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.
A recent advance in premedicating infants requiring intubation has
gained wide acceptance for humanitarian and physiological reasons.[1] The
use of muscle relaxation to facilitate intubation is quite separate from
sedation providing analgesia, amnesia and lack of awareness.
Practice is variable with little evidence-based guidance to suitable
drugs. Clinical Governance dictates continuing a...
A recent advance in premedicating infants requiring intubation has
gained wide acceptance for humanitarian and physiological reasons.[1] The
use of muscle relaxation to facilitate intubation is quite separate from
sedation providing analgesia, amnesia and lack of awareness.
Practice is variable with little evidence-based guidance to suitable
drugs. Clinical Governance dictates continuing audit of any such practice
supported with written guidelines. We advocate a minimum monitoring policy
(Saturation, Pulse, Non-Invasive Blood Pressure and Respiratory rate) and
the presence of at least two skilled operators, one of which should be an
experienced specialist registrar or consultant, when using neuromuscular blockade. This
exercise is reserved for elective intubations and tube changes but not for
use in resuscitation on the labour suite.
Recent reports to the CSM (Committee for the Safety of Medicines) via the UK Yellow Card Scheme of mortality
associated with premedication using atracurium (dose 500 mcg/kg) and
diamorphine (dose 50 mcg/kg) in three premature infants (24, 26 and 26 weeks' gestation) have attributed the problem mainly to using atracurium,
which we consider debatable (Nicholas Rutter, Nottingham; Personal Communication). In addition, neuromuscular blockade should
be unnecessary in pre-term infants.
Diamorphine is a prodrug that is metabolised to active 6-0-acetylmorphine and then to morphine. It has faster CNS penetration than
morphine due to increased lipid solubility but its side effects are
similar. Bradycardia of vagal origin (in combination with laryngoscopy)
and decreased sympathetic response can cause a fall in cardiac output.
Both morphine and atracurium cause histamine release that can precipitate
bronchospasm and a fall in systemic vascular resistance (SVR).
Atracurium is a non-depolarising muscle relaxant that is slow onset
and long acting. It provides intubating conditions within 90 seconds (dose
300-600 mcg/kg) and has a recovery index of 16 minutes (adult data).
Premature infants have a small functional residual capacity (FRC)
particularly when paralysed. A rapid fall in alveolar oxygen in an already
under-ventilated infant may lead to pulmonary hypertension and increase
V/Q mismatch. Consequently, mask ventilation or tube placement becomes
necessary before the 90 seconds, which may not be long enough to reach
therapeutic levels. Patients receiving a long acting muscle relaxant that
cannot be ventilated for whatever reason will not start any independent
respiratory effort for at least 16 minutes!
Our guidelines propose using fentanyl (dose 2 mcg/kg), which does not
cause histamine release, so there is no bronchospasm. Cardiac output,
systemic vascular resistance, pulmonary vascular resistance, and pulmonary
artery occlusion pressure are preserved. High doses (10-15 mcg/kg) can lead
to vagal bradycardias or chest wall rigidity. Where a muscle relaxant is
indicated, we suggest suxamethonium (dose 1 mg/kg) which is to be preceded
with atropine.
References
(1) Whyte S, Birrell G, Wyllie J. Premedication before intubation in UK neonatal units. Arch Dis Child Fetal Neonatal Ed 2000;82:F38-F41.
In their review on reducing the burden of neonatal sepsis[1] Modi and Carr discuss at length the role of colony stimulating
factors (CSFs) in neonatal sepsis.
The evidence thus far does not show either a reduction in incidence
or mortality from neonatal sepsis when this modality is used albeit
possibly in a small group of small for gestational age babies or babies
who develop neutropenia s...
In their review on reducing the burden of neonatal sepsis[1] Modi and Carr discuss at length the role of colony stimulating
factors (CSFs) in neonatal sepsis.
