Reports of microbial contamination of expressed unpasturised
breast milk (EBM)[1-3] are not new but the paper from Olver et al[4]
again highlights that this routine aspect of neonatal care has the
potential to provide a source for bacterial infection in immature
neonates.
Culture or pasturisation of a mother's own non-banked milk is
not however routine practice in neonatal units in the UK and may even b...
Reports of microbial contamination of expressed unpasturised
breast milk (EBM)[1-3] are not new but the paper from Olver et al[4]
again highlights that this routine aspect of neonatal care has the
potential to provide a source for bacterial infection in immature
neonates.
Culture or pasturisation of a mother's own non-banked milk is
not however routine practice in neonatal units in the UK and may even be
considered as "breastfeeding unfriendly" if associated processing delays
result in breast milk substitutes being administered to babies.
Unfortunately there is an absence of controlled trials examining what
constitutes significant contamination and addressing the appropriateness
or otherwise of bacteriological screening of unbanked EBM to assist units
in formulating an informed approach.
Our neonatal unit's policy of
culturing expressed milk prior to feeding it to sick preterm infants,
reflecting concern raised through case reports, has been controversial
particularly among midwifery staff and is currently under review. Olver et al's
triplets[4] have been timely for us in this regard and we are interested
to learn of other units' policies and practice.
Dr J McAloon
Dr J G Jenkins
NICU, Antrim Hospital
45 Bush Road
Antrim BT41 2LL, UK
References
(1) Davidson DC, Poll RA, Roberts C. Bacteriological monitoring of
untreated human milk. Arch Dis Child 1979;54:760-4.
(2) Eidelman IA, Szilagyi G. Patterns of bacterial colonization of human
milk. Obstet Gynecol 1979;53:550-2.
(3) Ng PC, Lewindon PJ, Siu YK, Wong W, Cheung KL, Liu K. Bacterial
contaminated breast milk and necrotizing enterocolitis in preterm twins.
J Hosp Infect 1995;31:105-10.
(4) Olver WJ, Bond DW, Boswell TC, Watkin SL. Neonatal group B streptoccal
disease associated with infected breast milk. Arch Dis Child Fetal
Neonatal Ed 2000;83:F48-9.
I refer to a comment made by Stalker[1] concerning the report by Slack
& Schapira[2] of severe apneas and bradycardia following DTP and Hib
vaccination in premature infants. No one would disagree that this
association deserves to be fully investigated as soon as possible. Yet
Stalker has said tha...
I refer to a comment made by Stalker[1] concerning the report by Slack
& Schapira[2] of severe apneas and bradycardia following DTP and Hib
vaccination in premature infants. No one would disagree that this
association deserves to be fully investigated as soon as possible. Yet
Stalker has said that it is neither ethical nor practical for this
association to be tested by randomised placebo controlled trials. However,
could not these trials be performed in a suitable animal model (eg, piglets or infant monkeys)?
Prospective cohort studies would be another practical option for
investigating this link. Temporary delay of vaccination until a goal
weight (eg, at least 2500g) has been achieved, would allow for a sizable
number of premature babies to be placed in the unvaccinated control group.
Vaccines could also be given separately, spaced apart by at least a few
days, in order to observe the effects of individual vaccines (eg, DTPa,
hepatitis B, Hib, IPV) on apnea/bradycardia, as has been done by Pourcyrous et
al.[3]
Will parents be told that up to 30% of premature infants may develop
abnormal cardiorespiratory responses such as apnea, bradycardia and oxygen
desaturation following vaccination?[3] And will they also be told that the
risk of severe life threatening reactions requiring resuscitation may be
as high as 8% in very low birth weight premature infants?[2] Parents deserve
to be fully informed about these risks. Those who have made a fully
informed decision to withhold vaccination would allow for their baby to be
included in a control group. This should be considered as an ethical
option.
Premature infants are well known to be at a greater risk of dying
from SIDS. Furthermore, studies that have performed cardiorespiratory
monitoring in infants subsequently dying from SIDS, have documented
bradycardia and apnea as important features that often occurred shortly
prior to death.[4, 5] Therefore the report by Slack & Schapira[2] again
raises the concern that vaccines may be a cause of SIDS.
The question needs to be raised: Has the routine practice of
vaccination of premature infants, with no adjustment for gestational age
or weight, contributed to an increased risk of SIDS in this group? I
believe that Slack & Schapira have indeed been wise in proposing that
vaccination may need to be delayed in premature infants.
Heidi White
Hospital Pharmacist
Lyell McEwin Health Service
Adelaide, South Australia
References
(1) Stalker DJ. Apnoea following immunisation in premature infants [letter]. Arch Dis Child Fetal Neonatal Ed 2000;83:F74.
