TG. Esophageal pH monitoring and impedance measurements: a
comparison of two diagnostic tests for gastroesophageal reflux. J Pediatr
Gastroenterol Nutr. 2002;34(5):519-23.
3.Loots C, Benninga M, Davidson G, Omari T. Addition of pH-impedance
monitoring to standard pH monitoring increases the yield of symptom
association analysis in infants and children with gastroesophageal reflux.
J Pediatr. 2009;154(2):248-52.
4.Orenstein SR, McGowan JD. Efficacy of conservative therapy as
taught in the primary care setting for symptoms suggesting infant
gastroesophageal reflux. J Pediatr. 2008;152(3):310-4.
5.Orenstein SR, Hassall E, Furmaga-Jablonska W, Atkinson S, Raanan M.
Multicenter, Double-Blind, Randomized, Placebo-Controlled Trial Assessing
the Efficacy and Safety of Proton Pump Inhibitor Lansoprazole in Infants
with Symptoms of Gastroesophageal Reflux Disease. J Pediatr. 2008; Epub
ahead of print.
6.Omari T, Lundborg P, Sandström M, Bondarov P, Fjellman M, Haslam
R, et al. Pharmacodynamics and systemic exposure of esomeprazole in
preterm infants and term neonates with gastroesophageal reflux disease. J
Pediatr. 2009;In Press.
Carter and Syed-Sabir1 gave a good account on the utility of rating
scales in ADHD. The time was appropriate when the new NICE guidance was
published. 2. However, I wish to emphasise to the readers that in UK, many
centres use the short version of Conners' Rating Scales- Revised (CRS-R).3
There are significant differences between the short and long versions of
the CRS.4 The Cognitive Problems / Inattention subscale on the...
Carter and Syed-Sabir1 gave a good account on the utility of rating
scales in ADHD. The time was appropriate when the new NICE guidance was
published. 2. However, I wish to emphasise to the readers that in UK, many
centres use the short version of Conners' Rating Scales- Revised (CRS-R).3
There are significant differences between the short and long versions of
the CRS.4 The Cognitive Problems / Inattention subscale on the teacher's
short CRS-R includes five questions as below:
Question No 4. Forgets things he/she has already learnt.
Question No 8. Poor in spelling.
Question 13. Not reading up to par.
18.Lacks interest in school work.
22. Poor in arithmetic.
All the above questions are related to the literacy difficulties rather
than indicating inattention. Therefore a high score in Cognitive Problems
/ Inattention subscale in the teacher's completed short CRS-R indicates a
child's literacy difficulties and not inattention. Clinicians need to be
aware that short CRS-R completed by teacher should not be used to evaluate
inattention in a child.
References:
1 Carter S and Syed-Sabir H. How to use: a rating score to diagnose
attention deficit hyperactivity disorder. Arch Dis Child Educ Pract Ed
2008; 93: 159-62. doi: 10.1136/adc.2008.139766
2. National Institute for Health and Clinical Excellence. Attention
deficit hyperactivity disorder: diagnosis and management of ADHD in
children, young people and adults- CG 72.September 2008 (available at
http://www.nice.org.uk/Guidance/CG72)
3. Conners CK. Conners' Rating Scales- Revised: Technical Manual,Multi-
Health Systems Inc, 1997, North Tonawanda, NY
4. Jacob J,Adesman A, Dimino R, Solanto M . Short Conners' Rating Scales:
Limitations for Diagnosing ADHD Inattentive Type. AACAP and CACAP Joint
Annual Meeting: Poster presentation 21 October. Toronto Canada 2005
I have just read this very good article in “Problem solving in
clinical practice” (Arch Dis Child Educ Pract Ed 2008:93;84-86)
Unfortunately Figure 1 is very unlikely to relate to the patient in
the case study as there are umbilical arterial and venous lines in situ
which would not be the case in a 3 week old. It is disappointing that the
authors could not find a suitable example from their extensive experience...
