We read with interest the paper by Verhulst et al 1 and there are a few areas that warrant further discussion.
On the accuracy of sleep polysomonography study, the accuracy of the thoracoabdominal strain gauge used in their study requires elaboration. Although strain gauge is one of the qualitative methods to measure thoracoabdominal circumference, it is not very sensitive to detect shallow...
We read with interest the paper by Verhulst et al 1 and there are a few areas that warrant further discussion.
On the accuracy of sleep polysomonography study, the accuracy of the thoracoabdominal strain gauge used in their study requires elaboration. Although strain gauge is one of the qualitative methods to measure thoracoabdominal circumference, it is not very sensitive to detect shallow breathing as seen in cases of patients with myopathy2. Hence, use of strain gauge may result in mislabeling of obstructive apnea as central apnea4.A better alternative would be respiratory inductive plethysmograph (RIP) that measures the change of the cross-sectional area of rib cage and abdomen. It is more sensitive and accurate in detecting lung volume change.2 According to the American Academy of Sleep Medicine, a quantitative measurement of ventilatory effort such as esophageal manometry, calibrated respiratory inductance plethysmography or diaphragmatic / intercostals EMG) should be performed for classifying obstructive, central or mixed hypopnea.3 The authors should also provide and justify the upper limit of normal for central apnea / hypopnea in their study. The absence of end-tidal CO2 monitor in the PSG set-up also decreased the sensitivity of diagnosing obstructive sleep-disordered breathing, i.e. obstructive sleep hypoventilation defined as end-tidal CO2 more than 45 mm Hg for more than 60% of total sleep time or more than 55mmHg for more than 8% of total sleep time.4 Verhulst et al. should also report the arousal index and wake after sleep onset (WASO) so as to allow comparison between normal and the apneic group.
On the analysis of data, this study evaluated the risk factors for obstructive sleep apnea and central apnea in a clinical sample of children referred to a pediatric obesity clinic. Verhulst et al concluded that “none of the anthropometric variables was a significant predictor for the presence of mild obstructive sleep apnea” although this conclusion was not supported by any quantitative analysis. Also the presentation of the results in Verhulst et al’s study did not conform to the standard suggested by Moss et al,5 e.g. inclusion of odds ratio and confidence intervals for the final model. The readers cannot judge for themselves if the conclusion was a result of insufficient statistical power. Some very important results were not presented, for example, the prevalence of tonsils hypertrophy, data on waist-hip ratio despite the fact that these results were used in their partially-disclosed logistic regression results.
We have conducted a systematic review of the literature and found that the prevalence of obstructive sleep apnea syndrome in obese children ranged from 13% to 36%.6 We also demonstrated a dose-response relationship between obstructive sleep apnea and obesity.7 We suspected that Verhulst et al’s failure to corroborate our findings was due to a type II error and misdiagnosis of obstructive sleep apnea as central apnea.
References:
Verhulst SL, Schrauwen N, Haentjens D, Rooman RP, Van Gaal L, De Backer WA, Desager KN. Sleep-disordered breathing in overweight and obese children and adolescents: prevalence, characteristics and the role of fat distribution. Arch Dis Child 2007;92:205-8
ATS/ERS Statement on Respiratory Muscle Testing. Am I Respir Care Med 2002, 166: 518-624.
The AASM Manual for the Scoring of Sleep and Associated Events. 2007.
Standards and Indications for Cardiopulmonary Sleep Studies in Children. Am J Respir Crit Care Med 1996; 153: 866-78.
Moss M, Wellman DA, Cotsonis GA. An appraisal of multivariable logistic models in the pulmonary and critical care literature. Chest. 2003;123:923-8.
Ng DK, Lam YY, Kwok KL, Chow PY. Obstructive sleep apnoea syndrome and obesity in children. Hong Kong Med J 2004; 10: 44-8.
Lam YY, Chan EY, Ng DK, Chan CH, Cheung JM, Leung SY, Chow PY, Kwok KL. The correlation among obesity, apnea-hypopnea index, and tonsil size in children. Chest. 2006;130:1751-6.
