This letter is in response to “Accuracy and Precision of Test
Weighing to Assess Milk Intake in Newborn Infants: 2006;91;F 330-332 (1),
in which the investigators conclude that test-weighing is too imprecise
for routine clinical use. This conclusion is contrary to a series of very
well-controlled studies on test-weighing in term and premature infants.
Our concerns with the conclusions of this study ar...
This letter is in response to “Accuracy and Precision of Test
Weighing to Assess Milk Intake in Newborn Infants: 2006;91;F 330-332 (1),
in which the investigators conclude that test-weighing is too imprecise
for routine clinical use. This conclusion is contrary to a series of very
well-controlled studies on test-weighing in term and premature infants.
Our concerns with the conclusions of this study are as follows.
First, the investigators’ use of the term “precision” is incorrect.
The precision of a measure (also known as its reliability) is the ability
of a measurement to be reproduced consistently; precision refers to the
repeatability of a measurement. To obtain a measure of precision, the
object of interest must be measured more than once under the same
circumstances. An assessment of the precision of test-weighing would
entail obtaining repeated measurements of the infants’ weights and/or the
milk volume before and after feedings such as performed in previous
studies of the reliability of test-weighing (2). However, these
investigators did not perform repeated infant or milk weights, so they did
not measure precision. Thus, their claim that test weights are imprecise
is incorrect. Similarly, the investigators’ conclusion that their data
demonstrate the accuracy of test-weighing is incorrect. Instead, their
data reveal large and clinically important differences between the actual
volume consumed and the volume estimated by test-weighing in many of the
cases. Thus, the test-weighing procedure, as reported in their
investigation, did not yield accurate results.
The large measurement error reported in this study is inconsistent
with the results of previously published research and is likely due the
lack of research control in this study. The lack of control is evident in
several aspects of the procedure, including the administration of infant
feedings, infant weighing procedures, evaluation of the volume of milk
consumed and the choice of an infant scale. In previous studies on this
topic, infants’ clothing and equipment have been standardized and
controlled, and the clinicians are well-prepared for their role in the
procedures. Previously published research has also demonstrated that the
reliability (precision) of infant weighing procedures is significantly
affected by the presence of equipment such as IVs and oxygen nasal
cannulae (3), so the management of that equipment during the test weighing
procedure requires careful control. Additionally, in previous studies,
infants were removed from analysis when regurgitation or spitting up
resulted in milk being spilled outside the clothing that was a part of the
pre- and post-weights. Obviously, when actual milk consumed is not
measured as a part of the test-weight, the estimate will be inaccurate.
Additionally, the scale used to obtain the test weights was not adequately
described. Although the investigators tested the repeatability of weights
obtained on the scales using 1500 and 4000 g weights, they did not report
whether the scale had the capability to accurately measure small weights –
such as oral intakes as small as 1-2 g. The scales used in previous
studies were specifically designed to detect these small differences in
weight. Finally, the practice of using syringes to measure milk volume
rather than weighing the milk before and after feeding is puzzling. All of
these factors may have contributed to the error in the test-weight
estimates in the current study.
Finally, there are incorrect statements in this research report. The
authors suggest that previous investigators have not adequately quantified
the precision and accuracy of test-weighing, and have reported only
correlation coefficients to describe the accuracy of test weights. This is
simply incorrect; our studies of test-weighing include numerous statistics
appropriate for quantifying the magnitude of error in physical measures
such as weight (4). The statistics reported in those studies included the
mean differences, standard deviation of the net differences, mean absolute
differences, maximal differences, percentage of differences exceeding 5
g, and the overall percentage of error in the measurement, calculated as
(((|actual-estimated values|) / actual value)*100) (5; 6). The
investigators also incorrectly assert that “differences of up to 30 ml”
have been reported by all previous studies. This is also incorrect; in our
1990 publication addressing the accuracy of test-weights for premature
infants (5), the maximum difference between the actual and estimated
values for the electronic scale was 10 ml, and only 6.25% of the
differences exceeded 5 ml.
