Vallabhaneni et al. describe a preterm infant developing obstruction secondary to bezoar formation. This is a rare but important occurence. The relationship with gaviscon (an un-licensed and un-proven treatment for gastro-oesophageal reflux) has been previously reported in this journal and is an alternative explanation. Should this be reported using the yellow card system to the BNF?
Vallabhaneni et al. describe a preterm infant developing obstruction secondary to bezoar formation. This is a rare but important occurence. The relationship with gaviscon (an un-licensed and un-proven treatment for gastro-oesophageal reflux) has been previously reported in this journal and is an alternative explanation. Should this be reported using the yellow card system to the BNF?
Dr. Millar raises the point that an alternative broader-spectrum (and
more expensive) antibiotic combination could be considered for empirical
therapy of neonates with suspected early-onset sepsis in preference to
penicillin and gentamicin which (based on our data) he estimated to be
ineffective for 6% of cases.
We support Dr Millar's view on the importance of appropriate
empirical antibiotic treatment for septi...
Dr. Millar raises the point that an alternative broader-spectrum (and
more expensive) antibiotic combination could be considered for empirical
therapy of neonates with suspected early-onset sepsis in preference to
penicillin and gentamicin which (based on our data) he estimated to be
ineffective for 6% of cases.
We support Dr Millar's view on the importance of appropriate
empirical antibiotic treatment for septic neonates and the need to discuss
acceptable thresholds for antibiotic resistance. However, extrapolating
the number of neonates experiencing clinical failure of treatment and
subsequent adverse effects from the proportion of pathogens resistant to
the empiric antimicrobials used for treatment should be treated with
caution since in vitro resistance does not necessarily equate to treatment
failure in vivo. We were unable to address this important issue in our
published study due to the lack of clinical information and outcome data
in the laboratory surveillance data analysed. Our recommendation was based
on a value judgement where we weighed poorly quantified but serious risk
and costs of increased antibiotic resistance for future patients against a
potentially serious adverse effect of using less effective antibiotics in
a small number of patients.
Avoiding selection pressure, particularly for carbapenem resistance
in Gram-negative bacteria, should be paramount in Neonatal Intensive Care
Units. Furthermore, clinical experience suggests that although antibiotics
should be stopped by 48 hours when cultures are found to be negative, this
will not always be the case. Further research is needed to evaluate
outcomes for neonates receiving empirical antibiotic treatment in order to
define appropriate therapy and subsequently identify 'high risk' patients
for whom guidelines might need to be amended. The National Institute for
Health and Clinical Excellence (NICE) is currently reviewing the
management of neonatal infections and this could perhaps be one of the key
areas of future research.
Black women produce more testosterone than white women and, I
suggest, this is directly involved in problematic birth weights of
offspring which occur more often in black women. Additionally, I think
testosterone is increasing in women of different races and may account for
ongoing changes in birth weight of offspring as well as a group of other
negative pregnancy outcomes and problems in these offspring in later life....
Black women produce more testosterone than white women and, I
suggest, this is directly involved in problematic birth weights of
offspring which occur more often in black women. Additionally, I think
testosterone is increasing in women of different races and may account for
ongoing changes in birth weight of offspring as well as a group of other
negative pregnancy outcomes and problems in these offspring in later life.
A syndrome is occurring in America and other countries, the cause of
which is often attributed to one part or another of the syndrome and more
often attributed to the environment or life style. I suggest a single
cause may be involved that is biological and evidence of ongoing
evolution.
It is my hypothesis that the "secular trend," the increase in size and
earlier puberty occurring in children, is caused by an increase in the
percentage of individuals of higher testosterone. More specifically, I
suggest this is due to an increase in the percentage of mothers of higher
testosterone with time within the population. This exposes more fetuses to
increased maternal testosterone with time within the population. This
causes permanent effects in the fetus which persist throughout the life
span. I suggest this is the cause of the parallel increases in morbidity
occurring within the population, such as obesity, cancer, breast cancer,
diabetes, etc., including prematurity, small for gestational age, etc.,
including less obvious gross effects which later contribute to "failing
schools" and other adverse behavioral outcomes in children.
I have come to the conclusion that the "increase in testosterone" may
partially be due to a reduction in "sex hormone binding globulin (SHBG)"
as a number of phenomena explained by the secular trend may be based on
changes in SHBG. A decrease in SHBG increases free testosterone levels.