Figure 1 in this study shows a rise in autism incidence (recorded)
from 22 cases in the birth cohort of 1989 to 46 in 1991. R Lingam, A
Simmons, N Andrews, E Miller, J Stowe and B Taylor fail to take into
consideration the introduction of the accelerated Diptheria, Pertussis,
Tetanus (DPT) as a potential confounder, advancing the doses from 3, 5 and
10 months to 2, 3 and 4 months [1]: each dose also c...
Figure 1 in this study shows a rise in autism incidence (recorded)
from 22 cases in the birth cohort of 1989 to 46 in 1991. R Lingam, A
Simmons, N Andrews, E Miller, J Stowe and B Taylor fail to take into
consideration the introduction of the accelerated Diptheria, Pertussis,
Tetanus (DPT) as a potential confounder, advancing the doses from 3, 5 and
10 months to 2, 3 and 4 months [1]: each dose also containing 50 µg
Thiomersal (Thimerosal) including 25 µg mercury [1]. This is a surprising
omission as N Andrews, E Miller, J Stowe and B Taylor were also co-authors
of [1], which though not published at the time of this study had already
been delivered privately to the World Health Organization in June 2002
[1]. Equally in [1] they failed to note the rise aforementioned in this
present study as possible evidence of a population effect of the
accelerated schedule.
John Stone
Reference:
[1] Andrews N, Miller E, Grant A, Stowe J, Osborne V, and Taylor B,
'Thimerosal Exposure in Infants and Developmental Disorders: A
Retrospective Cohort Study in the United Kingdom Does Not Support a Causal
Association', PEDIATRICS Vol. 114 No. 3 September 2004, pp. 584-591
(doi:10.1542/peds.2003-1177-L),
http://pediatrics.aappublications.org/cgi/content/full/114/3/584
We would like to reply to the letter by Murugan [1] following our article on
Kawasaki disease.[2] We have suggested that children with known Kawasaki
disease and normal coronary arteries should have lifelong follow-up. The
long term vascular damage from Kawasaki Disease is uncertain, but evidence
from Dhillon et al suggests that abnormalities of systemic endothelial
function are present many years after...
We would like to reply to the letter by Murugan [1] following our article on
Kawasaki disease.[2] We have suggested that children with known Kawasaki
disease and normal coronary arteries should have lifelong follow-up. The
long term vascular damage from Kawasaki Disease is uncertain, but evidence
from Dhillon et al suggests that abnormalities of systemic endothelial
function are present many years after resolution of acute KD, even in
patients without coronary artery abnormalities on echocardiography.[3] We
recommend that children with KD have echocardiography at 6-8 weeks and
subsequent follow-up to six months for those with no coronary artery
abnormalities to ensure resolution of symptoms, such as behavioural
problems and skin re-peeling. Clearly there are resource issues here for
paediatric cardiology and specialist Kawasaki clinics. Some balance has to
be struck between the observation that few cardiac sequelae are found in
the long-term follow-up of children with normal coronary arteries at
original presentation, and case reports to the contrary.[4] For this
reason, we advocate long-term annual follow-up by General Practitioners to
monitor for and minimise risk factors for coronary vascular disease in
adolescent and adult life. Prospective follow-up of children with KD will
also be important in estimating the long-term cardiac risk of this
disorder.
References
(1) Murugan SJ, Thomson J, Parsons JM. Is Life long Follow up for patients with Kawasaki disease indicated? [electronic response to Brogan PA et al, Kawasaki disease: an evidence based approach to diagnosis, treatment, and proposals for future research]. archdischild.comhttp://adc.bmjjournals.com/cgi/eletters/archdischild;86/4/286.
(2) Brogan PA, Bose A, Burgner D, Shingadia D, Tulloh R, Michie C,
Klein N, Booy R, Levin M, Dillon MJ. Kawasaki disease: an evidence based
approach to diagnosis, treatment, and proposals for future research. Arch
Dis Child 2002 Apr;86(4):286-90.
(3) Dhillon R, Clarkson P, Donald AE, Powe AJ, Nash M, Novelli V, Dillon
MJ, Deanfield JE. Endothelial dysfunction late after Kawasaki Disease. Circulation 1996;94:2103-6
Dr. Kanjilal makes some important observations but is mistaken in
several of her assertions. First, she suggests that because we limited
our study sample to infants for whom pre and post discharge TSBs were
performed our results are affected by some form of selection bias. The
bias she is referring to is verification bias, in which only patients with
“positive” or more concerning test results have a...