In summary, test-weighing, when performed with standard research
controls and electronic scales that weigh to the nearest 1 to 2 g, has
been demonstrated to be accurate in well-controlled clinical trials and
has been endorsed by the World Health Organization as a method of
accurately estimating intake. The lower accuracy in measures reported by
these investigators underscore the need to carefully select a scale and
control for the procedures used for test-weighing in the clinical setting
to the extent possible, but do not indicate that test-weighing is too
inaccurate for clinical use.
Paula P. Meier, DNSC, RN
Janet L. Engstrom, PhD, RNC, CNM
Rush University Medical Center
Chicago Illinois United States
References:
1. Savenije OEM, Brand PLP. Accuracy and precision of test weighing
to assess milk intake in newborn infants. Arch Dis Child Fetal Neonatal Ed
2006; 91 (5): F330-332.
2. Kavanaugh K, Engstrom JL, Meier PP, Lysakowski TY. How reliable
are scales for weighing preterm infants. Neonatal Network 1990;9(3): 29-
32.
3. Engstrom JL, Kavanugh K, Meier PP, Boles E, Hernandez J, Wheeler
D, Chuffo R. Reliability of in-bed weighing procedures for critically ill
infants. Neonatal Network 1995;14(5):27-33.
4. Engstrom JL. Assessment of the reliability of physical measures.
Research in Nursing and Health 1988;11:383-389.
5. Meier PP, Lysakowski, TY, Engstrom JL, Kavanaugh KL, Mangurten H.
The accuracy of test weighing for preterm infants. Journal of Pediatric
Gastroenterology and Nutrition 1990;10:62-5.
6. Meier, PP, Engstrom JL, Crichton CL, Clark DR, Williams MM,
Mangurten HH. A new scale for in-home test-weighing for mothers of preterm
and high risk infants. Journal of Human Lactation 1994;10:163-8.
Persistent patent ductus arteriosus (PDA) is a common pathology in
the preterm whose traditional treatment has been indomethacin. Recently,
ibuprofen has shown its effectiveness in closing the PDA with less
hemodynamic effects.
I read different various studies on Ibuprofen versus indomethacin in
the treatment of PDA with great interest. Despite this common occurrence,
opinion about the u...
Persistent patent ductus arteriosus (PDA) is a common pathology in
the preterm whose traditional treatment has been indomethacin. Recently,
ibuprofen has shown its effectiveness in closing the PDA with less
hemodynamic effects.
I read different various studies on Ibuprofen versus indomethacin in
the treatment of PDA with great interest. Despite this common occurrence,
opinion about the use of interventions to promote closure of a PDA is
controversial (1). There are no universal guidelines. There is no clear
benefit of one therapy or intervention over other. However, now with more
and more studies evidence is accumulating.
Su et al (2) clearly demonstrated from their study that Ibuprofen is
as effective as indomethacin for the early-targeted PDA treatment in
extremely premature infants, without increasing the incidence of
complications. These results are similar to the metaanalysis from 11
studies by Gimeno Navarro et al (3) where they found that ibuprofen was as
effective as indomethacin in closing PDA. There was no significant
differences were found in the incidence of complications except for less
renal impairment with ibuprofen.
Some studies have raised concerns regarding the incidence of raised
bronchopulmonary dysplasia (BPD) in patients treated with ibuprofen as
compared to indomethacin. However, most of the studies have shown lower
incidence of oliguria (renal complications) in patients treated with
ibuprofen as compared to indomethacin.
In my experience from working in the different neonatal units I have
found ibuprofen equally effective to indomethacin. We have tried to treat
patients with indomethacin if they are few days old and in that case
indomethacin also prevents the intraventricular haemorrhage. If a patient
with haemodynamically significant PDA has been about 2 weeks old or had
other recent medications with renal side effects then ibuprofen may prove
safer.
Now evidence is accumulating that if PDA is not haemodynamically
significant then it may be best to leave untreated. Because of the lack of
evidence of benefit from treatments for closure, and recent data that
suggest that both medical (4) and surgical (5) treatments for the PDA are
associated with poor outcomes, an increasing number of clinicians rarely
treat PDAs, unless haemodynamically significant.