Low SHBG has been found in obese children who do not produce excessive
testosterone. A number of negative phenomena which may be caused by
increased testosterone are found with low SHBG and a number of positive
effects of reduced SHBG exist.
It is my hypothesis that human evolution is driven by increases in
testosterone ("Androgens in Human Evolution," Rivista di Biologia /
Biology Forum 2001; 94: 345-362). This was directly supported by research
in 2003; see the chart of testosterone levels in humans and related great
apes, upper left at www.anthropogeny.com . I suggest that periodically
testosterone increases excessively and the exposure to excessive maternal
testosterone causes negative and evolutionarily consequential changes to
the human population. We may be experiencing this effect at this time.
It is not true that the bronze baby syndrome "has never been
pictorially described" (1). The first description of the syndrome in 1972
(2), to which De Luca et al did not refer (1), was illustrated with
striking color photographs. Other color photographs of bronze babies have
been published since then (3-5).
The notion that the syndrome is caused by bilirubin-sensitized
phototransformation of Cu(II)-protoporphy...
It is not true that the bronze baby syndrome "has never been
pictorially described" (1). The first description of the syndrome in 1972
(2), to which De Luca et al did not refer (1), was illustrated with
striking color photographs. Other color photographs of bronze babies have
been published since then (3-5).
The notion that the syndrome is caused by bilirubin-sensitized
phototransformation of Cu(II)-protoporphyrin is also probably incorrect
(6).
References
1 De Luca D, Picone S, Fabiano A, Paolillo P, Images in neonatal
medicine. Bronze baby syndrome: pictorial description of a rare condition.
Arch Dis Child Fetal Neonatal Ed, 2010; 95(5):F325.
2 Kopelman AE, Odell GB, Brown RS, The "bronze" baby syndrome: A
complication of phototherapy. J Pediatrics, 1972; 81(3):466-72.
3 Onishi S, Bronze baby syndrome: and its allied diseases. Asian Med
J, 1978; 21(11):53-6.
4 Ashley JR, Littler CM, Burgdorf WH, Brann BS, Bronze baby syndrome.
Report of a case. J Am Acad Dermatol, 1985; 12(2 Pt 1):325-8.
5 Purcell SM, Wians FH, Ackerman NB, Davis BM, Hyperbiliverdinemia in
the bronze baby syndrome. J Am Acad Dermatol, 1987; 16(1 Pt 2):172-7.
6 McDonagh AF, Bilirubin, Copper-porphyrins, and the bronze-baby
syndrome. J Pediatrics, 2010; [Epub ahead of print]
doi:10.1016/j.jpeds.2010.08.014)
We are very grateful to Caroline for the very thoughtful and well-
timed review of evidence for the feeding practices in neonates. We agree
with the summary of this review.
It is true that feeding of the preterm neonate has undergone major change
since the beginning of the 20th century [1]. However, we remain far off
from having evidence-based protocols for feeding the preterm or very low
birth weight infant. The main que...
We are very grateful to Caroline for the very thoughtful and well-
timed review of evidence for the feeding practices in neonates. We agree
with the summary of this review.
It is true that feeding of the preterm neonate has undergone major change
since the beginning of the 20th century [1]. However, we remain far off
from having evidence-based protocols for feeding the preterm or very low
birth weight infant. The main questions being the timing of initiating
feeds especially how quickly to increase this, for fear of precipitating
necrotising enterocolitis [1].
While it is widely accepted that risk factors for necrotising
enterocolitis include intra-uterine growth retardation, abnormal antenatal
umbilical dopplers and formula feeding [2], the evidence for necrotising
enterocolitis and exact practices regarding the timing and progression of
enteral feeds is somewhat based on observational studies [2]. Moreover, in
establishing feeding guidelines for the preterm infant, one has to
consider not only the risks of necrotising enterocolitis, but also the
potential benefits of gut maturation provided by early feeding and the
potential risks of sepsis and metabolic disturbances associated with
prolonged parenteral feeding [3].