Dr. Kanjilal makes some important observations but is mistaken in
several of her assertions. First, she suggests that because we limited
our study sample to infants for whom pre and post discharge TSBs were
performed our results are affected by some form of selection bias. The
bias she is referring to is verification bias, in which only patients with
“positive” or more concerning test results have a follow-up test to verify
the original results. By decreasing the number of patients with
“negative” test results, this bias has the effect of overestimating test
sensitivity and underestimating specificity. However, as we point out in
our manuscript, we studied infants enrolled in an early discharge follow-
up program and minimized the potential for verification bias by
restricting our sampling frame to months during which >75% of enrolled
infants had postdischarge TSB measurements performed. In fact, for the
majority of these months, >90% of enrolled infants had postdischarge
TSBs measured.
The second point on which Dr. Kanjilal is mistaken concerns the
inclusion of “interrelated” factors “like vacuum and cephalohematoma” in
our clinical risk factor scoring system. As summarized in Table 2, vacuum
extraction is included in the scoring system but cephalohematoma is not.
In fact, contrary to our expectation, cephalohematoma was not associated
with development of postdischarge TSB>95%ile. This simply may be a
result of poor documentation of cephalohematoma in the admission and
discharge physical examinations (misclassification bias), but it raises
concerns about the use of subjective factors in clinical risk factor
scoring systems. Our results suggest that using more objective findings,
such as use of vacuum extraction during delivery--a common cause of
cephalohematoma-- may provide more accurate information about subsequent
risk of hyperbilirubinemia.
Finally, our finding that breastfeeding increases the risk of
hyperbilirubinemia is not new and should not be interpreted as a
recommendation against breastfeeding. As pediatricians who routinely care
for newborn infants, we recognize the benefits of breastfeeding and
strongly support its use. However, at the same time we are cognizant of
the potential risks of dehydration and hyperbilirubinemia posed by
inadequate intake in breastfed infants. The results of our study should
be interpreted as yet another invocation for healthcare systems and
providers to guarantee adequate lactation support for breastfeeding
mothers and early identification and treatment of breastfeeding problems
that may result in inadequate intake for infants.
As Dr. Kanjilal suggests, a prospective validation of alternative
risk assessment strategies is needed to confirm the results of our study
as well as other studies of alternative screening strategies. Further
studies are needed to evaluate the incremental benefit of using clinical
risk factors in addition to the predischarge TSB to predict which infants
are at risk of developing severe hyperbilirubinemia. And finally, more
studies are needed to evaluate the cost-effectiveness of alternative
strategies for screening and tracking infants for their risk of developing
severe hyperbilirubinemia in order to prevent the occurrence of
kernicterus, an uncommon but devastating, costly, and entirely preventable
condition.
We would like to take into consideration recent publications that
have recently appeared about the possibility of developing hyponatraemia
in children with gastroenteritis treated with intravenous hypotonic saline
and the risks derived from such complication.[1-3]
Even though we belive these papers have been well designed and
developed, we cannot agree with their results for we are carrying...
We would like to take into consideration recent publications that
have recently appeared about the possibility of developing hyponatraemia
in children with gastroenteritis treated with intravenous hypotonic saline
and the risks derived from such complication.[1-3]
Even though we belive these papers have been well designed and
developed, we cannot agree with their results for we are carrying out a
similar study in our centre (81 cases up to now) that is leading to the
opposite conclusion: our children with gastroenteritis didn’t develop
hyponatraemia although they were all treated with hypotonic intravenous
solutions (0.3% saline with 5% glucose) while isotonic fluids were only
used in the “pre-sock” situations.
To begin with, the incidence of hyponatraemia at the time of diagnosis is
lower in our study (9%) than in those published before (range from 30% to
50%), dates that can be due to differences in climate or diet.