References:
1. Laughon MM, Simmons MA, Bose CL. Patency of the ductus arteriosus
in the premature infant: is it pathologic? Should it be treated? Curr Opin
Pediatr 2004; 16:146–51.
2. Su BH, Lin HC, Chiu HY, Hsieh HY, Chen HH, Tsai YC. Comparison of
ibuprofen and indomethacin for early-targeted treatment of patent ductus
arteriosus in extremely premature infants: a randomised controlled trial.
Archives of Disease in Childhood - Fetal and Neonatal Edition 2008;93:F94-
F99.
3. Gimeno Navarro A, Modesto Alapont V, Morcillo Sopena F, Fernández
Gilino C, Izquierdo Macián I, Gutiérrez Laso A. Ibuprofen versus
indomethacin in the preterm persistent patent ductus arteriosus therapy:
review and meta-analysis. An Pediatr (Barc) 2007; 67(4):309-18.
4. Schmidt B, Roberts RS, Fanaroff A, et al. Indomethacin
prophylaxis, patent ductus arteriosus, and the risk of bronchopulmonary
dysplasia: further analyses from the Trial of Indomethacin Prophylaxis in
Preterms (TIPP). J Pediatr 2006; 148: 730–4.
5. Kabra NS, Schmidt B, Roberts RS, et al. Neurosensory impairment
after surgical closure of patent ductus arteriosus in extremely low birth
weight infants: results from the Trial of Indomethacin Prophylaxis in
Preterms. J Pediatr 2007; 150: 129–34.
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
In response to the subject, i wish to pen down my recent experience
of normal growth of twins till 6 months on exclusive breast feeding.
A pair of male twins were born to at term to a 2nd gravida mother by
normal vaginal route, the birth weight was 3.2kg and 3.0kg. The mother was
motivated and advised breast feeding in delivery room and subsequently in
postnatal ward. The parents belonged to lower socico...
In response to the subject, i wish to pen down my recent experience
of normal growth of twins till 6 months on exclusive breast feeding.
A pair of male twins were born to at term to a 2nd gravida mother by
normal vaginal route, the birth weight was 3.2kg and 3.0kg. The mother was
motivated and advised breast feeding in delivery room and subsequently in
postnatal ward. The parents belonged to lower socicoeconomic status.
the babies were followed up after discharge every fortnight for 2 months
and later every month till 6 months age. they were exclusively breast fed,
and weighed 7.6 and 7.3 kg at 6 months. The only advise given to mother
was nutrion advise and eating for three(mother and twins).She was advised
and motivated for benefits of breast feeding.The mother had some extra
calories about 6 kg of fats with suji and nuts(panjeeree) which is
commonly given to lactating mothers in northern India.
I feel breast feeding of twins is possible if the health personnel give 5
min advise tomother in delivery room and followed up by same person
subsequently.
It is not unusual that health personnel shift feeding to other milks
rather than giving ear to her problems and nutrition advise. although all
mothers may not produce as much milk as this mother , but most can hanve
enoughmilk for abot 4 months with some supplemntary feeds by katori or
spoon; my advise is" eat more of all food items from family pot".
Herrman et al demonstrated that patent ductus arteriosus (PDA) closes
spontaneously in most of the cases of a select group of very low birth
weight infants. We did a similar retrospective observational study, at
North Trent Regional Intensive Care Unit (Jessop Wing) in Sheffield, in
infants diagnosed with PDA on echocardiogram, done for the murmur on
routine baby check examination or for other clini...
Herrman et al demonstrated that patent ductus arteriosus (PDA) closes
spontaneously in most of the cases of a select group of very low birth
weight infants. We did a similar retrospective observational study, at
North Trent Regional Intensive Care Unit (Jessop Wing) in Sheffield, in
infants diagnosed with PDA on echocardiogram, done for the murmur on
routine baby check examination or for other clinical indication as per our
unit policy.