Neonatal units tend to have very varied protocols and practice for
feeding preterm infants. At our unit, a level 2 neonatal unit with 3500
deliveries (Becomes level 3 in 2011) we use an adaptation of the Yorkshire
Neonatal Network feeding protocol. This protocol defines six feeding
groups that are assigned to infants depending on their gestation, weight
and the presence of risk factors like intrauterine growth retardation or
abnormal antenatal umbilical dopplers. A quick survey in our neonatal unit
shows that most clinical staff appreciate the advantage the protocol
offers of being well defined in terms of when to start and how quickly to
advance feeds. However, some feel that the protocol over-generalises and
would like to see clear categorisation of infants between very low birth
weight and extremely low birth weight infants as its lack, results in
feeds being unnecessarily delayed in some babies. This over-generalisation
probably reflects the lack of evidence in this area.
In this paper we also reviewed the present randomised control trial
evidence over feeding practices for the preterm neonate, more specifically
the evidence behind the use of trophic feeds over enteral fasting, the
evidence behind delaying the progression of enteral feeds beyond trophic
amounts, and also the evidence behind the rate of advancement of feeds
advocated for preterm infants.
There is evidence that enteral feeds can cause better adaptation of
gastro-intestinal motility [4] and gastrointestinal hormone production [5]
and it has been postulated that this can lead to better feed tolerance,
less time taken to reach full feeds and better growth in preterm infants.
However, it is more important to find out whether this translates into any
clinical benefits for the preterm infant.
Trophic feeds, also called minimal enteral feeds or hypocaloric feeds
which generally involves giving 12-24 mls/kg/day of feeds in small volumes
and starts within the first few days of life and continuing until days 7-
10 without increasing the amounts.
Several papers have tried to research the clinical implications of
trophic feeds. While some have shown beneficial effects on
hyperbilirubinaemia and osteopenia of prematurity [6], most have shown
little change in feed tolerance and growth parameters. Indeed a Cochrane
review on trophic feeds [7] shows no statistically significant difference
in feed tolerance or necrotising enterocolitis between starting trophic
feeds and enteral starving for the first week or so of life in preterm
infants.
Although this does not provide any evidence of any beneficial effects
of trophic feeds clinically, it does not show trophic feeds to be harmful.
However, the authors warn against jumping to conclusions in view of the
flaws of the studies included, such as a lack of blinding. On the other
hand, they do point out that blinding would be difficult and the lack of
blinding would have theoretically caused an increased reporting of feed
intolerance and necrotising enterocolitis by default.
When we look at the issue of delaying the advancement of feeds beyond
"trophic amounts", the main evidence for this comes from observational
studies as the evidence from randomised control trials is limited [8].
Cochrane review [8] looks at randomised control trials comparing earlier
and later progression of enteral feeds, starting days 1-4 as opposed to
days 4-10 respectively. They found a limited number of trials on the
subject. None of the trials showed a statistically significant difference
in risks of necrotising enterocolitis and mortality, nor in feed tolerance
and growth parameters. Although this seems to suggest that early
advancement of feeds as safe, none of the studies were sufficiently
powered and conclusions reached should be interpreted with care. None of
the studies looked at the risks of parenteral feeding as an outcome, which
is an important part of the balance of risk that needs to be considered in
these scenarios.
A meta-analysis [3] of three studies has also looked at the evidence
behind the rate of advancement of enteral feeds. None of the studies
involved showed any significant difference between the rates of
necrotising enterocolitis in groups where feeds were advanced at a rate of
15-20 mls/kg/day as opposed to a rate of 30-35 mls/kg/day. At the same
time, all the studies showed that the groups where feeds were advanced
more rapidly established full enteral feeds and regained their birth
weights quicker.
While this seems to show that rapid progression of feeds do not
increase the risks of necrotising enterocolitis, it is to be noted that in
these studies, as in most of the other randomised control trials looking
at other aspects of feeding mentioned above, high risk infants are either
not included or no subgroup analysis provided. The evidence can therefore
not be generalised to infants of extreme prematurity, extreme low birth
weight, small for gestational age or infants with abnormal antenatal
umbilical dopplers. These are all recognised risk factors for necrotising
enterocolitis. However, there is a lack of studies on such infants looking
at the optimum timing of initiation or progression of feeds for them.
While the Yorkshire Neonatal Network feeding guideline for preterm
infants is clear-cut with its suggestions, the compilation still relies on
limited evidence. More evidence is now required especially looking at
specific questions of when and how quickly to feed preterm infants
enterally and specific groups like the extremely low birth weight infant
or infant with intra-uterine growth retardation need to be looked at
separately in order to develop a better feeding protocol for these
infants. Such trials need to be sufficiently powered and need to also to
consider possible adverse effects of parenteral feeding in the questions
asked.