In the analysis, we separated children according to whether they were
hyponatraemic, normonatraemic or hypernatraemic at presentation: in the
first group the hypotonic intravenous saline increased their mean plasma
sodium (132.4 mEq/l, standard derivation, SD: 2.07, to 135.3, SD: 2.21),
while decreased lightly in the second group without leading to
hyponatraemia (139.2, SD: 2.9, to 137.3, SD: 2.9), and also did in the
third group (150.4, SD: 4.12, to 140.6, SD: 3.6). No cases of
hyponatraemia post-infussion were detected. Hoorn et al[4] with a sample
of 1586 children pointed out that the cases of hyponatraemia in their
study were all due to wrong treatments with fluid apports higher than
needed.
We also want to emphasize the fact that we have found an important number
of children (10 cases: 16,3%) in our study that presented glucose levels
lower than 70 mg/dl, and in one case it was as low as 40 mg/dl. If these
children were treated with isotonic fluids without addecuate apports of
glucose, their levels would never increase as needed, with serious
consequences.
These dates are not deffinitive but we think that should be taken into
consideration before taking decissions about which solution should be
better to treat these patients and carry out new studies with different
designs to increase the existing evidence.
References:
1 Neville KA, Verge CF, Rosenberg AR, et al. Isotonic is better than
hypotonic saline for intravenous rehydration of children with
gastroenteritis: a prospective randomised study. Arch Dis Child.
2006;91:226-32.
2 Duke T, Molyneux EM. Intravenous fluids for seriously ill children: time
to consider. Lancet. 2003;362:1320-3.
3 Neville KA, Verge CF, O’Meara MW, et al. High antidiuretic hormone
levels and hyponatraemia in children with gastroenteritis. Pediatrics.
2005;116:1401-7.
4 Hoorn EJ, Geary D, Robb M, et al. Acute hyponatremia related to
intravenous fluid administration in hospitalized children: an
observational study. Pediatrics. 2004;113:1279-84.
The report by Stenhouse and colleagues on obesity trends in Plymouth
toddlers [1]. is important since there are still few data on when and how
obesity begins in the pre-school years.
Unfortunately, the data they
present, though suggestive, do not make the case as strongly as they
might. The paper implies that during the years in question there was a
policy of universal review at 6-9 mon...
The report by Stenhouse and colleagues on obesity trends in Plymouth
toddlers [1]. is important since there are still few data on when and how
obesity begins in the pre-school years.
Unfortunately, the data they
present, though suggestive, do not make the case as strongly as they
might. The paper implies that during the years in question there was a
policy of universal review at 6-9 months and at 24-30 months. Yet BMI
data were only available for 2829 / 4665 (64%) of the birth cohort. Why
were there no data on the other third? It may be that the health visitors
did not see some children because they defaulted, or they may have been
unofficially operating a selective policy of health visiting in order to
manage the workload, or perhaps they only recorded both height and weight
when they thought it was necessary. Either way, the number of children
without BMI measurements is sufficiently large to prompt the question –
was there a systematic bias that meant the measured children had higher
(or lower) BMIs than the population as a whole?
The question of social
class bias could be addressed by using postcode analysis. Health visitor
behaviour is more difficult to examine but it would help to know more
about their attitudes and their actual policies and practice, as opposed
to what is written in their policy manual.
The report also demonstrates once again that in reality it is
extremely difficult to engage all pre-school children in a programme of
health surveillance, whatever policy one adopts. This in turn emphasises
the need for caution when interpreting community datasets.
Reference
(1). Stenhouse et al: “Weight differences in Plymouth
toddlers compared to the British Growth Reference population”. Archives
of Disease in Childhood, 2004, 89, 843-844.
It would be churlish to write expressing criticism of the recent
study by the Welsh Child Protection Systematic Review Group (1) without
first acknowledging the important contribution they have made to bringing
an evidence base to the practice of child protection. However, I was
surprised that the study group should make the statement that a torn
frenum is widely regarded as pathognomonic and note there is only one
art...
It would be churlish to write expressing criticism of the recent
study by the Welsh Child Protection Systematic Review Group (1) without
first acknowledging the important contribution they have made to bringing
an evidence base to the practice of child protection. However, I was
surprised that the study group should make the statement that a torn
frenum is widely regarded as pathognomonic and note there is only one
article cited to support this statement. This article did not present any
data but was an educational review of the responsibilities of dentists in
notifying child abuse.
