The team from leed have highlighted a very important area of neonatal
practice that is still seeking clarification and enlightenment.
Neonates do have a high incidence of reflux due to physiologic and
iatrogenic causes. These have been clearly highlighted in this review. The
choice and rationale for treating these babies clearly shows that more
work still needs to done before we can be sure that the doctors and nurses
are u...
The team from leed have highlighted a very important area of neonatal
practice that is still seeking clarification and enlightenment.
Neonates do have a high incidence of reflux due to physiologic and
iatrogenic causes. These have been clearly highlighted in this review. The
choice and rationale for treating these babies clearly shows that more
work still needs to done before we can be sure that the doctors and nurses
are using appropriate measures to address the real problem and not just
propagating a placebo effect and using medications that are not only
unnecessary but potentially dangerous.
The following questions may help to concentrate the thinking about this
problem.
Do we know if reflux in neonates is the
cause of apnoeas? If not why treat
If we believe there is an association in the
absence of aspiration, what is the mechanism?
It is agreed that the stomach of milk fed
neonate is unlikely to suffer from the effect of acid (buffering effect)
what then is the rationale for prescribing gaviscon? Could it be acting as
a thickening agent?
In the absence of proven oesophageal irritation
or inflammation why do we need to further reduce acid production by using
H2 blocker or even worse a proton pump inhibitor in the face of
significant side effects with this substance?
Is there a place for using ph study with
modified (acidified) feeds for testing to demonstrate acid reflux and how
significant is the position of non acid reflux in this group of patients?
Should positioning not be routinely adhered to
as part of routine neonatal care since gastro oesophageal reflux is common
in this age group?
Surgical intervention in my experience is mainly
offered for severe reflux especially in patients with neurological disease
or do the authors have a different experience?
Is contrast study underused in these patients?
And could this be a better test in this uncertain field? I concede that
reflux episde may be missed during this test but its presence can be noted
in addition to any anatomical defect.
Although I have raised a few questions, I appreciate the efforts of the
authors who have tried to highlight the clear difficulties with the
investigation and treatment of reflux in this age group. Neonatologists in
the front line have to deal with problems using best evidence and in most
cases extrapolate from management strategies of older children. It is how
ever the time to look again at the evidence and adjust practice
accordingly. I remember not long ago cisapride was the standard prokinetic
agent used to treat gastroesophageal reflux in neonatal units even when
the evidence was not there. Tertiary neonatal units had in their
formularies this dangerous medicine which was dished out routinely and
thanks to the responsible authorities for the withdrawal of this product
from the UK, meaning that neonates have been spared the dangers of
arrhythmias.
I have an interest in paediatric gastroenterology and have practised in a
DGH with sessions in gastroenterology at the
Children's hospital. In my practice I have
investigated neonates with symptoms suggestive of gastroesophageal reflux
and also suggested and advised on treatment regimes. Having looked at the
evidence, I still advice on ph studies with its flaws after initiation of
treatment which had failed to resolve the observed symptoms. In addition,
neonates with acute life threatening events in addition to Ph studies are
subjected to contrast studies to make sure no anatomical defect exists.
On the use of pharmacology agents, my emphasis is on the use of prokinetic
agents and less of H2 blockers or proton pump inhibitors unless evidence
of oesophagitis exists or the neonate is not enterally fed with milk while
symptomatic. In my experience, surgical intervention for managing
gastroesophageal reflux is only common with those neonates with
neurological problem with severe reflux disease.
The take home message for me after reading this article is that there is a
presumption by some medical practitioners that gastroesophageal Reflux
disease is associated with neonatal apnoes and bradcardias and also that
no reliable form of investigation exists to confirm this and that
pharmacological agents though lacking in evidence remain the mainstay of
treatment. It also tells me that more research is needed to provide the
necessary answers. I will be very willing to be a participant in any such
study.
Reference:
Peter CS, Sprodowski N, Bohnhorst B,et al Gastroesophageal reflux and
apnoea of prematurity: No temporal relationship. Pediatrics
2002;109:8-11
Birch JL; Newell SJ; Gastroesophageal reflux disease in preterm
infants: Current management and diagnostic dilemmas ; Arch Dis Child fetal
Neonatal Ed 2009;94:F379-F383 doi:10.1136/adc.2008.149112.
