Premedication for neonatal intubation has become a hot topic
recently, and in their letter Attardi et al[1] make an interesting
contribution to the debate. However the significant increase in
oxyhaemaglobin desaturation in those neonates intubated following
administration of midazolam when compared to placebo is not surprising.
Midazolam is a hypnotic agent and as such can only be useful as part
of...
Premedication for neonatal intubation has become a hot topic
recently, and in their letter Attardi et al[1] make an interesting
contribution to the debate. However the significant increase in
oxyhaemaglobin desaturation in those neonates intubated following
administration of midazolam when compared to placebo is not surprising.
Midazolam is a hypnotic agent and as such can only be useful as part
of an anaesthetic procedure. The so called triad of anaesthesia comprises
hypnosis, analgesia and muscle relaxation. Modern practice commonly
employs a number of drugs each with a single primary effect which are
combined in low doses to allow the minimum effective dose of each to be
used - this is termed balanced anaesthesia. As a single agent midazolam
does not produce anaesthesia and will not confer good intubating
conditions. Any cardiovascular and respiratory depression during its long
onset time of up to 5 minutes will also make adverse events more likely.
If we are to truly move forward in our goal to make intubation of
neonates both safer and less stressful we must follow the lead given to us
by our colleagues in paediatric anaesthesia. Careful assessment of the
airway, a skilled operator with an experienced assistant and application
of the principles of balanced anaesthesia are the keys to success.
References
(1) Attardi DM, Paul DA, Tuttle DJ, Greenspan JS. Premedication for intubation in neonates [letter]. Arch Dis Child Fetal Neonatal Ed 2000;83:F160.
The authors of this paper need all appreciation in trying out this
“magic cream” on babies, which already finds an established role in
children as a topical anaesthetic.
However as one goes through this interesting article, a striking feature
is the small numbers in the study. I find no mention as regards to the
power of the study. The confidence limits while expressing significant p
values is...
The authors of this paper need all appreciation in trying out this
“magic cream” on babies, which already finds an established role in
children as a topical anaesthetic.
However as one goes through this interesting article, a striking feature
is the small numbers in the study. I find no mention as regards to the
power of the study. The confidence limits while expressing significant p
values is not mentioned.
Assessment of pain in neonates is a difficult area. The use of
validated pain scores as a bedside tool is well taken. However in
literature published on this subject, many authors express the importance
of assessing the physiological response of babies to pain, like changes
in heart rate, respiration, blood pressure,and saturation of oxygen. Moreover the level
of arousal at the time of stimulation seems to hold a lot of importance.
A baby who is asleep is far less prone to cry than one who is awake. In the
present paper there seems to be no mention of the state of arousal of the
baby at the moment of cannulation. Inclusion of neonatal behaviour scales
would have boosted the value of this useful study.
As regards to the safety profile of the drug, it is not clear as to
whether one could use 4% amethocaine in preterm babies as well. In
preterm babies the risk of systemic absorption needs further looking into.
It is interesting to see in the future how topical amethocaine and
oral sucrose fare against each other or add up to provide effective pain
relief to the neonate.
Dr R Srinivasan
Department of Paediatrics
Scunthorpe General Hospital
North Lincolnshire, UK
References
(1) Jain A, Rutter N. Does topical amethocaine gel reduce the pain of venupuncture in newborn infants? A randomised double blind controlled trial. Arch Dis Child Fetal Neonatal Ed 2000:83:F207-10.
(2) Bozzette M. Observation of pain behavior in the NICU: an exploratory study. J Perinat Neonatal Nurs 1993;7:76-87.
(3) Grunau RV, Craig KD. Pain expression in neonates: facial action and cry. Pain 1987;28:395-410.
(4) Rushforth JA, Levene MI. Behavioral response to pain in healty neonates. Arch Dis Child Fetal Neonatal Ed 1994;70:F174-6.
(5) Ramenghi LA, Wood CH,Griffith GC, Levene MI. Reduction of pain response in premature infants using intraoral sucrose. Arch Dis Child Fetal Neonatal Ed 1996;74:F126-8.