My own experience leads me to believe firmly that a torn labial
frenum may occur accidentally in older infants. I have previously been
involved in a case where a 12 month infant who had recently started
cruising, had been standing exploring the top of a coffee table with her
mouth and gums in the way that small infants often do. She had
unexpectedly lost her balance whilst her mouth was still in contact with
the edge of the table and had been reported by her parents as falling.
She had immediately cried, had been noted to have blood in her mouth and
parents attended the Accident and Emergency Department where they gave
this plausible and consistent history for the injury.
In an attempt to clarify whether my personal experience of this
injury was unusual, I recently asked a group of 30 paediatricians whether
there was support for the proposition that a torn labial frenulum is
pathognomonic of child abuse. No one was prepared to support this and two
other consultant paediatricians cited examples of accidental trauma
involving a similar mechanism to that described above – one in his own
child.
However, my concern is that whilst the possibility of accidental
causation in the older child appears to be widely accepted, the same may
not be so for babies.
The literature supports the idea that non-mobile infants are unlikely
to bruise accidentally. (2,3,4). The presence of a torn labial frenulum
in an non-mobile infant (where a previous history of general anaesthetic
and intubation have been excluded) is highly suggestive (and even, dare I
say, possibly pathognomonic) of non accidental injury.
My belief is that the courts would follow and support the logic
inherent in the proposition that babies who are non-mobile do not generate
sufficient forces to bruise the skin spontaneously and are similarly
exceedingly unlikely to occasion accidental tears to the labial frenum.
REFERENCES:
1. Maguire S, Hunter B, Hunter L et al Diagnosing abuse:a systematic
review of torn frenum and other oral injuries. Archives of Disease in
Childhood. 2007; 92: 1113-1117
2. Sugar N F, Taylor J A and Feldman K W. Bruises in Infants and
Toddlers: those who don’t cruise rarely bruise. Archives of Paediatric
and Adolescent Medicine 1999, April 153 (4): 399-403.
3. Mortimer P E and Freeman M. Are Facial Bruises in Babies Ever
Accidental? Archives of Disease in Childhood 1983; 58: 75-80
4. Labbè J, Caouette G. Recent Skin Injuries in Normal Children.
Paediatrics, 2001 (August) 108(2): 271-276.
Campbell and Spencer have enumerated the challenges that the European
Working Time Directive (EWTD) presents(1). The basis of the problem
appears to be that doctors in training will have to be grouped together in
larger cells with a minimum of 10 on each rota. The rationale behind this
assertion is that exposure to useful training time in clinics and non-
acute work will be eroded with smaller numbers...
Campbell and Spencer have enumerated the challenges that the European
Working Time Directive (EWTD) presents(1). The basis of the problem
appears to be that doctors in training will have to be grouped together in
larger cells with a minimum of 10 on each rota. The rationale behind this
assertion is that exposure to useful training time in clinics and non-
acute work will be eroded with smaller numbers on a rota(2). This may well
be the case in the context of a large hospital with many sub-specialist
clinics and day time training opportunities, but it does not recognise the
importance of learning to asses and manage the acutely ill child.
Our experience is that 62% of admissions from the Emergency
Department occur outside of the normal working day. These unwell children
are a precious training resource which is only of value at the time when
they are assessed and managed in the acute situation. If these admissions
are to provide useful training opportunities trainees must have access to
appropriate supervision out of hours.
The corollary of increasing numbers on a rota is that more doctors
are present during the normal working day. With 10 in a cell there will be
an average of 6 doctors present during the normal working day. This is
more than is needed in a smaller District General Hospital.
We have maintained a 2009 EWTD compliant middle grade rota over the
last year with 7 doctors. The educational value of the training posts has
been affirmed by both the College and the Deanery and this has been
achieved by ensuring an appropriate level of out of hours Consultant
supervision. We believe that this model should be considered when facing
the challenges of the EWTD, particularly in the context of more remote
District General Hospitals.
References:
1.Campbell C, Spencer SA. The Implications of the Working Time
Directive: how can paediatrics survive? Arch Dis Child 2007; 92: 573-5.