Dhillon AS, Ewer AK Diagnosis and management of gastroesophageal
reflux in preterm infants in neonatal intensive care units. Acta
Paediatrica 2004;93:88-93
Omari TI, Haslam RR, Lundborg P, et al Effect of omeprazole on acid
gastroesophageal reflux and gastric acidity in preterm infants with
pathological acid reflux. J Pedr Gastroenterol Nutr
2007;44:41-44.
The paper by Sarkar et al[1] addresses a question of considerable
practical and ethical importance for parents and clinicians caring for
asphyxiated newborn infants. Which infants are so severely affected that
they will not benefit from attempted neuroprotection with therapeutic
hypothermia?[2]
However, it is not clear that their paper answers this question. They
focus on risk of mortality...
The paper by Sarkar et al[1] addresses a question of considerable
practical and ethical importance for parents and clinicians caring for
asphyxiated newborn infants. Which infants are so severely affected that
they will not benefit from attempted neuroprotection with therapeutic
hypothermia?[2]
However, it is not clear that their paper answers this question. They
focus on risk of mortality, but do not provide any data on the mechanism
of demise in dying infants. What proportion of infants died despite full
attempts to save their lives, and what proportion died following
withdrawal or withholding of life-sustaining treatment? This is critically
important since in previous studies of infants with HIE the majority of
deaths followed treatment limitation decisions.[3]
The problem is that if a significant proportion of deaths did follow
treatment limitation decisions, the statistical association between an
Apgar score of 0 and death may reflect a self-fulfilling prophecy.[4]
Given the recommendation by the Neonatal Resuscitation Program and
previous evidence of poor outcome in infants with such Apgar scores, it
would not be surprising if an Apgar score of 0 at 10 minutes made
clinicians more pessimistic about outcome and more likely to subsequently
limit treatment.
Secondly, the authors suggest that infants surviving with Apgar
scores of 0 at 10 minutes are "likely to have severe disability". They
base this claim on the finding that there were no non-disabled survivors
in the cohort. However, the absence of an event does not provide good
evidence of its rarity in the presence of small sample sizes.[5]
The authors note in passing that their results differ from those of
the NICHD sub-study.[6] But they understate the significance of those
results. In that study there were 13 survivors with an Apgar score of 0 at
10 minutes, of whom 6 (46%) had mild or no disability.[6] Although that
report did not distinguish between cooled and non-cooled infants, if the
two reports are combined they suggest a 38% chance of favourable outcome
among surviving infants, with a confidence interval of 18-61%.
Further follow-up data of infants with HIE treated with cooling may
help clarify which infants do not benefit from therapeutic hypothermia.
But at present it would be premature to deny infants treatment based
solely on their Apgar score at 10 minutes of age.
Dr Dominic Wilkinson, Neonatologist, Nuffield Medical Research
Fellow, The Ethox Centre, University of Oxford
REFERENCES
1. Sarkar S, Bhagat I, Dechert RE, Barks JD. Predicting death despite
therapeutic hypothermia in infants with hypoxic-ischaemic encephalopathy.
Arch Dis Child Fetal Neonatal Ed. 2010; [published Online First
doi:10.1136/adc.2010.182725].
2. Wilkinson DJ. Cool heads: ethical issues associated with
therapeutic hypothermia for newborns. Acta Paediatrica. 2008;98:217-20
doi: 10.1111/j.1651-2227.2008.01127.x [published Online First 28/11/2008].
3. Pierrat V, Haouari N, Liska A, et al. Prevalence, causes, and
outcome at 2 years of age of newborn encephalopathy: population based
study. Arch Dis Child Fetal Neonatal Ed. 2005;90:F257-61 doi:
10.1136/adc.2003.047985.
4. Wilkinson D. The self-fulfilling prophecy in intensive care. Theor
Med Bioeth. 2009;30:401-10 doi: 10.1007/s11017-009-9120-6.
5. Eypasch E, Lefering R, Kum CK, Troidl H. Probability of adverse
events that have not yet occurred: a statistical reminder. BMJ.