184 cardiac echocardiograms were done between Sept 2007 and Sept 2008
by the consultant radiologists. Mean age of echocardiograms was 2.3 days
(Range from 0-17 days). 83 cases were found to have PDA with or without
persistent foramen ovale (PFO), without any other significant pathology.
42 Cases had only PDA while 41 had both PDA and PFO. PDA was categorised
into three categories: small (< 2mm), moderate (2-4mm) and large (>
4mm).
Out of 83 cases, 60 had small PDA, moderate PDA in 21 cases while 2
cases had large PDA. All the infants were followed up in the neonatal
follow up clinic by the consultant neonatologists with special interest
in cardiology. PDA was assigned as closed either by the repeat
echocardiogram in the clinic or in presence of entirely normal cardiac
examination. No infant went into cardiac failure and none of them required
bacterial endocarditis prophylaxis.
In agreement to Hermann et al, our data showed that PDA spontaneously
closed in all cases except 2 cases. One case had congenital rubella and
this infant needed duct ligation surgically. While second case is being
followed up for small PDA but with a strong family history of duct
ligation. In the second very interesting case significant number of the
family members had duct ligation.
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.
Thank you for your response to our research "Non-invasive
measurements of ductus arteriosus flow directly after birth".
We agree with Dr. Hutchon that a caesarian section can influence the
respiratory transition of a newborn infant. As such, our results reflect
the transition after elective caesarian section with cord clamping within
1 minute after birth, which...
Thank you for your response to our research "Non-invasive
measurements of ductus arteriosus flow directly after birth".
We agree with Dr. Hutchon that a caesarian section can influence the
respiratory transition of a newborn infant. As such, our results reflect
the transition after elective caesarian section with cord clamping within
1 minute after birth, which we have indicated is a limitation of our study
as stated in the Discussion section of our manuscript. However, as cord
clamping was delayed between 30-60 s after birth, most newborns will have
commenced breathing before the cord was clamped. While many guidelines
suggest a fixed time interval of 1-3 minutes between birth and cord
clamping, this is not physiological and is only relevant to individual
infants because most infants will have commenced breathing within this
time. We agree that infants that did not started breathing sufficiently
before cord clamping could have had a less efficient transition, but our
small sample size prohibits a more detailed subgroup analysis. However, as
all of these infants had a normal "clinical" transition and did not
require respiratory support or any other specialized medical care, we feel
that the potential influence of cord clamping before the start of
breathing had no significant clinical impact. With regard to the WHO
advice, the observations from Bhatt et al. show that the timing of cord
clamping is probably less important than the occurrence of breathing
before the cord is clamped.(1)
It would be interesting to compare the transition of neonates after
vaginal delivery to our results. However, no data within the first 10
minutes after vaginal delivery is present as our report is the first to
assess hemodynamic changes during this time frame. This study may
therefore be regarded as a starting point for future research on
hemodynamic changes directly after birth.
As we have described in a previous publication, aeration of the lung
and the consequent rise in preload is most likely responsible for the
increase in left ventricular output (LVO).(2) The increase in preload will
cause a pressure gradient to exist over the Ductus Arteriosus (DA) and
foramen ovale (FO). As Dr. Hutchon suggests the resulting shunt over the
FO could explain differences between LVO and right ventricular output
(RVO). However, we must stress that the simple mathematical calculation of
adding or subtracting mean blood flows and outputs from a group of
infants, which were measured using echocardiography at different time
points is not a legitimate way of making comparisons. The values stated in
our manuscript are mean values and although they were all measured within
a small time range, it is not possible to make these measurements
simultaneously. As these parameters are very dynamic and change over time,
ideally they should be measured simultaneously and comparisons should be
made in individual infants rather between groups means. Furthermore,
Doppler derived measurements of absolute volume are based on several
assumptions and cardiac output can range from 150 ml/kg/min to 273
ml/kg/min for LVO and from 200 to 310 ml/kg/min for RVO in term neonates
depending on the site of measurement, the vascular diameter and Doppler
method used.(3) As such we believe that the calculation of shunting across
the FO as done by Dr. Hutchon is based on too many assumptions for any
valid conclusions to be drawn. We consider that our figures are neither an
anomaly nor a sign of a disrupted transitional circulation, but merely
reflect the suboptimal assessment of absolute volumes with
echocardiography.