Nitric oxide (NO) is frequently used as a selective pulmonary
vasodilator in neonates. Since its metabolite, methaemoglobin can
potentially cause tissue hypoxia it is considered mandatory to measure
methaemoglobin levels when using NO. In an attempt to review and
rationalise our own practice of methaemoglobin measurement when using NO
we undertook a search of current literature and conducted a postal surv...
Nitric oxide (NO) is frequently used as a selective pulmonary
vasodilator in neonates. Since its metabolite, methaemoglobin can
potentially cause tissue hypoxia it is considered mandatory to measure
methaemoglobin levels when using NO. In an attempt to review and
rationalise our own practice of methaemoglobin measurement when using NO
we undertook a search of current literature and conducted a postal survey
of current practice.
38 questionnaires were sent to level II or III neonatal units in
England, Scotland and Wales. Of the 32 (84%) returned, 24 were from
centres using NO (63%). We asked about their timing for methaemoglobin
levels and what level was considered to warrant intervention. Our replies
found no standardised protocol for the timing of levels and no recognised
‘toxic’ level. The range of timings for levels was large varying from
every 4 hours to every 24 hours after starting NO therapy. Most hospitals
considered a methaemoglobin level of 4% needed a reduction in the dose of
NO and that levels of 5 to 7% required the NO to be stopped. All centres
agreed on the treatment of choice for toxic levels, ie, an infusion of
methylene blue, but there was no agreement on what level required
treating, quoted levels ranging from 5 to 15%.
From the literature it would appear that neonates tolerate relatively high
methaemoglobin levels well. Normal blood levels of methaemoglobin have
been quoted as 0 to 1.9% for adults, 0 to 2.8% for term neonates and 0.08 to 4.7% for premature babies.[1] The higher level in neonates being due to
their immature enzymatic system and the fact that fetal haemoglobin is
more prone to oxidation. Furthermore, in a case where NO was inadvertently
given in extremely high concentrations, a neonatal methaemoglobin level of
13.4% was measured with no clinical deterioration and no other
intervention than stopping the NO therapy being required.[2]
Methaemoglobin has been shown to follow first order kinetics for both
its formation and metabolism with a time constant of 39 to 91 minutes. Peak
methaemoglobin levels occurred 3 to 5 hours after starting NO therapy after
which steady state concentrations were achieved.[3] From this data it would
seem appropriate to take a methaemoglobin levels 4 hours and 8 hours after
starting NO and then daily unless the dose is increased, when levels
should be re-measured at 4 and 8 hours after the change. Once the dose of
NO is being decreased levels should no longer be necessary.
Our survey has highlighted a lack of agreement for the safe use of
nitric oxide in neonates with regard to methaemoglbinaemia. The
pharmacokinetic data quoted was from healthy adults inhaling NO and
therefore may not be comparable to that of sick neonates. We therefore
feel this is an area that warrants further research and would be grateful
of other unit’s advice and experience in this area.
Dr RD Taylor*
Dr SA Calvert**
*Specialist Registrar anaesthetics Frenchay Hospital Bristol, UK
**Consultant Neonatologist
Neonatology Unit St George’s Health Care Trust London SW17 OQT, UK
References
(1) Bowman WC, Rand MJ. Methaemoglobinaemia. In: Textbook of
Pharmacology. Second edition. Blackwell Scientific publications.1984:21.45 – 48.
(2) Heal CA, Spencer SA. Methaemoglobinaemia with high dose nitric oxide administration. Acta Paediatr 1995;84:1318-19.
(3) Young JD, Dyar O, Xiong L, Howell S. Methaemoglobin production in normal adults inhaling low concentrations of nitric oxide. Intensive Care Med 1994;20:581-4.
Whitelaw and Thoresen recently reviewed the current evidence
concerning the effects of antenatal steroids on brain development, and
made suggestions for clinical practice.
We believe that interpretation of current evidence is not yet clear
enough to determine clinical practice, and further research is necessary
before such recommendations are possible. No randomised controlled trials
comparing si...
Whitelaw and Thoresen recently reviewed the current evidence
concerning the effects of antenatal steroids on brain development, and
made suggestions for clinical practice.