1995;311:619-20.
6. Laptook AR, Shankaran S, Ambalavanan N, et al. Outcome of term
infants using apgar scores at 10 minutes following hypoxic-ischemic
encephalopathy. Pediatrics. 2009;124:1619-26.
In their retrospective observational study of 1960 preterm infants
over a 7-year period, Aralikatti et al reported an increased risk of
developing threshold retinopathy of prematurity (ROP) in Asian and black
infants compared to white infants [1]. The proportion of small for
gestational age (SGA), by standard growth charts, was also higher in Asian
(36.19%) than in white (29.45%) and black infants (...
In their retrospective observational study of 1960 preterm infants
over a 7-year period, Aralikatti et al reported an increased risk of
developing threshold retinopathy of prematurity (ROP) in Asian and black
infants compared to white infants [1]. The proportion of small for
gestational age (SGA), by standard growth charts, was also higher in Asian
(36.19%) than in white (29.45%) and black infants (27.81%) and the authors
speculated that this might explain the increased risk of ROP in Asian
infants. They also adjusted for birthweight and gestational age through
logistic regression analysis and reported that the results still supported
the increased risk of ROP in non-white infants.
SGA, as defined by standard growth standards, is a known risk factor
for ROP in the preterm infant [2-5]. When looking for an association
between ethnicity and the risk of ROP in a logistic regression model which
adjusts for birthweight and gestational age, the model calculates the odds
ratio of ROP for each ethnicity by adjusting separately for each unit
increment in birthweight and for each unit increment in gestational age,
while maintaining the other factor constant. The classification of each
infant as SGA or AGA is totally ignored in the model used, as the
birthweight and the gestational age of each infant are separately taken
into account, without any indication whether each infant's birthweight is
appropriate for his/her gestational age or not. We believe that this
deficiency in the model they used prevented the authors from reliably
studying whether the relationship they found between ethnicity and the
risk of ROP was not confounded by growth retardation.
Furthermore, the observed ethnic differences in foetal growth are
often physiologic rather than pathologic [6]. Customised birth weight
percentiles, by adjusting for the variables found to be associated with
normal variation in birth weight, such as maternal height, weight, parity,
ethnic origin and the baby's gender, better distinguish growth-restricted
from constitutionally small but healthy neonates and have been proven to
be superior to standard growth charts in detecting foetal and neonatal
complications associated with poor foetal growth [7-8]. Using these
customised birth weight percentiles [9], we found that, regardless of
gestational age, SGA infants identified exclusively by the customised
method, and therefore missed by the standard growth charts, accounted for
50% of all infants diagnosed with ROP in a cohort of 6125 neonates. We
also found that, after adjusting for prematurity, SGA infants exclusively
identified by the customised method, still had a higher risk of
complications, including an increased risk for all grades of ROP,
confirming previous reports that morbidities associated with preterm
delivery, including ROP [2-5], are compounded by foetal growth restriction
[10].
We therefore believe that adding a classification of birthweight as
SGA (or not) in their regression model, even using the standard growth
charts, was needed, and would have allowed the authors to reliably confirm
if the role of ethnicity in the risk of ROP is not confounded by SGA.
Better still, using the customised growth percentiles instead of standard
growth charts to classify infants' growth in their model would have been
more appropriate, as maternal ethnicity is already integrated in the
customised classification of the infant's birth weight.
Hassib Narchi, Alyson Skinner
References
1. Aralikatti AKV, Mitr A, Denniston AKO, Haque MS, Ewer AK, Butler
L. Is ethnicity a risk factor for severe retinopathy of prematurity? Arch
Dis Child Fetal Neonatal Ed 2010;95:F174-F176.
2. Zaw W, Gagnon R, da Silva O. The risks of adverse neonatal outcome
among preterm small for gestational age infants according to neonatal
versus fetal growth standards. Pediatrics 2003;111 (Part 1):1273-1277.
3. 26. Slidsborg C, Olesen HB, Jensen PK, Jensen H, Nissen KR,
Greisen G, Rasmussen S, Fledelius HC, la CM. Treatment for retinopathy of
prematurity in Denmark in a ten-year period (1996-2005): is the incidence
increasing? Pediatrics 2008; 121:97-105.