(2) Slack MH, Schapira D. Severe apnoeas following immunisation in premature infants. Arch Dis Child Fetal Neonatal Ed 1999;81:F67-8.
(3) Pourcyrous M, Korones SB, Crouse D, Bada HS. Interleukin-6, C-reactive protein, and abnormal cardiorespiratory responses to immunization in
premature infants. Pediatrics 1998;101:e3 [http://www.pediatrics.org/cgi/content/full/101/3/e3]
(4) Meny RG, Carroll JL, Carbone MT, Kelly DH. Cardiorespiratory recordings
from infants dying suddenly and unexpectantly at home. Pediatrics 1994;93:44-9.
(5) Poets CF, Meny RG, Chobanian MR, Bonofiglo RE. Gasping and other
cardiorespiratory patterns during sudden infant deaths. Pediatr Res 1999;45:350-4.
We read with interest the paper by Olver et al[1]
describing triplets with group B streptococcal (GBS) infections acquired
from breast milk. We have recently seen a case of GBS meningitis in a 34
week gestation infant and suspect that the source of infection was the
maternal breast milk.
At delivery there were no risk factors for sepsis. In particular, the
baby was delivered by elective Caes...
We read with interest the paper by Olver et al[1]
describing triplets with group B streptococcal (GBS) infections acquired
from breast milk. We have recently seen a case of GBS meningitis in a 34
week gestation infant and suspect that the source of infection was the
maternal breast milk.
At delivery there were no risk factors for sepsis. In particular, the
baby was delivered by elective Caesarian section for growth retardation,
without any prior rupture of membranes. No organisms were grown from
routine admission blood culture and surface swabs. During the first week
of life, our infant remained asymptomatic. The white cell count and C
reactive protein levels remained within the normal range. On day 7, a full
septic screen was performed for recurrent bradycardias. The white cell
count was 3.9 x 109/l (neutrophils 0.3 x 109/l) and the C reactive
protein was less than 7mg/l. GBS (serotype III) was isolated from both the
blood and CSF cultures. The C reactive protein started to rise after
twelve hours, and reached a peak of 353mg/l. As the source of the
infection was not clear, a sample of maternal breast milk was cultured and
the same serotype of GBS was isolated. There was no clinical evidence of
mastitis.
Following the development of meningitis, cranial ultrasonography
demonstrated periventricular vasculitis and increased echogenicity of the
caudothalamic nucleus. No haemorrhagic lesions or structural abnormalities
were detected either before or after the onset of this illness. On day 12
our infant became polyuric with dilute urine (osmolarity 70mOsm/kg) in the
face of a high serum osmolarity (314mOsm/kg). A diagnosis of diabetes
insipidus was therefore made and treatment with ddAVP was commenced.
Subsequent investigations revealed evidence of hypopituitarism requiring
replacement therapy. Cortisol was undetectable. Free thyroxine was low
with a TSH level of 3.52mIU/l.
We agree that GBS transmission in breast milk may have been
underestimated as a cause of late-onset sepsis and agree that breast milk
should be screened in all such cases. Larger studies would be required to
determine the true incidence of the problem. This case also underlines the
need to actively look for the known-but-uncommon complications following
neonatal meningitis such as diabetes insipidus and hypopituitarism.[2]
Anjum Deorukhkar
Robin Miralles
Jessop Hospital for Women
Sheffield, South Yorkshire, UK
References
(1) Olver WJ, Bond DW, Boswell TC, Watkin SL. Neonatal group B
streptococcal disease associated with infected breast milk. Arch Dis Child
Fetal Neonatal Ed 2000;83:F48-9.
(2) Cohen C, Rice EN, Thomas DE, Carpenter TO. Diabetes insipidus as a
hallmark neuroendocrine complication of neonatal meningitis. Current
Opinion in Pediatrics 1998;10:449-52.
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.
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.
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.
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.
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.
We read the article by Kumar et al[1] with interest especially in light
of the changing profiles of NICU practices as applicable to a developing
nation with limited resources and lack of uniform parameters for
antibiotic usage, resulting in the emergence of drug resistant strains.
However, the utility of a rapid diagnostic system has to be viewed in the
light of its universal applicability. The cost of s...
We read the article by Kumar et al[1] with interest especially in light
of the changing profiles of NICU practices as applicable to a developing
nation with limited resources and lack of uniform parameters for
antibiotic usage, resulting in the emergence of drug resistant strains.
However, the utility of a rapid diagnostic system has to be viewed in the
light of its universal applicability. The cost of setup and subsequent
maintenance of a rapid culture system like BacT/Alert needs to be looked
into vis a vis the traditional culture methodologies, which still are high
yield relative to their low cost and results are available within 48-72
hours. Appearance of a growth itself can be taken as a decision tool for
continuation of antibiotics pending the subculturing process in an
appropriate clinical scenario. Automation has its advantages but need for
calibration and standardization should not be ignored. Possibilities of
false positive signals do remain and in a scenario of frequent power
failures the performance of such a system may be far from ideal and can
lead to potentially disastrous decisions.