We believe that interpretation of current evidence is not yet clear
enough to determine clinical practice, and further research is necessary
before such recommendations are possible. No randomised controlled trials
comparing single with multiple courses of corticosteroids have been
completed, and current evidence is from observational studies of humans
and animal experiments. There are several problems with interpretation of
these results.
Firstly, animal experiments have demonstrated impaired
growth of the brain after antenatal exposure to corticosteroids, but it is
not known to what extent similar changes may occur in human brains, nor
whether they lead to functional problems. Secondly, observational studies
may suffer from several sources of bias; for example, infants exposed to
single and multiple courses of antenatal steroids may be born at different
gestational ages, may be born to mothers suffering from different
conditions, or may be exposed to a high-risk situation for different
amounts of time. These biases could influence the results of observational
studies in either direction. Finally, publication bias may have
influenced the available evidence; papers suggesting harmful effects from
multiple courses of steroids may have been more readily published during
recent years than those showing no effect or benefit. No firm conclusions
can be drawn from the available evidence and we cannot say whether
multiple courses of antenatal steroids are beneficial, harmful or have no
effect.
Better evidence is needed to resolve this issue, and several large
randomised controlled trials comparing single and multiple courses of
antenatal steroids are either planned or in progress around the world.
Until these trials are completed the uncertainty about the risks and
benefits of multiple courses of antenatal steroids must remain. The best
policy for obstetricians would therefore be to take part in the current
trials in order to resolve this issue as quickly as possible.
In the UK the TEAMS trial is currently recruiting, and more centres
are needed. The study can be contacted by telephone (+44 (0) 1865 227122), or
email (teams@perinat.ox.ac.uk).
Simon Gates
Peter Brocklehurst
Ann Johnson
National Perinatal Epidemiology Unit Institute of Health Sciences
Old Road, Oxford OX3 7LF, UK
Zarko Alfirevic
Department of Obstetrics and Gynaecology Liverpool Women's Hospital
Crown Street, Liverpool L8 7SS, UK
Geoffrey Chamberlain
Department of Gynaecology, Singleton Hospital Sketty, Swansea SA2 8QA, UK
We appreciate Dr Pharoah's comments on the definitions of incidence
and prevalence.[1] However, his interpretation of the data appears
erroneous.[2]
Dr Pharoah suggests that perhaps the dexamethasone-treated infants
were sicker than the control infants and were saved by the intervention
only to go on to suffer from cerebral palsy. This interpretation is
incompatible with the data. There were...
We appreciate Dr Pharoah's comments on the definitions of incidence
and prevalence.[1] However, his interpretation of the data appears
erroneous.[2]
Dr Pharoah suggests that perhaps the dexamethasone-treated infants
were sicker than the control infants and were saved by the intervention
only to go on to suffer from cerebral palsy. This interpretation is
incompatible with the data. There were no differences in the prenatal
characteristics, delivery type or severity of disease after birth between
the groups. There was no evidence to suggest that dexamethasone improves
survival as has been borne out by other studies.
In addition, Dr Pharoah points to the infant who had cerebral palsy
with normal ultrasound scans. The most likely explanation of these
findings is that ultrasound has inadequate sensitivity in order to detect
subtle fidings which may be picked up by other methods such as MRI.
Thus, our study does not address issues of prenatal timing of the
pathogenesis of cerebral palsy, but rather points to a serious and
potentially preventable postnatal cause.
References
(1) Pharoah POD. Dexamethasone treatment and cerebral palsy [Rapid Response]. http://adc.bmjjournals.com/cgi/eletters/fetalneonatal;83/3/F177#EL1 (8 November 2000)
(2) Shinwell ES, Karplus M, Reich D, et al. Early postnatal dexamethasone treatment and increased incidence of cerebral palsy. Arch Dis Child Fetal Neonatal Ed 2000;83:F177-81.
In view of the increasing interest in the special nutritional care of
nutritionally-compromised infants, we should like to identify an incorrect
description of our work on the subject. In their Current Topic article
on Feeding issues in preterm infants, Cooke and Embleton[1] cited our
randomised trial[2] showing faster linear growth and weight gain in post-discharged preterm infants assigned to a specially...