4. Allegaert K, Vanhole C, Casteels I, Naulaers G, Debeer A, Cossey
V, Devlieger H. Perinatal growth characteristics and associated risk of
developing threshold retinopathy of prematurity. J AAPOS 2003;7:34-37.
5. Regev RH, Lusky A, Dolfin T, Litmanovitz I, Arnon S, Reichman B.
Excess mortality and morbidity among smallfor- gestational-age premature
infants: a population-based study. J Pediatr 2003;143:186-191.
6. Kierans WJ, Joseph KS, Luo ZC, Platt R, Wilkins R, Kramer MS. Does
one size fit all? The case for ethnic-specific standards of fetal growth.
BMC Pregnancy Childbirth 2008;8:1.
7. Gardosi J. New definition of small for gestational age based on
fetal growth potential. Horm Res 2006;65 (Suppl 3):15-18.
8. Reddy UM. Prediction and prevention of recurrent stillbirth.
Obstet Gynecol 2007;110:1151-1164
9. Narchi H, Skinner A, Williams B. Small for gestational age
neonates- are we missing some by only using standard population growth
standards and does it matter? J Matern Fetal Neonatal Med. 2009; 29:1-7.
10. Pallotto EK, Kilbride HW. Perinatal outcome and later
implications of intrauterine growth restriction. Clin Obstet Gynecol
2006;49:257-269
We congratulate Sehgal and colleagues for their study (1) that found
prophylactic surfactant causes major haemo-dynamic changes in preterm
babies. This publication follows close on the heels of a study in the NEJM
that found that prophylactic surfactant was no better than continuous
positive airway pressure (CPAP)ventilation (2). It is significant that
both these papers (1,2) quote a Cochrane meta-analysis in there
intro...
We congratulate Sehgal and colleagues for their study (1) that found
prophylactic surfactant causes major haemo-dynamic changes in preterm
babies. This publication follows close on the heels of a study in the NEJM
that found that prophylactic surfactant was no better than continuous
positive airway pressure (CPAP)ventilation (2). It is significant that
both these papers (1,2) quote a Cochrane meta-analysis in there
introduction to suggest that prophylactic surfactant reduces mortality
(3). This is a misinterpretation of the Cochrane report. The meta-analysis
had found that there was no difference in the in-hospital deaths, after
use of surfactant (Risk Ratio: 0.70, 95% C.I. 0.47 - 1.06). It however
found that surfactant reduces incidence of deaths in the first 30 days of
life and this was then reported as a reduction in neonatal mortality (Risk
Ratio: 0.80, C.I. 0.72 - 0.88). The Cochrane meta-analysis was revised
recently (4) but this misleading statement in the abstract has survived
into the new version also. The fact that leading researchers working with
surfactant carry this wrong impression from the Cochrane report suggests
that the report needs to be revised for clarity.
We hope that this letter will in a small way, add to the results of newer
studies on surfactant(1,2), to clarify the issue that prophylactic
surfactant is not useful in reducing mortality.
References
1. Haemodynamic changes after delivery room surfactant administration
to very low birth weight infants Arvind Sehgal, Wendy Mak, Michael Dunn,
Edmond Kelly, Hilary Whyte, B McCrindle, Patrick J McNamara Arch. Dis.
Child. Fetal Neonatal Ed. published 10 June 2010, 10.1136/adc.2009.173724
2. SUPPORT Study Group of the Eunice Kennedy Shriver NICHD Neonatal
Research Network. Early CPAP versus Surfactant in Extremely Preterm
Infants. N Engl J Med. 2010 May 16. [Epub ahead of print] PMID: 20472939
3. Soll RF. Prophylactic natural surfactant extract for preventing
morbidity and mortality in preterm infants. Cochrane Database Syst Rev
2000;2:CD000511.