References:
1. Greer FR, Feeding the premature infant in the 20th century,
Journal of Nutrition, 2001; 131: 426S-430S
2. McGuire W, Bombell S, Slow advancement of enteral feed volumes to
prevent necrotising enterocolitis in very low birth weight infants,
Cochrane Database of Systematic Reviews, 2008, Issue 2. Art. No.:
CD001241. DOI: 10.1002/14651858.CD001241.pub2.
3. Williams AF, Early enteral feeding of the preterm infant, Arch Dis
Child Fetal Neonatal Ed, 2000; 83: F219-F220
4. Berseth CL, Neonatal small intestinal motility: motor responses to
feeding in term and preterm infants, Journal of Paediatrics, 1990; Nov:
117(5):777-82.
5. Lucas A, Bloom SR, Aynsley-Green A, Gut hormones and "minimal enteral
feeding", Acta Paediatrica, Sept 1986; 75:5; 719-723
6. Beneficial effects of early hypocaloric enteral feeding on neonatal
gastrointesting function: Preliminary report of a randomized trial,
Journal of Pediatrics; April 1988; 112: 4; 622-629
7. Bombell S, McGuire W. Early trophic feeding for very low birth weight
infants. Cochrane Database of Systematic Reviews 2009, Issue 3. Art. No.:
CD000504. DOI: 10.1002/14651858.CD000504.pub3.
8. Bombell S, McGuire W. Delayed introduction of progressive enteral feeds
to prevent necrotising enterocolitis in very low birth weight infants.
Cochrane Database of Systematic Reviews 2008, Issue 2. Art. No.: CD001970.
DOI: 10.1002/14651858.CD001970.pub2.
Ponnusamy et al report on the availability of cooling equipment
within UK neonatal units in 2009 (1). They conclude that only 28% of all
units and 78% of level 3 units possess such equipment despite evidence
supporting therapeutic hypothermia. Whilst we agree with the authors in
supporting universal access to cooling for asphyxiated infants, the lack
of local availability of equipment need not equate to a lack of access...
Ponnusamy et al report on the availability of cooling equipment
within UK neonatal units in 2009 (1). They conclude that only 28% of all
units and 78% of level 3 units possess such equipment despite evidence
supporting therapeutic hypothermia. Whilst we agree with the authors in
supporting universal access to cooling for asphyxiated infants, the lack
of local availability of equipment need not equate to a lack of access to
therapeutic hypothermia.
From March 2009 the Scottish Cooling Group has cooperated to provide
therapeutic hypothermia within Scotland, supporting neonatal units whether
they choose to deliver cooling or not. Some level 3 units who anticipate
small numbers of asphyxiated infants have rightly had concern about
maintenance of expertise and have chosen to transfer out eligible infants.
Within Scotland there is now national provision of therapeutic
hypothermia delivered by six out of ten level 3 units and achieved through
cooperation, sharing of experience and outreach education. All non-cooling
units have clear referral criteria and guidance to undertake passive
cooling with strict temperature monitoring and the support of a cooling
centre whilst awaiting retrieval. The national transport service has
collaborated on the production of comprehensive cooling guidelines and is
able to initiate cooling at the referring centre and continue on transport
using servocontrol cooling systems.
We support the collection of national data but suggest that further
surveys should not focus solely on local availability of equipment but
should also investigate accessibility of hypothermia for asphyxiated
infants.
1. Ponnusamy V, Nath P, Bissett L, Willis K, Clarke P. Current
availability of cerebral function monitoring and hypothermia therapy in UK
neonatal units. Arch. Dis. Child. Fetal Neonatal Ed. 2010 95:F383-F384
Preer and Philipp have drawn attention to inadequate breastfeeding
and neonatal jaundice but omitted to mention the most important factor in
breastfeeding success: the let-down reflex.1
In addition to prolactin, oxytocin (the hormone associated with the
reflex) stimulates milk production: numerous oxytocin receptors on the
milk secreting cells of the breast alveoli mediate a massive release of
casein (milk protein) into...