2. Royal College of Physicians. Designing safer rotas for junior
doctors in the 48-hour week. Report of a multidisciplinary working group.
http://www.rcplondon.ac.uk/pubs
I would like to thank Dr Reimer for his interest in our work and
reciprocate by correcting his flawed understanding of the paper. Perhaps
it would be helpful to start by summarising the hypothesis, results and
interpretation of the study. Our a priori hypothesis was that positive
physical contact between mother and child in early life may result in
enhanced control of the stress response as indicate...
I would like to thank Dr Reimer for his interest in our work and
reciprocate by correcting his flawed understanding of the paper. Perhaps
it would be helpful to start by summarising the hypothesis, results and
interpretation of the study. Our a priori hypothesis was that positive
physical contact between mother and child in early life may result in
enhanced control of the stress response as indicated by animal studies (1,
2). We could not test this directly, but used breast feeding as an
indirect marker of close contact in early life. Among breast fed children
there was no statistically significant or notable association of parental
divorce with anxiety, but among bottle fed children the association was
more pronounced and statistically significant. This does not prove that
early physical contact associated with breast feeding confers resilience
against psychosocial stress, but is consistent with the hypothesis.
Further research should have a more detailed focus on mother-child
interactions (not just breast feeding) during the first months of life.
Our abstract concludes: ‘This could be because breast feeding is a marker
of exposures related to maternal characteristics and parent-child
interaction.’
This study forms part of a collaborative programme of work
investigating the concept of resilience, which is defined as a factor that
limits the damaging consequences of adverse exposures.(3) To investigate
this concept using statistical effect modification, it is necessary to
consider the difference in outcome between those with and without an
adverse exposure and how this difference varies by presence of the
putative resilience factor using interaction testing. Dr Reimer seems to
misunderstand interaction testing when he complains that reduced anxiety
is only observed among those who experienced divorce. We chose divorce as
a marker of exposure to chronic psychosocial stress as we have evidence
from earlier studies of its potentially profound effect on child
development.(4) The hypothesis being tested concerned children’s anxiety
following exposure to stress reflecting differences in reactivity of the
stress response. A limitation of the study is that we did not have acute
measures of exposure and response to stress and only a proxy measure of
maternal contact in early life (breast feeding): use of such measures
means that associations are likely to be conservative. In claiming that
the differences in anxiety are ‘clinically irrelevant’ Dr Reimer misses
the point: we were not suggesting breast feeding as an intervention for
families at a high risk of divorce, but identifying associations that may
provide information about processes relevant to resilience. We have
identified a potentially useful indirect marker of resilience against some
forms of psychosocial stress that should now be confirmed and elucidated
by further investigation.
Dr Reimer claims that ‘adjustment has only been made for very serious
mental illness,’ but reading the paper shows this statement to be entirely
inaccurate. Multiple potential confounding factors were included in the
multivariate analysis, including the Malaise Inventory, which is a 24-item
measure of tendency to depression.(5, 6) We modelled this information both
as a dichotomous variable and using all of the 24 items as separate
variables (hardly measuring just serious mental illness) in an attempt to
perform the most comprehensive adjustment possible for maternal
characteristics. This measure of depression is likely to be strongly
associated with anxiety. Other relevant measures include cigarette smoking
during pregnancy, which is associated both with maternal personality
characteristics and adverse outcomes in offspring. While we do not have
perfect measures, if the observed effect modification was mediated
exclusively through maternal anxiety then a greater reduction in magnitude
of association might be expected following adjustment for the potential
confounding factors. The concern that father’s characteristics influence
both exposure and outcome differentially by early breast feeding is of
course possible but less plausible as a major source of confounding.
Observational studies cannot prove causation. In contrast with Dr
Reimer’s assertion that the paper is trying to show ‘breast milk to be the
best thing,’ the paper outlines several potential explanations for the
results that may not be mutually exclusive, including: the influence of
early physical contact on neuro-endocrine mechanisms; maternal personality
characteristics associated both with breast feeding and other aspects of
mother-child interactions; breast feeding may indicate a non-causal
association with parental attachment or may be implicated in the
development of parental attachment.