This is the main reason that we did not focus on the absolute
differences between LVO and RVO at the described time points. Instead we
used the Doppler derived measurements to assess differences over time
during the first 10 minutes after birth in LVO, RVO and blood flow shunt
over the DA. Furthermore, we calculated the ratio between DA right-to-left
vs. left-to-right flow based on the velocity time integral of the flow
patterns. As this is a dimensionless parameter that is not influenced by
assumptions or inaccuracies in the measurement of vessel diameter, it is
more appropriate to use for investigations into the hemodynamic
transition.
The matter of whether left-to-right shunting across the FO is a
normal physiological process is an interesting point and one that hasn't
really been addressed previously, mostly because it was previously
considered to be a one way valve. Nevertheless, as the two ventricles act
as two independent pumps working at different outputs throughout fetal
life, we consider that it is unrealistic to expect that the ventricles
will immediately synchronize their outputs at birth. Instead we believe
that there will be a period of adjustment during the immediate newborn
period and theoretically bidirectional flows in both the FO and the DA
would allow both ventricular outputs to come into balance without
triggering systemic hypotension or pulmonary hypertension.
References
(1) Bhatt S, Alison BJ, Wallace EM, Crossley KJ, Gill AW, Kluckow M,
et al. Delaying cord clamping until ventilation onset improves
cardiovascular function at birth in preterm lambs. J Physiol 2013;591:2113
-26.
(2) van Vonderen JJ, Roest AA, Siew ML, Blom NA, van Lith JM, Walther
FJ, et al. Noninvasive measurements of hemodynamic transition directly
after birth. Pediatr Res 2014;75:448-52.
(3) de Waal KA. The methodology of Doppler-derived central blood flow
measurements in newborn infants. Int J Pediatr 2012;2012:680162.
In this study it was reported that, the "frequency of apnoea in the
30 seconds after GER (GER-triggered apnoeas) was greater than that
detected in the 30 seconds before (p = 0.01). ..A strong correlation
between total number of apnoeas and the difference between apnoeas
detected 30 seconds after and before GER was found (p = 0.034)"(1).
These data are consistent with both apnoea and GER being caused by an
enrgy...
In this study it was reported that, the "frequency of apnoea in the
30 seconds after GER (GER-triggered apnoeas) was greater than that
detected in the 30 seconds before (p = 0.01). ..A strong correlation
between total number of apnoeas and the difference between apnoeas
detected 30 seconds after and before GER was found (p = 0.034)"(1).
These data are consistent with both apnoea and GER being caused by an
enrgy deficit. The presence of an energy deficit in adults, identified
from the presence of a gastric intramucosal acidosis, is predictive of
weaning failure (2).
1. L Corvaglia, D Zama, S Gualdi, M Ferlini, A Aceti, and G Faldella
Gastro-oesophageal reflux increases the number of apnoeas in very preterm
infants
Arch. Dis. Child. Fetal Neonatal Ed. 2009; 94: F188-F192
2. Mohsenifar; Angela Hay; Jeffrey Hay; Michael I. Lewis; and Spencer
K. Koerner. Gastric Intramural pH as a Predictor of Success or Failure in
Weaning Patients from Mechanical Ventilation Annals of Internal Medicine.
Gastric Intramural pH as a Predictor of Success or Failure in Weaning
Patients from Mechanical Ventilation
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 read with interest the case report of Dharmaraj et al. published
in your journal (1). The authors described a full term infant born by an
emergency caesarean section. At birth this newborn had a depressed skull
fracture on the right parietal bone. Neurosurgical elevation of the
fracture was performed at age of 2 weeks after birth. In the discussion
the authors mentioned that reduction by vacuum...