Authors emphasise that the clinical status of the neonate still
remains the most important factor in deciding the management of neonatal
sepsis and therefore, a symptomatic neonate will continue to get
antibiotics even in the absence of laboratory support, for a duration, if
the clinical condition so demands. In asymptomatic neonates, there is need
to have more clear guidelines about the duration of therapy once the
antibiotics were started initially, may be based upon either
symptomatology or high perinatal risk scores. In this study, the authors
have not spelt out the clinical or laboratory criteria utilized after
negative blood culture results at 36 hours, so as to consider presence or
absence of sepsis and to justify continuation or discontinuation of
antibiotics beyond 36 hours, awaiting the final culture report at 72
hours. It will be pertinent for the practice that between 36 and 72 hours
period, the decisions about antibiotic therapy should not be based on
negative culture test at 36 hours alone but must additionally utilize the
rapid diagnostic tests (RDT), like use of IL-6 and C-reactive protein or
TNF alpha. These RDTs have good cumulative accuracies for the diagnosis
and exclusion of sepsis. [2,3] RDTs negativity after 36 hours, in culture
negatives will give additional strength to decision of stopping of
antibiotics. If these RDTs remain positive at 36 hours in culture
negatives, then it will be justified to continue antibiotics till the
final blood culture report becomes available at 72 hours and decision
about antibiotic continuation taken accordingly. Therefore, it will be
interesting to have information from the current study, on clinical
condition and RDTs status of neonates, after obtaining 36 hours report of
culture till 72 hours of life and final decisions about use of
antibiotics. A rapid diagnostic blood culture system is likely to be most
relevant in a clinical scenario of high perinatal sepsis risk score
dictating use of antibiotics [4], asymptomatic neonate and with early
negative RDT. An early negative blood culture result at 36 hours then
could be the gold standard proof for absence of sepsis and mandating
discontinuation of antibiotics in this subset of neonates.
Lastly the study in its retrospective design has limitations of
applicability. There appears to be a bias towards LBW/prematures in the
study, as data regarding term/AGA babies is not available in this study.
The definitive pathogens in term babies are likely to be different and
there may not be predominance of coagulase negative staphylococcus in
them.
References:
(1) Kumar Y, Qunibi M, Neal TJ, Yoxall CW Time to positivity of neonatal
blood cultures. Arch Dis Child Fetal Neonatal Ed 2001 Nov;85(3):F182-6
(2) Ng PC, Cheng SH, Chui KM, Fok TF, Wong MY, Wong W, Wong RP, Cheung
KL.Diagnosis of late onset neonatal sepsis with cytokines, adhesion
molecule, and C-reactive protein in preterm very low birthweight infants.
Arch Dis Child Fetal Neonatal Ed 1997 Nov;77(3):F221-7)
(3) Philip AG, Mills PC Use of C-reactive protein in minimizing antibiotic
exposure: experience with infants initially admitted to a well-baby
nursery. Pediatrics 2000 Jul;106(1):E4
(4) Singh M, Narang A, Bhakoo ON Predictive perinatal score in the
diagnosis of neonatal sepsis J Trop Pediatr 1994 Dec;40(6):365-8
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.
Reports of microbial contamination of expressed unpasturised breast milk (EBM)[1-3] are not new but the paper from Olver et al[4] again highlights that this routine aspect of neonatal care has the potential to provide a source for bacterial infection in immature neonates.
Culture or pasturisation of a mother's own non-banked milk is not however routine practice in neonatal units in the UK and may even b...
Dear Editor:
I refer to a comment made by Stalker[1] concerning the report by Slack & Schapira[2] of severe apneas and bradycardia following DTP and Hib vaccination in premature infants. No one would disagree that this association deserves to be fully investigated as soon as possible. Yet Stalker has said tha...
Dear Editor:
We read with interest the paper by Olver et al[1] describing triplets with group B streptococcal (GBS) infections acquired from breast milk. We have recently seen a case of GBS meningitis in a 34 week gestation infant and suspect that the source of infection was the maternal breast milk.
At delivery there were no risk factors for sepsis. In particular, the baby was delivered by elective Caes...
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...
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:
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...
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:
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
We read the article by Kumar et al[1] with interest especially in light of the changing profiles of NICU practices as applicable to a developing nation with limited resources and lack of uniform parameters for antibiotic usage, resulting in the emergence of drug resistant strains. However, the utility of a rapid diagnostic system has to be viewed in the light of its universal applicability. The cost of s...
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...
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