4. Soll R, Ozek E. Prophylactic animal derived surfactant extract for
preventing morbidity and mortality in preterm infants. Cochrane Database
of Systematic Reviews 1997, Issue 4. Art. No.: CD000511. DOI:
10.1002/14651858.CD000511
With great interest we read the article by Sehgal et al describing
the hemodynamics of surfactant administration in the delivery room. The
authors found a low RVO, low LVO, low to normal SVC flow and an increasing
RVO:LVO ratio in the first 60 minutes after surfactant administration.
Surprisingly, SVC flow is responsible for 62% of RVO in the pre-surfactant
measurement and up to 79% of LVO at 1 hour...
With great interest we read the article by Sehgal et al describing
the hemodynamics of surfactant administration in the delivery room. The
authors found a low RVO, low LVO, low to normal SVC flow and an increasing
RVO:LVO ratio in the first 60 minutes after surfactant administration.
Surprisingly, SVC flow is responsible for 62% of RVO in the pre-surfactant
measurement and up to 79% of LVO at 1 hour after surfactant. This combined
with a large duct and exclusive left-to-right shunting would mean there is
very little blood flow to the lower body. However, this was not reflected
by the arterial pH. The authors provide hemodynamic explanations, but do
not discuss methodological issues surrounding Doppler-derived cardiac
output measurements. Delivery room hemodynamics are not extensively
studied, but some information is available for healthy term newborns.
Agata et al. measured 34 healthy term infants at 1 hour of age and found a
LVO of 327 /- 66 ml/kg/min, followed by a decrease.1 Walther et al.
showed comparable findings in a group of 32 term infants starting at 30
minutes after birth.2 We re-analysed a previously published cohort of
preterm infants who were studied during lung recruitment.3 There were 9
infants who were measured within 1 hour after birth immediately after the
change to high frequency ventilation. In this group the median (range) RVO
and SVC flow was 325 (251-541) and 74 (48-126) ml/kg/min respectively. The
ductal diameter was 2.9 (1.7-3.6) mm with total ductal shunting always
left-to-right.
We suggest that differences in methodology may explain the differences in
findings. Detailed information on where LVO and RVO diameters were
determined was not provided. The Pa Vmax is suggestive of an expected RVO
of 150-300 ml/kg/min 4 so it is possible that a reduced diameter
measurement could explain the low RVO and LVO compared to values found
using other referenced methodology.5 Further investigations into whether
the low-normal SVC flow is caused by the early surfactant administration
and if this coincides with low peripheral blood flow will be required to
establish the full picture and potential consequences of these
observations.
1. Agata Y, Hiraishi S, Oguchi K, Misawa H, Horiguchi Y, Fujino N,
Yashiro K,
Shimada N. Changes in left ventricular output from fetal to early neonatal
life.
J Pediatr. 1991;119(3):441-5
2. Walther FJ, Benders MJ, Leighton JO. Early changes in the neonatal
circulatory transition. J Pediatr. 1993;123(4):625-32
3. de Waal K, Evans N, van der Lee J, van Kaam A. Effect of lung
recruitment on
pulmonary, systemic, and ductal blood flow in preterm infants. J Pediatr.
2009;154(5):651-5
4. Evans N. Support of the preterm circulation: keynote address to
the Fifth Evidence vs Experience Conference, Chicago, June 2008. J
Perinatol. 2009;29 Suppl 2:S50-7
5. Evans N, Kluckow M. Early determinants of right and left
ventricular output in ventilated preterm infants. Arch Dis Child Fetal
Neonatal Ed. 1996;74(2):F88-94
Dear editor,
We read with great interest the recent article by Aralikatti et al.1 The
authors conducted a well designed study regarding the effect of ethnicity
on developing severe retinopathy of prematurity (ROP). They concluded that
asians and black infants have a higher risk of developing threshold ROP
compared to white infants. Although ethinicity might be a risk factor, we
think that it can hardly be considered as a...