In view of the increasing interest in the special nutritional care of
nutritionally-compromised infants, we should like to identify an incorrect
description of our work on the subject. In their Current Topic article
on Feeding issues in preterm infants, Cooke and Embleton[1] cited our
randomised trial[2] showing faster linear growth and weight gain in post-discharged preterm infants assigned to a specially designed post-discharge
formula - the first of its type at the time. Cooke and Embleton state
that in our trial "no differences were detected in nutrient intake between
groups [making differences in growth difficult to explain]". Had this
been so, we agree our study would appear to disobey the laws of
thermodynamics.
However, it was volume intake, not nutrient intake that was the same
between those fed the nutrient enriched versus standard formulas.[2]
Clearly, if the two groups consumed formulas with different nutrient
concentrations and the volume intake did not differ between groups, then
the nutrient intake would be higher in the group that consumed the more
nutrient enriched formula - hence the better growth.
This has biological and practical implications. In previous attempts
to make growth -retarded infants grow, energy supplements were used, which
resulted in down-regulation of milk volume intake by the infant,[3]
counteracting the effect of the enriched diet on weight gain. When we
designed our post-discharge formula in the mid 1980s for our first trial,
we decided to use a predominantly protein-enriched rather than energy-
enriched formula since protein was arguably the most limiting major
nutrient for tissue growth (our formula was also enriched in minerals and
micronutrients to fuel the predicted increase in growth). Based on our
findings on the similar formula volume consumed by the protein-enriched
versus standard formula-fed groups, a key message of our study, perhaps
overlooked by Cooke and Embleton, is that protein, as opposed to energy,
does not appear to cause down-regulation of milk volume intake.[2] [4]
Thus, infants fed on protein-enriched formula grew well. This has
practical importance for the design of future post discharge formulas and
for any feeding regime aimed at producing catch-up growth in ad-libitum
fed infants.
We have now confirmed the validity of this principle in two
further large nutritional intervention trials involving around 600 infants
that show catch-up growth can be achieved, well beyond the period of
dietary intervention, in both post discharge preterm and full term small-
for-gestational age infants.[5] [6]
A Lucas
M Fewtrell
MRC Childhood Nutrition Research Centre
Institute of Child Health
30 Guilford Street, London, UK
cnrc@ich.ucl.ac.uk
References
(1) Cooke RJ, Embleton ND. Feeding issues in preterm infants. Arch Dis Child Fetal Neonatal Ed 2000;83:F215-17.
(2) Lucas A, Bishop NJ, Cole TJ. Randomised trial of nutrition for
preterm infants after discharge. Arch Dis Child 1992;67:324-7.
(3) Brooke OG, Kinsey JM. High energy feeding in small for gestation
infants. Arch Dis Child 1985;60:42-6.
(4) Lucas A, King FJ, Bishop NJ. Postdischarge formula consumption in
infants born preterm. Arch Dis Child 1992;67:691-2.
(5) Fewtrell MS, Morley R, Abbott RA, Stephenson T, MacFadyen UM, Lucas A. Randomised trial of high protein and energy formula versus standard
formula in growth retarded term infants [abstract]. Arch Dis Child 1999;80(Suppl I):A4.
(6) Lucas A, Fewtrell MS, Abbott RA, Stephenson T, MacFadyen UM, Morley R. Randomised trial of nutrient enriched formula versus standard formula
for post-dishcharge preterm infants [abstract]. Arch Dis Child 1999;80(Suppl I):A31.
In a recent article Stevenson and colleagues[1] report further data
showing increased vulnerability of male compared to female infants in
early life, and comment that the biological mechanisms contributing to the
male disadvantage or female advantage have not been elucidated.
In fact, male vulnerability in early life is consistent with an
aspect of evolutionary theory described by Trivers...
In a recent article Stevenson and colleagues[1] report further data
showing increased vulnerability of male compared to female infants in
early life, and comment that the biological mechanisms contributing to the
male disadvantage or female advantage have not been elucidated.