We read with interest the case report of Dharmaraj et al. published
in your journal (1). The authors described a full term infant born by an
emergency caesarean section. At birth this newborn had a depressed skull
fracture on the right parietal bone. Neurosurgical elevation of the
fracture was performed at age of 2 weeks after birth. In the discussion
the authors mentioned that reduction by vacuum extraction (obstetric
vacuum or breast milk extractor) has been described as a possibility of
treatment. In our paper (2) we distinguished two types of congenital
depression of the neonatal skull: deformed skull depression (deformation
without fracture) and fractured skull depression (fracture accompanied by
depression). Clinically it is impossible to differentiate between these
two entities. We used a non-surgical approach (application of obstetric
vacuum extractor on the newborn's skull depression) for the treatment of
skull depression without fracture. There exists some concern regarding the
use of non-surgical methods (especially in the presence of a skull
fracture) due to the possibility of intracranial complications such as
subdural hematoma or the presence of extradural or subdural of clot or
bone fragment (3). In order to exclude this concern we suggest Dharmaraj
et al to recommend a head CT scan prior to the initiation of a non-
surgical treatment. This precaution is essential for selection of cases of
congenital skull depression that are appropriate for a non-surgical
approach.
References
1.Dharmaraj ST, Embleton ND, Jenkins A, Jones G. Depressed skull
fracture in a newborn baby. Arch Dis Child Fetal Neonatal Ed 2009;
94:F137.
2.Ben-Ari J, Merlob P, Hirsch M, Reisner SH. Congenital depression of
the neonatal skull. Eur J Obstet Gynecol Reprod Biol 1986;22:249-55
3.Volpe JJ. Skull fracture. In Neurology of the Newborn, W B Saunders
Comp. Philadelphia, 4th ed, 2001, p 815-7.
Dear Editor,
This letter is in response to “Accuracy and Precision of Test Weighing to Assess Milk Intake in Newborn Infants: 2006;91;F 330-332 (1), in which the investigators conclude that test-weighing is too imprecise for routine clinical use. This conclusion is contrary to a series of very well-controlled studies on test-weighing in term and premature infants. Our concerns with the conclusions of this study ar...
Dear Editor,
Persistent patent ductus arteriosus (PDA) is a common pathology in the preterm whose traditional treatment has been indomethacin. Recently, ibuprofen has shown its effectiveness in closing the PDA with less hemodynamic effects.
I read different various studies on Ibuprofen versus indomethacin in the treatment of PDA with great interest. Despite this common occurrence, opinion about the u...
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...
Dear Editor,
In response to the subject, i wish to pen down my recent experience of normal growth of twins till 6 months on exclusive breast feeding. A pair of male twins were born to at term to a 2nd gravida mother by normal vaginal route, the birth weight was 3.2kg and 3.0kg. The mother was motivated and advised breast feeding in delivery room and subsequently in postnatal ward. The parents belonged to lower socico...
Dear Editor,
Herrman et al demonstrated that patent ductus arteriosus (PDA) closes spontaneously in most of the cases of a select group of very low birth weight infants. We did a similar retrospective observational study, at North Trent Regional Intensive Care Unit (Jessop Wing) in Sheffield, in infants diagnosed with PDA on echocardiogram, done for the murmur on routine baby check examination or for other clini...
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...
Response to "Physiological transition ?"
Thank you for your response to our research "Non-invasive measurements of ductus arteriosus flow directly after birth".
We agree with Dr. Hutchon that a caesarian section can influence the respiratory transition of a newborn infant. As such, our results reflect the transition after elective caesarian section with cord clamping within 1 minute after birth, which...
In this study it was reported that, the "frequency of apnoea in the 30 seconds after GER (GER-triggered apnoeas) was greater than that detected in the 30 seconds before (p = 0.01). ..A strong correlation between total number of apnoeas and the difference between apnoeas detected 30 seconds after and before GER was found (p = 0.034)"(1).
These data are consistent with both apnoea and GER being caused by an enrgy...
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...
Dear Editor,
We read with interest the case report of Dharmaraj et al. published in your journal (1). The authors described a full term infant born by an emergency caesarean section. At birth this newborn had a depressed skull fracture on the right parietal bone. Neurosurgical elevation of the fracture was performed at age of 2 weeks after birth. In the discussion the authors mentioned that reduction by vacuum...
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