Dear editor,
We read with great interest the recent article by Aralikatti et al.1 The
authors conducted a well designed study regarding the effect of ethnicity
on developing severe retinopathy of prematurity (ROP). They concluded that
asians and black infants have a higher risk of developing threshold ROP
compared to white infants. Although ethinicity might be a risk factor, we
think that it can hardly be considered as an independent factor. To our
knowledge2,3 lower socio-economical status of the black and Asian race in
most areas of the world might be the main contributing factor for the
increase in severe retinopathy of prematurity incidence requiring
treatment. The lower socio-economical status means lower educational level
and less reliability on the data collected from the parents with respect
to correct gestational age, maternal smoking and nutrition, infant
nutrition. The infants born in developing countries carry greater risk of
acquiring infectious, inherited and malnutrition diseases. It is well
known that these all are risk factors for ROP.
In our study a screening was performed on neonates born between 32 and 35
weeks gestation and referred for ROP screening between 1 January 2004 and
31 December 2008. Our unpublished data suggested that, in developing
countries attention must be paid to increase awareness among
neonatologists and widely used screening criteria for ROP must be revised
to decrease the risk of blindness due to ROP in larger babies as it can be
treatable to a great extent. From this point of view, some different
aspects should be stressed. We think that though ethnicity may be an
independent risk factor for developing severe ROP, concomitant attributes
of the infants of the black and asian race are the main underlying factors
for greater risk for severe ROP.
References
1. Aralikatti AK, Mitra A, Denniston AK et al. Is ethnicity a risk factor
for severe retinopathy of prematurity? Arch Dis Child Fetal Neonatal Ed.
2009 Nov 29. (Epub)
2. Silva AM, de Almeida MF, Matsuo T, Soares DA. Risk factors for pre-term
birth in Londrina, Parana State, Brazil. Cad Saude Publica. 2009; 25: 2125
-38.
3. Maida JM, Mathers K, Alley CL. Pediatric ophthalmology in the
developing world. Curr Opin Ophthalmol 2008; 19(5):403-8.
The case report by R. Negrine and colleagues(1) is of considerable
interest. However, testicular trauma following breech delivery is not
extremely rare as they suggest. In 1975 I reported 11 cases of scrotal
bruising and significant testicular enlargement among 114 consecutively
breech-born male infants over a two year period(2). Those affected tended
to be large, first-born, singleton and term or post-term infants. O...
The case report by R. Negrine and colleagues(1) is of considerable
interest. However, testicular trauma following breech delivery is not
extremely rare as they suggest. In 1975 I reported 11 cases of scrotal
bruising and significant testicular enlargement among 114 consecutively
breech-born male infants over a two year period(2). Those affected tended
to be large, first-born, singleton and term or post-term infants. One
infant with particularly severe damage was found to have soft and
hypoplastic testicles at the age of 10 years. It is therefore not
improbable that the damage at birth may be another cause of the vanishing
testicle and for sterility or gonadal dysfunction. It would be of
interest to study the prior incidence of breech delivery in a large series
of sterile adult males.
Correspondence to:
Professor Peter M. Dunn
University of Bristol, Southmead Hospital, Bristol, BS10 5NB
p.m.dunn@bristol.ac.uk
References
1. Negrine, R., Easter, W., Fraser, I. and Ellis, S. Neonatal
testicular trauma: scrotal rupture. Arch. Dis. Child. Fetal Neonatal Ed.,
2010; 95, F.193.
The swedish observational study on neonatal thiopentone
pharmacokinetics provides some interesting data. The authors rightly point
out that the duration of anaesthesia following a thiopentone bolus is
determined by redistribution rather than metabolism. It is interesting
that blood levels in the mother at six minutes following induction with a
dose of 5.5mg/kg were three times the average level in the neonate five
minute...
The swedish observational study on neonatal thiopentone
pharmacokinetics provides some interesting data. The authors rightly point
out that the duration of anaesthesia following a thiopentone bolus is
determined by redistribution rather than metabolism. It is interesting
that blood levels in the mother at six minutes following induction with a
dose of 5.5mg/kg were three times the average level in the neonate five
minutes after a dose of 3mg/kg. This is likely due to the higher blood
volume per kg in neonates, as well as their relatively large brains, so
leading to a higher initial volume of distribution.
It is unfortunate that umbilical arterial thiopentone levels were not
measured in infants delivered by caesarean section. The venous values only
confirm that placental transfer is very efficient. The total dose the
infant receives (and their corresponding blood level) will also be
affected by the umbilical blood flow. Without this data, how can the
author's claim that one should wait 4 hours before giving thiopentone to
an infant already exposed via its mother?