In fact, male vulnerability in early life is consistent with an
aspect of evolutionary theory described by Trivers and Willard in 1973.[2] Their theory addressed changes in the sex ratio at birth in relation
to the quality of the maternal environment during pregnancy. Further
elaboration of the theory allows post-natal morbidity and mortality to be
included within the same mechanism.[3] Relative to female infants, male
infants represent a better maternal "strategy" for maximising reproductive
success in a good environment, but a worse maternal "strategy" in a poor
environment. Evolution has therefore favoured enhanced male vulnerability
in poor environments as a means of maximising maternal lifetime
reproductive success.[2] [3]
Increased male mortality and morbidity have been reported throughout
the 20th century,[3] and are reflected in increased male rates of
hospitalisation and outpatient admission. The male disadvantage may
therefore be considered a natural aspect of human biology, although
differential medical care appears to overcome the deficit in societies
where male offspring are preferred to female offspring.[4] As medical
care improves, and more low birth weight and preterm infants initially
survive, excess male morbidity and subsequent mortality are predicted to
increase, as has already been observed in recent decades.[3]
Jonathan CK Wells
MRC Childhood Nutrition Research Centre
Institute of Child Health
30 Guilford Street
London WC1N 1EH
References
(1) Stevenson DK, Verter J, Faranoff AA, et al. Sex differences in
outcomes of very low birthweight infants: the newborn male disadvantage.
Arch Dis Fetal Neonatal Ed 2000;83:F182-5.
(2) Trivers RL, Willard DE. Natural selection of parental ability to
vary the sex ratio of offspring. Science 1973;179:90-2.
(3) Wells JCK. Natural selection and sex-differences in morbidity and
mortality in early life. J Theor Biol 2000;202:65-76.
(4) Xu B, Rantakallio P, Järvelin M-J, Fang XL. Sex differentials in
perinatal mortality in China and Finland. Soc Biol 1997;44:170-8.
The three excellent articles on twin to twin transfusion syndrome
(TTTS) provide futher important data for clinical decisions and parental
counselling. We would like to comment on the paper by Cincotta et al.[1]
We are interested in the incidence of hydrops and absence of end
diastolic velocity of the umbilical artery in the cohort and their
correlation with outcome. A recent study of 33 pregn...
The three excellent articles on twin to twin transfusion syndrome
(TTTS) provide futher important data for clinical decisions and parental
counselling. We would like to comment on the paper by Cincotta et al.[1]
We are interested in the incidence of hydrops and absence of end
diastolic velocity of the umbilical artery in the cohort and their
correlation with outcome. A recent study of 33 pregnancies with TTTS by
Mari et al[2] showed that the presence of hydrops of the recipient and
absence of the end-diastolic velocity of the umbilical artery in one of
the twins were associated with poor prognosis.
In contrast with the findings of Mari et al[2] the Brisbane group did
not find any significant difference in the mean weight between the donor
and recipient twins. We wondered whether this is due to efficacy of
obstetrics interventions, a less severe nature of the TTT or a shorter
duration between time of diagnosis and delivery. We believe that the data
should have included a comparison between the donor and recipient twins in
both short term and longer-term outcomes. Interestingly Mari et al found
3 of 28 recipient twins had periventricular leukomalacia compared with
none of the 23 donor live born twins although the difference was not
significant.
The authors should state how many of the babies in their cohort were
less than 27 weeks' gestation at birth as one study of 112 cases of TTTS
showed a drop in survival from 70% at 27 weeks to less than 25% at 26
weeks or earlier.[3]
We also note that 8 babies in the cohort had chronic lung disease.
The findings by Shinwell et al published in the same issue of the ADC
emphasised yet again the worrisome association between post natal steroids
with increased cerebral palsy[4]; it would therefore be useful to know
how many of the babies in the TTTS group had post natal steroids and
whether these babies were over represented in those with cerebral palsy.