I have just read this very good article in “Problem solving in
clinical practice” (Arch Dis Child Educ Pract Ed 2008:93;84-86)
Unfortunately Figure 1 is very unlikely to relate to the patient in
the case study as there are umbilical arterial and venous lines in situ
which would not be the case in a 3 week old. It is disappointing that the
authors could not find a suitable example from their extensive experience
to demonstrate the plain film findings of malrotation in a 3 week old.
If authors are forced to use an example from a different patient it
would have been appropriate to acknowledge this.
These criticisms apart I enjoyed this Education section very much.
Yours
David Pilling
Consultant Paediatric Radiologist
Royal Liverpool Children’s Hospital
Dear Dr. Acheson
Many thanks for an excellent update on Appendicitis. Only comment I would like to make is about the bottom line.
A review by a paediatric surgeon for all suspected Appendicitis to decide on further management is almost impossible in the existing NHS. I have worked in 5 different DGH's and one Children's hospital A&E. In DGH, its hard to get a paediatric surgeons review even for pro...
Dear Editor,
in the interesting paper “Is it my calcium, Doctor?” (1), the authors concluded that “Amy’s hypercalcaemia” is due to a “primary hyperparathyroidism” and they don’t cite celiac disease (CD) as a specific cause of hyperparathyroidism (HPT), although they first wrote that “she had a previous history of celiac disease for which she was on a gluten free diet” (GFD).
CD is frequently associated...
Blair and colleagues mentioned CHILD2015 in their article and I would like to invite all ADC readers with an interest in this subject to join. Please see invitation below. To join, please go to: www.hifa2015.org/child2015-forum and click on 'Join CHILD2015'.
With thanks, Dr Neil Pakenham-Walsh MB,BS Co-moderator, CHILD2015
Coordinator, HIFA2015 Global Healthcare Information Network 16 Woodfield Drive C...
The authors of a recent article1 reporting on the management of an outbreak of tuberculosis in a crèche in Cork had difficulties with the explanation of what we currently manage as latent M. tuberculosis infection. In their first paragraph they defined “TB” as active pulmonary tuberculosis. Where they reported on communication to the parents of the differences between tuberculosis infection and active disease they menti...
Sir, Your two recent articles dealing with malrotation of the intestine (1,2), whilst being very specific with regard to the colour of the vomitus (green), were perhaps not specific enough. Yellow vomiting as a sign of malrotation has been noted by Millar et al (3), Walker et al (4) and personal experience some years earlier. Awareness of this may aid early diagnosis.
Reflux of yellow bile into the stomach,...
Dear editor,
Kempley et al (1) have recommended the length based on the gestation of the neonates rather than the rule of ‘7-8-9’, which has been being used traditionally over the years. I have read both articles with great interest – excellent review by Wylie’s (2) on neonatal resuscitation published in education and practice of Archives diseases in childhood and Endotracheal tube length for neonatal intubation...
Dear Sir,
With interest we read the paper by Tighe et al about the use of pH- monitoring in childhood.(1) However, we believe that the authors overestimate the role of this technique and their omission of a detailed discussion of the utility of pH-impedance monitoring renders this review incomplete.
The term ‘gold standard’ can no longer be applied to 24-hour pH- monitoring because pH-probes only d...
Carter and Syed-Sabir1 gave a good account on the utility of rating scales in ADHD. The time was appropriate when the new NICE guidance was published. 2. However, I wish to emphasise to the readers that in UK, many centres use the short version of Conners' Rating Scales- Revised (CRS-R).3 There are significant differences between the short and long versions of the CRS.4 The Cognitive Problems / Inattention subscale on the...
I have just read this very good article in “Problem solving in clinical practice” (Arch Dis Child Educ Pract Ed 2008:93;84-86)
Unfortunately Figure 1 is very unlikely to relate to the patient in the case study as there are umbilical arterial and venous lines in situ which would not be the case in a 3 week old. It is disappointing that the authors could not find a suitable example from their extensive experience...
Sir, Should all infants less than three months of age with fever be investigated, including those in the "low risk" category?
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