Preer and Philipp have drawn attention to inadequate breastfeeding
and neonatal jaundice but omitted to mention the most important factor in
breastfeeding success: the let-down reflex.1
In addition to prolactin, oxytocin (the hormone associated with the
reflex) stimulates milk production: numerous oxytocin receptors on the
milk secreting cells of the breast alveoli mediate a massive release of
casein (milk protein) into the lumen of the alveoli.2 The let-down reflex
(via oxytocin) then transfers milk to the infant: in between the positive
pressure waves of the reflex milk flows back towards the breast alveoli,
away from the infant.3
Frequent feeding in the early postpartum period is associated with lower
bilirubin levels whilst jaundiced infants may be lethargic and feed
poorly.4 Good positioning and latching and relying on infant demand may,
of themselves, not be sufficient to ensure frequent feeding, good milk
production and transfer.
Mothers need to know how to institute a beneficial feeding pattern to
optimise the milk intake of their infant and avoid 'not enough breast
milk' jaundice.
References
1 Prier GL, Philipp BL. Understanding and managing breast milk jaundice.
Arch Dis Child Fetal Neonatal Ed August 5 2010 doi:10.1136/adc2010.184416
2 Lollivier V, Marnet PG, Delpal S, Rainteau D, Achard C, Rabot A et al.
Oxytocin stimulates secretory processes in lactating rabbit mammary
epithelial cells. J Physiol. 2006;570 (Pt 1):125-40.
3 Ramsay DT, Kent JC, Owens RA, Hartman PE. Ultrasound imaging of milk
ejection in the breast of lactating women. Pediatrics 2004; 113; 361-367
4 de Carvalho M, Klaus MH, Merkatz RB. Frequency of breast-feeding and
serum bilirubin concentration. Am J Dis Child 1982 Aug 136(8):737-8
I read this paper with interest and would like to comment on some of
the results and conclusions reached.
The authors have studied changes in regional cerebral saturation
(RSO2) using near infrared spectroscopy and used these to calculate
fractional tissue oxygen extraction (FTOE) in babies felt to require blood
transfusion and have made measurements before and after transfusion. They
describ...
I read this paper with interest and would like to comment on some of
the results and conclusions reached.
The authors have studied changes in regional cerebral saturation
(RSO2) using near infrared spectroscopy and used these to calculate
fractional tissue oxygen extraction (FTOE) in babies felt to require blood
transfusion and have made measurements before and after transfusion. They
describe that if the haemoglobin concentration (Hb) is low and the
cerebral FTOE is high before transfusion the FTOE tends to improve
afterwards leading them to conclude that cerebral oxygenation may be at
risk when the Hb is below 6g/dl. The authors used a restrictive
transfusion guideline and most of the babies studied therefore had quite
low haemoglobin concentrations. However I do not think that these
conclusions are completely supported by their data.
When transfusions are given the FTOE tends to decrease in all three
groups whether the Hb is low or higher. This result is surprising but is
consistent with the data from our study which was similar in design,
although slightly different methodology was used (1). Notably the babies
in our study had higher haemoglobin concentrations and yet still
demonstrated decreases in FTOE after transfusion (1).
FTOE represents the balance between oxygen delivery and consumption.
A decrease in FTOE implies either that oxygen delivery has increased or
oxygen consumption has fallen (or both). When giving a blood transfusion
one would expect consumption to remain constant unless other changes such
as changes in temperature or activity level have occurred. Cerebral
oxygen delivery is dependent on main three factors: the Hb, cerebral blood
flow (CBF) and the arterial oxygen saturation (SaO2). SaO2 should remain
constant within the monitored limits. Hb will obviously increase following
a transfusion. One might expect cerebral blood flow to decrease in
proportion to the increase in Hb so that delivery also remained constant,
a notion which is supported by clinical and animal studies (2-4). If this
occurred then FTOE should remain constant after transfusion. The decrease
in FTOE therefore implies that delivery increases with transfusion. CBF
may not therefore decrease as much as expected as a result of a
transfusion.
This result could suggest, as I think the authors imply, that
cerebral oxygen consumption is delivery dependent in these babies - in
other words the brain is dependent on the level of oxygen delivery and is
extracting oxygen at its maximum such that when oxygen delivery is
increased by transfusion FTOE decreases. This seems very unlikely in
clinical well babies. Changes in FTOE may therefore be more complex and a
decrease in FTOE after an intervention may not necessarily imply that
delivery was compromised before the intervention.
One factor which may be important could be the HbF fraction. Giving
a blood transfusion with adult red cells will increase the proportion of
HbA in most preterm babies. HbA has a lower affinity for oxygen and this
will therefore increase the availability of oxygen to the cells even
though delivery does not change and this may explain why FTOE decreases.