The evidence thus far does not show either a reduction in incidence
or mortality from neonatal sepsis when this modality is used albeit
possibly in a small group of small for gestational age babies or babies
who develop neutropenia secondary to pregnancy induced hypertension in the
mother.
I was surprised that in a "Current Topic" the authors
failed to mention one of the most exciting development in the management
of neonatal sepsis since their earlier review of CSFs three years ago.[2]
Pentoxifylline a carbonic anhydrase inhibitor is known to "exert numerous
potential beneficial effects in human and animal models of sepsis".[3]
Lauterbach and colleagues[4] have shown that pentoxifylline
significantly affects the synthesis of tumour necrosis factor (TNF) and (interleukin) IL-6 as well as reducing
mortality in neonatal sepsis (mortality 1/40 versus 6/38 p=0.046).
While anti-TNF strategies have been associated with increases in adverse outcome, it is likely that pentoxifylline, like intravenous
immunoglobulin (IVIG), attenuates rather than eliminates TNF enhanced
bacterial clearance and provides anti-inflammatory effect and improves
outcome.
It is therefore much more likely that pentoxifylline either alone or
in conjunction with IVIG would be the combination to study, particularly
in the light of Bialek and Bartman's,[5] work who have shown that any
benefits of either CSF or IVIG therapy cannot be attributed to an
immediate increase in and direct effect on neutrophil phagocytic activity.
With the above in mind we are participating in the International Neonatal Immunotherapy Study funded by the MRC and are
initiating a large pentoxifylline study in Pakistan.
Dr K N Haque
Epsom & St Helier NHS Trust St Helier
Hospital Wrythe Lane Carshalton, Surrey SM1 5AA, UK
References
(1) Modi N, Carr R. Promising stratagems for reducing the burden of neonatal sepsis. Arch Dis Child Fetal Neonatal Ed 2000;83:F150-3.
(2) Carr R, Modi N. Haemopoietic colony stimulating factors for preterm neonates. Arch Dis Child Fetal Neonatal Ed 1997;76:F128-F33.
(3) Zimmerman JJ. Appraising the potential of pentoxifylline in septic preemies. Crit Care Med 1999;27:695-6.
(4) Lauterbach R, Pawlik D, Kowalczyk D, et al. Effect of immunomodulating agent, pentoxifylline, in
the treatment of sepsis in prematurely delivered infants: A placebo-controlled double-blind trial. Crit Care Med 1999;27:807-14.
(5) Bialek R, Bartman P. Is there an effect of immunoglobulins and G-CSF on neutrophil phagocytic activity in preterm infant? Infection 1998;26:375-8.
Katz-Salamon et al[1] make the important point that children with
chronic lung disease (CLD) need careful neurodevelopmental follow up
irrespective of whether or not they suffered from intraventricular
haemmorhage or periventricular leucomalacia.
Visual dysfunction due to retinopathy of prematurity (ROP) could
contribute to defects in control of hand and eye coordination.
Katz-Salamon et al[1] make the important point that children with
chronic lung disease (CLD) need careful neurodevelopmental follow up
irrespective of whether or not they suffered from intraventricular
haemmorhage or periventricular leucomalacia.
Visual dysfunction due to retinopathy of prematurity (ROP) could
contribute to defects in control of hand and eye coordination.
It would be interesting to know if they found a greater incidence of
ROP in the preterm infants with CLD as compared to the control group.
Reference
(1) Katz-Salamon M, Gerner E M, Jonsson B, Lagercrantz H. Early motor and mental development in very preterm infants with chronic lung disease. Arch Dis Child Fetal Neonatal Ed 2000;83:F1-6.
Beardsall et al are to be congratulated on presenting further evidence
that group B streptococcus (GBS) gives rise to a significant burden of
disease in some areas of the United Kingdom.[1] Retrospective data collected
at St George’s is in agreement with the authors’ suggestion that culture
proven sepsis under-represents the true burden of disease.