It would also be interesting to know what percentage of the cohort
were IUGR. We believe that TTTS could provide an ideal situation to test
Barker’s hypothesis of in utero programming for morbidities during later
life.[5]
THHG Koh MA FRCPCH FRACP Senior Staff Specialist in Neonatal
Paediatrics
Collie L RN Neonatal Research Nurse
Budge D RN Neonatal Research Nurse
Regional NICU, Kirwan Hospital
Townsville, Great Barrier Reef Queensland 4817 Australia
fax 0747730320
References
(1) Cincotta RB, Gray PH, Phythian G, Rogers YM, Chan FY. Long term outcome of twin-twin transfusion syndrome. Arch Dis Child Fetal Neonatal Ed 2000;83:F171-6.
(2) Mari G, Detti L, Oz U, Abuhamad AZ. Long-term outcome in twin-twin transfusion syndrome treated with serial aggressive amnioreduction. Am J Obstet Gynecol 2000;183:211-17.
(3) Dickinson JE, Evans SF. Obstetric and perinatal outcomes from the
Australian and New Zealand Twin-Twin Syndrome Registry. Am J Obstet Gynecol 2000;182:706-12.
(4) Shinwell ES, Karplus M, Reich D, Weintraub Z, Blazer S, Bader D, Yurman S, Dolfin T, Kogan A, Dollberg S, Arbel E, Goldberg M, Gur I, Naor N, Sirota L, Mogilner S, Zaritsky A, Barak M, Gottfried. Early postnatal
dexamethasone treatment and increased incidence of cerebral palsy. Arch Dis Child Fetal Neonatal Ed 2000;83:F177-F81.
(5) Barker DJ. In utero programming of cardiovascular disease. Theriogenology. 2000;53:555-74.
Both the title of this paper and the first paragraph of the
discussion imply that the use of postnatal dexamethasone may lead to
cerebral palsy. However, it is the misuse of the term "incidence" that
gives rise to this interpretation. The authors did not, neither could
they, provide incidence data. What they presented was cerebral palsy
prevalence data.
Both the title of this paper and the first paragraph of the
discussion imply that the use of postnatal dexamethasone may lead to
cerebral palsy. However, it is the misuse of the term "incidence" that
gives rise to this interpretation. The authors did not, neither could
they, provide incidence data. What they presented was cerebral palsy
prevalence data.
If it is accepted that prevalence and not incidence data are
provided, then a very different interpretation of the findings can be
made. Supposing the cerebral impairment of cerebral palsy occurred
prepartum, then the use of dexamethasone may have allowed these children
to survive whereas, had they received the placebo, they would have died
before a diagnosis of cerebral palsy could be made. This would account for
the higher prevalence of cerebral palsy in the dexamethasone compared with
the placebo group. Support for this interpretation comes from the author's
statement:
Eleven (22%) of the 51 children with cerebral palsy had normal
neonatal ultrasound scans. All 11 of these infants were treated with
dexamethasone.
This suggests that the cerebral impairment was prenatal in
timing. Further support comes from the observation that there were fewer
IVH in the dexamethasone group, although the difference did not quite
attain the conventional level of statistical significance.
It needs to be appreciated that:
Prevalence = Incidence x Duration of disease.
The duration of the disease is affected by how long the child (or
fetus) survives. Unless it is known what happens to the fetus from the
time of conception, it is not possible to determine incidence in those
diseases that have their origin during uterine development.
We are grateful for the response to our article on the
neurodevelopment of infants with CLD. The comment as to the possible
contribution of ROP to deficient eye-hand coordination is supported by the
Swedish study published in British Journal of Ophthalmology (1991;75;527-31). The study clearly showed higher prevalence of ocular abnormalities in
children with a birth weight below 1000 g and gesta...
We are grateful for the response to our article on the
neurodevelopment of infants with CLD. The comment as to the possible
contribution of ROP to deficient eye-hand coordination is supported by the
Swedish study published in British Journal of Ophthalmology (1991;75;527-31). The study clearly showed higher prevalence of ocular abnormalities in
children with a birth weight below 1000 g and gestational age (GA) <_30 weeks.="weeks." we="we" were="were" aware="aware" of="of" this="this" during="during" the="the" preliminary="preliminary" analysis="analysis" our="our" data.="data." p="p"/>We checked the
prevalence of ROP in both groups of infants. Surprisingly, the over-all
prevalence of ROP was the same among infants with and without CLD.