HbF was not measured in this study. Although we measured it in our study
(1) no correlation with FTOE was demonstrated but this may have been
because of other confounding factors and a larger sample with a wider
range of values might be more likely to demonstrate a relationship. There
is a relationship between HbF and FTOE measured in peripheral tissues (the
forearm) (5).
This question could be answered by measuring cerebral FTOE in two
groups of babies one with significant proportions of HbF and one group
with no HbF to see if there was a change in cerebral FTOE after
transfusion.
The authors seem to suggest that they expect a particular level of Hb
which would be associated with important changes in cerebral oxygenation.
In fact they suggest that 6g/dl is this value however this is not
supported by their data. A particular cut-off is also unlikely for
several reasons: preterm babies have varying abilities to compensate
depending on their cardio-respiratory status, they will have varying
amounts of HbF which might influence oxygen availability to the tissues
and finally the Hb does not accurately reflect the red cell volume (6).
For all of these reasons, as one observes clinically, anaemia may become
clinically important at different levels of Hb in different babies.
A better marker of significant anaemia is required and measurements
of tissue oxygenation either cerebral or peripheral made using NIRS may be
useful for this although the ideal measurement which best indicates at an
early enough stage when anaemia is starting to compromise tissue
oxygenation is not yet clear and more studies are required.
One factor which is missing is knowledge of what is 'abnormal'. How
high does the value of FTOE need to be to represent impaired cerebral
oxygenation? Although reference ranges are available in well infants it is
not clear when increases in cerebral FTOE are significant. What is
required is data which demonstrates whether some values of FTOE are
associated important clinical changes or morbidity so that changes or
values which are truly clinically important can be recognised. This sort
of data will clearly require much larger studies.
References
1. Wardle SP, Yoxall CW, Weindling AM. Cerebral Fractional Oxygen
Extraction Using Near Infrared Spectroscopy During Hypotension and Anaemia
in Preterm Infants. Journal of Cerebral Blood Flow and Metabolism
2000;20(2):272-279
2. Brown MM, Marshall J. Regulation of cerebral blood flow in response
to changes in blood viscosity. Lancet 1985; i:604-609.
3. Ramaekers VT, Casaer P, Marchal G, et al. The effect of blood
transfusion on cerebral blood-flow in preterm infants: a Doppler study.
Dev.Med.Child Neurol. 1988;30:334-341.
4. Younkin 1981) Younkin DP, Reivich M, Obrist WD, et al. Physiologic
responses of neonatal rCBF. J Cereb Blood Flow Metab 1981;1:S273-S274.
5. Peripheral Oxygenation and Anaemia in Preterm Babies. SP Wardle, CW
Yoxall, E Crawley, AM Weindling. Pediatric Research 1998;44(1):125-131
6. Hudson I, Cooke A, Holland B, Houston A, Jones JG, Turner T, Wardrop
CA 1990 Red cell volume and cardiac output in anaemic preterm infants.
Arch Dis Child 65:672-5
Sir,
The authors have rightly made a retrospective diagnosis of benign tonic
gaze in the three infants described. However, no mention is made of
whether or not tests for hypoglycemia and hypocalcemia were done at the
time of occurance as subtle seizures not picked up on later EEG may
present in this way and should be ruled out immedietely.
Sir,
The authors have rightly made a retrospective diagnosis of benign tonic
gaze in the three infants described. However, no mention is made of
whether or not tests for hypoglycemia and hypocalcemia were done at the
time of occurance as subtle seizures not picked up on later EEG may
present in this way and should be ruled out immedietely.
Dr. Mactier has done an excellent service by writing this article and
bringing this issue to the fore front. It is indeed a huge public health
problem and we do need many more studies to understand better treatment
for long term outcomes for children of opiate dependent mothers. However,
until such treatments and alternatives to methadone/buprenorphine are
available, we need to keep treating these women with
methadone/bu...