References:
1. Sapolsky RM. The importance of a well-groomed child. Science
1997; 277:1620-1621.
2. Liu D, Diorio J, Tannenbaum B, Caldji C, Francis D, Freedman A et
al. Maternal care, hippocampal glucocorticoid receptors, and hypothalamic-
pituitary-adrenal responses to stress. Science 1997; 277:1659-1662.
3. Osika W, Ehlin A, Montgomery SM. Does height modify the risk of
angina associated with economic adversity? Economics and Human Biology
2006; 4: 398-411.
4. Montgomery SM, Bartley MJ, Wilkinson RG. Family conflict and slow
growth. Archives of Disease in Childhood 1997; 77: 326-330.
5. Rutter M, Graham P, Yule W. A neuropsychiatric study in childhood.
London: Heinemann; 1970.
6. Grant G, Nolan M, Ellis N. A reappraisal of the Malaise Inventory.
Social Psychiatry and Psychiatric Epidemiology 1990; 25:170-178.
Dear Editor,
We read with interest the paper by Verhulst et al 1 and there are a few areas that warrant further discussion.
On the accuracy of sleep polysomonography study, the accuracy of the thoracoabdominal strain gauge used in their study requires elaboration. Although strain gauge is one of the qualitative methods to measure thoracoabdominal circumference, it is not very sensitive to detect shallow...
Dear Editor,
Figure 1 in this study shows a rise in autism incidence (recorded) from 22 cases in the birth cohort of 1989 to 46 in 1991. R Lingam, A Simmons, N Andrews, E Miller, J Stowe and B Taylor fail to take into consideration the introduction of the accelerated Diptheria, Pertussis, Tetanus (DPT) as a potential confounder, advancing the doses from 3, 5 and 10 months to 2, 3 and 4 months [1]: each dose also c...
Dear Editor
We would like to reply to the letter by Murugan [1] following our article on Kawasaki disease.[2] We have suggested that children with known Kawasaki disease and normal coronary arteries should have lifelong follow-up. The long term vascular damage from Kawasaki Disease is uncertain, but evidence from Dhillon et al suggests that abnormalities of systemic endothelial function are present many years after...
Dear Editor,
Dr. Kanjilal makes some important observations but is mistaken in several of her assertions. First, she suggests that because we limited our study sample to infants for whom pre and post discharge TSBs were performed our results are affected by some form of selection bias. The bias she is referring to is verification bias, in which only patients with “positive” or more concerning test results have a...
Dear Editor,
We would like to take into consideration recent publications that have recently appeared about the possibility of developing hyponatraemia in children with gastroenteritis treated with intravenous hypotonic saline and the risks derived from such complication.[1-3]
Even though we belive these papers have been well designed and developed, we cannot agree with their results for we are carrying...
Dear Editor
It was the Broad Street (currently Broadwick Street) pump that John Snow had the parish elders remove the handle of, not Bond Street.
Dear Editor,
The report by Stenhouse and colleagues on obesity trends in Plymouth toddlers [1]. is important since there are still few data on when and how obesity begins in the pre-school years.
Unfortunately, the data they present, though suggestive, do not make the case as strongly as they might. The paper implies that during the years in question there was a policy of universal review at 6-9 mon...
It would be churlish to write expressing criticism of the recent study by the Welsh Child Protection Systematic Review Group (1) without first acknowledging the important contribution they have made to bringing an evidence base to the practice of child protection. However, I was surprised that the study group should make the statement that a torn frenum is widely regarded as pathognomonic and note there is only one art...
Dear Editor,
Campbell and Spencer have enumerated the challenges that the European Working Time Directive (EWTD) presents(1). The basis of the problem appears to be that doctors in training will have to be grouped together in larger cells with a minimum of 10 on each rota. The rationale behind this assertion is that exposure to useful training time in clinics and non- acute work will be eroded with smaller numbers...
Dear Editor,
I would like to thank Dr Reimer for his interest in our work and reciprocate by correcting his flawed understanding of the paper. Perhaps it would be helpful to start by summarising the hypothesis, results and interpretation of the study. Our a priori hypothesis was that positive physical contact between mother and child in early life may result in enhanced control of the stress response as indicate...
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