Beardsall et al are to be congratulated on presenting further evidence
that group B streptococcus (GBS) gives rise to a significant burden of
disease in some areas of the United Kingdom.[1] Retrospective data collected
at St George’s is in agreement with the authors’ suggestion that culture
proven sepsis under-represents the true burden of disease.
Firstly we conducted a retrospective search for cases of culture-
positive GBS (either blood or cerebrospinal fluid) among a cohort of
consecutive births at St George’s between 1/1/94 and 31/10/98, comprising 16,910 births.
Secondly we conducted a retrospective analysis of all babies
colonised with GBS (deep ear swabs taken in the first 6 hours of life
which were positive for GBS), and who were screened and treated for
suspected early onset infection in the first 72 hours of life, during the
period 01/04/97 to 31/03/98. Probable early onset GBS (EOGBS) infection
was defined as: a positive deep ear swab in a baby with clinical pneumonia
or sepsis (either fever >38oC on one occasion or >37.5oC on 2 occasions separated by at least one hour
or 2 or more of: poor
perfusion, respiratory distress, thrombocytopenia, leucopenia <_5 x="x" _10sup="_10sup"/>9/l,
persisting glucose imbalance or abdominal distension, bilious aspirates or
blood in stool) in a baby <_72 hours="hours" of="of" age.="age." p="p"/> Twelve of 16,910 babies had blood cultures positive for GBS, and GBS
was cultured from cerebrospinal fluid of one baby whose blood culture was
negative. This gives an infection rate of 0.77/1000.
Of 3438 deliveries from 01/04/97 to 31/03/98, there were 9 babies
with probable GBS infection, giving an incidence of 2.6/1000.
Because of the usual problems related to retrospective data analysis
this figure is likely to still under-represent the true burden of disease.
We are currently prospectively evaluating the incidence of probable as
well as proven GBS infection in order to estimate the true burden of
disease in our local population. It is only in the light of such data that
we will be able to develop evidence-based guidelines for the prevention
and management of this disease.
AR Bedford Russell
Aodhan Breathnach*
Paul Sender
Neonatal Unit and Medical Microbiology & PHLS Collaborating Centre*
St George’s Hospital
Blackshaw Road, London SW17 OQT, UK
(1) Beardsall K, Thompson MH, Mulla RJ. Neonatal group B streptococcal
infection in South Bedfordshire 1993-1998. Arch Dis Child Fetal Neonatal
Ed 2000;82:F205-7.
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...
Dear Editor:
A recent advance in premedicating infants requiring intubation has gained wide acceptance for humanitarian and physiological reasons.[1] The use of muscle relaxation to facilitate intubation is quite separate from sedation providing analgesia, amnesia and lack of awareness.
Practice is variable with little evidence-based guidance to suitable drugs. Clinical Governance dictates continuing a...
Dear Editor:
In their review on reducing the burden of neonatal sepsis[1] Modi and Carr discuss at length the role of colony stimulating factors (CSFs) in neonatal sepsis.
The evidence thus far does not show either a reduction in incidence or mortality from neonatal sepsis when this modality is used albeit possibly in a small group of small for gestational age babies or babies who develop neutropenia s...
Katz-Salamon et al[1] make the important point that children with chronic lung disease (CLD) need careful neurodevelopmental follow up irrespective of whether or not they suffered from intraventricular haemmorhage or periventricular leucomalacia.
Visual dysfunction due to retinopathy of prematurity (ROP) could contribute to defects in control of hand and eye coordination.
It would be in...
Dear Editor:
Beardsall et al are to be congratulated on presenting further evidence that group B streptococcus (GBS) gives rise to a significant burden of disease in some areas of the United Kingdom.[1] Retrospective data collected at St George’s is in agreement with the authors’ suggestion that culture proven sepsis under-represents the true burden of disease.
Firstly we conducted a retrospective search...
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