Dr. Mactier has done an excellent service by writing this article and
bringing this issue to the fore front. It is indeed a huge public health
problem and we do need many more studies to understand better treatment
for long term outcomes for children of opiate dependent mothers. However,
until such treatments and alternatives to methadone/buprenorphine are
available, we need to keep treating these women with
methadone/buprenorphine. Leaving them in the street and allowing them to
use heroin is not only a disservice to these patients but also to future
generation. People working in the field of addiction are not arguing that
methadone/buprenorphine is the best alternative but they are better than
using the heroin during pregnancy as use of heroin brings other lifestyle
issues and dangers to the pregnant mother as well as the fetus. NAS is an
important issue with respect to newborns, but proper management of NAS can
far minimize the adverse consequences. It is true that there are trans-
atlantic differences in attitude with regards to this population but this
is true in lot of other areas of health care. Having a comprehensive
system of primary care, UK can do better job of providing the adequate
care to these pregnant women. The essential thing is that we need to keep
an eye on the future generation. If these women are entered into a long
term comprehensive program with a support structure that is not only good
for their recovery but also provides a better future to these children,
the outcome will be drastically different. As the author has indicated,
the poor suffer from ongoing social deprivation. Right at the time of
their first encounter with the health care system, pregnant women can be
entered into a training/job/recovery program which will provide them
future support and lead to a better environment for growing children.
Lastly, since this article is focussed on pharmacotherapy, we do not need
to discuss much about behavior therapy/modification but one thing that has
proven extremely useful for this population is CM (contingency management)
and we should look to exploit the good effects of this very important tool
The key is to keep an eye on the future generation in spite of maternal
drug use.
Reference
(1) Sorbie AL, Symon DN,...
Dr. Millar raises the point that an alternative broader-spectrum (and more expensive) antibiotic combination could be considered for empirical therapy of neonates with suspected early-onset sepsis in preference to penicillin and gentamicin which (based on our data) he estimated to be ineffective for 6% of cases.
We support Dr Millar's view on the importance of appropriate empirical antibiotic treatment for septi...
Black women produce more testosterone than white women and, I suggest, this is directly involved in problematic birth weights of offspring which occur more often in black women. Additionally, I think testosterone is increasing in women of different races and may account for ongoing changes in birth weight of offspring as well as a group of other negative pregnancy outcomes and problems in these offspring in later life....
It is not true that the bronze baby syndrome "has never been pictorially described" (1). The first description of the syndrome in 1972 (2), to which De Luca et al did not refer (1), was illustrated with striking color photographs. Other color photographs of bronze babies have been published since then (3-5).
The notion that the syndrome is caused by bilirubin-sensitized phototransformation of Cu(II)-protoporphy...
We are very grateful to Caroline for the very thoughtful and well- timed review of evidence for the feeding practices in neonates. We agree with the summary of this review. It is true that feeding of the preterm neonate has undergone major change since the beginning of the 20th century [1]. However, we remain far off from having evidence-based protocols for feeding the preterm or very low birth weight infant. The main que...
Ponnusamy et al report on the availability of cooling equipment within UK neonatal units in 2009 (1). They conclude that only 28% of all units and 78% of level 3 units possess such equipment despite evidence supporting therapeutic hypothermia. Whilst we agree with the authors in supporting universal access to cooling for asphyxiated infants, the lack of local availability of equipment need not equate to a lack of access...
Preer and Philipp have drawn attention to inadequate breastfeeding and neonatal jaundice but omitted to mention the most important factor in breastfeeding success: the let-down reflex.1 In addition to prolactin, oxytocin (the hormone associated with the reflex) stimulates milk production: numerous oxytocin receptors on the milk secreting cells of the breast alveoli mediate a massive release of casein (milk protein) into...
Dear Sir,
I read this paper with interest and would like to comment on some of the results and conclusions reached.
The authors have studied changes in regional cerebral saturation (RSO2) using near infrared spectroscopy and used these to calculate fractional tissue oxygen extraction (FTOE) in babies felt to require blood transfusion and have made measurements before and after transfusion. They describ...
Sir, The authors have rightly made a retrospective diagnosis of benign tonic gaze in the three infants described. However, no mention is made of whether or not tests for hypoglycemia and hypocalcemia were done at the time of occurance as subtle seizures not picked up on later EEG may present in this way and should be ruled out immedietely.
Conflict of Interest:
None declared...
Dr. Mactier has done an excellent service by writing this article and bringing this issue to the fore front. It is indeed a huge public health problem and we do need many more studies to understand better treatment for long term outcomes for children of opiate dependent mothers. However, until such treatments and alternatives to methadone/buprenorphine are available, we need to keep treating these women with methadone/bu...
Pages