Therefore we excluded ROP as a risk factor that could influence the
development in our study population.
We should have mentioned this in the Results
and/or the Discussion. Unfortunately none of the reviewers pointed at this
important fact and required clarification.
The letter prompted us to go further in the analysis and to see whether
there was any discrepancy in the grades of ROP between the groups. The
more thorough statistical analysis did not reveal any difference.
Below you will find our data.
ROP type
CLD (n=43)
Controls (n=43)
No ROP
13
13
ROP
30
30
ROP I
6
8
ROP II
12
15
ROP III + cryotherapy
12
7
The chi squared analysis that we used to test the possible differences
showed that:
1. The prevalence of ROP I and II was the same in both groups of infants (p=0.55)
2. The prevalence of ROP III did not differ between the groups (p=0.17).
Thus, on the basis of our results, we can rule out the ROP as a
contributing factor to the deterioration in eye-hand coordination in
infants with CLD.
Premedication for neonatal intubation has become a hot topic recently, and in their letter Attardi et al[1] make an interesting contribution to the debate. However the significant increase in oxyhaemaglobin desaturation in those neonates intubated following administration of midazolam when compared to placebo is not surprising.
Midazolam is a hypnotic agent and as such can only be useful as part of...
The authors of this paper need all appreciation in trying out this “magic cream” on babies, which already finds an established role in children as a topical anaesthetic.
However as one goes through this interesting article, a striking feature is the small numbers in the study. I find no mention as regards to the power of the study. The confidence limits while expressing significant p values is...
Nitric oxide (NO) is frequently used as a selective pulmonary vasodilator in neonates. Since its metabolite, methaemoglobin can potentially cause tissue hypoxia it is considered mandatory to measure methaemoglobin levels when using NO. In an attempt to review and rationalise our own practice of methaemoglobin measurement when using NO we undertook a search of current literature and conducted a postal surv...
Whitelaw and Thoresen recently reviewed the current evidence concerning the effects of antenatal steroids on brain development, and made suggestions for clinical practice.
We believe that interpretation of current evidence is not yet clear enough to determine clinical practice, and further research is necessary before such recommendations are possible. No randomised controlled trials comparing si...
We appreciate Dr Pharoah's comments on the definitions of incidence and prevalence.[1] However, his interpretation of the data appears erroneous.[2]
Dr Pharoah suggests that perhaps the dexamethasone-treated infants were sicker than the control infants and were saved by the intervention only to go on to suffer from cerebral palsy. This interpretation is incompatible with the data. There were...
In view of the increasing interest in the special nutritional care of nutritionally-compromised infants, we should like to identify an incorrect description of our work on the subject. In their Current Topic article on Feeding issues in preterm infants, Cooke and Embleton[1] cited our randomised trial[2] showing faster linear growth and weight gain in post-discharged preterm infants assigned to a specially...
Dear Editor,
In a recent article Stevenson and colleagues[1] report further data showing increased vulnerability of male compared to female infants in early life, and comment that the biological mechanisms contributing to the male disadvantage or female advantage have not been elucidated.
In fact, male vulnerability in early life is consistent with an aspect of evolutionary theory described by Trivers...
The three excellent articles on twin to twin transfusion syndrome (TTTS) provide futher important data for clinical decisions and parental counselling. We would like to comment on the paper by Cincotta et al.[1]
We are interested in the incidence of hydrops and absence of end diastolic velocity of the umbilical artery in the cohort and their correlation with outcome. A recent study of 33 pregn...
Both the title of this paper and the first paragraph of the discussion imply that the use of postnatal dexamethasone may lead to cerebral palsy. However, it is the misuse of the term "incidence" that gives rise to this interpretation. The authors did not, neither could they, provide incidence data. What they presented was cerebral palsy prevalence data.
If it is accepted that prevalence and no...
Dear Editor:
We are grateful for the response to our article on the neurodevelopment of infants with CLD. The comment as to the possible contribution of ROP to deficient eye-hand coordination is supported by the Swedish study published in British Journal of Ophthalmology (1991;75;527-31). The study clearly showed higher prevalence of ocular abnormalities in children with a birth weight below 1000 g and gesta...
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