After redistribution has occurred, thiopentone, in common with other
barbiturates and alcohol, is metabolized at a constant rate. The half life
will vary with blood level. This may explain the discrepancy between the
author's calculations and earlier studies using higher doses of
thiopentone for neuroprotection. It is meaningless to calculate the half
life of a drug which is metabolized by zero order kinetics. It is better
to simply state the rate at which blood levels fall.
It was with great interest that we read the article by Choong et al.
- Remifentanil for endotracheal intubation in neonates: a randomised
controlled trial. First of all, we would like to congratulate the authors
for their relevant RCT. However, there are some aspects that should be
pointed out.
The premedication protocol for endotracheal intubation of this study
includes many classes of drugs besid...
It was with great interest that we read the article by Choong et al.
- Remifentanil for endotracheal intubation in neonates: a randomised
controlled trial. First of all, we would like to congratulate the authors
for their relevant RCT. However, there are some aspects that should be
pointed out.
The premedication protocol for endotracheal intubation of this study
includes many classes of drugs besides opioids that might interfere with
physiological responses. For instance, the administration of
succinylcoline (a short action muscle relaxant) might have biased the
results. Indeed, premedication with succinylcoline could be able to
influence the evaluation of intubation conditions by intubators. Since
both groups received atropine, the pharmacodynamic responses were probably
more influenced by this drug than by the opioids themselves. It should
have been more appropriate if the comparison had included only the opioids
(remifentanil versus fentanyl).
Another issue is the evaluation of intubation conditions per se. The use
of subjective impression of intubation rather than specific and validated
scores1 seems to be not the ideal approach. In addition, the enrollment
of six different intubators instead of just one2 could also have
influenced this evaluation.
The authors did not show any sample size calculation to support one of the
outcomes (adverse events) and also one of the main conclusions of this
trial. Even though, no differences in adverse events were detected in the
comparison between groups. However, the study suggested that remifentanil
was more frequently responsible for chest wall rigidity. To date,
synthetic opioid administration as a cause of chest wall rigidity in
adults has been recently questioned3. The general idea is that the opioids
produce transient vocal cord closure rather than chest wall rigidity and
this phenomenon could also happen with neonates. In this regard,
succinylcoline administration might again avoid this adverse event in the
group treated with fentanyl.4
Finally, the experience with remifentanil in neonates is not large enough
and the RCTs with this opioid are very important. Indeed, the American
Academy of Pediatrics has recently recommended the use of remifentanil as
a possible premedication for neonatal endotracheal intubation.5,6
However, further properly designed and larger clinical trials are needed
before any conclusion concerning the best opioid recommended for neonatal
intubation.
Yerkes Pereira e Silva, MD, PhD; Juliana Marcatto, RN; Rosilu
Barbosa, MD, MSc; Ana Cristina Simoes e Silva, MD, PhD
1- Viby-Mogensen J, Engbaek J, Eriksson LI et al. Good clinical
research practice (GCRP) in pharmacodynamic studies of neuromuscular
blocking agents. Acta Anaesthesiol Scand 1996;40:59-74.
2- E Silva Y, Gomez R, de Oliveira Marcatto J, et al. Morphine versus
remifentanil for intubating preterm neonates. Arch Dis Child Fetal
Neonatal Ed 2007;18:176-83.
3- Bennett JA, Abrams JT, Van Riper DF, et al. Difficult or
impossible ventilation after sufentanil-induced anesthesia is caused
primarily by vocal cord closure. Anesthesiology 1997;87:1070-1074.
4- Fahnenstich H, Steffan J, Kau N et al. Fentanyl induced chest wall
rigidity and laryngospasm in preterm and term infants. Crit Care Med,
2000;28:836-839.
5- Kumar P, Denson, SE, Mancuso TJ and Committee of Fetus and
Newborn, Section on Anesthesiology and Pain Medicine. Pediatrics
2010;125;608-615.
6- Greenwood CS, Colby CE. Pharmacology Review: Premedication for
endotracheal intubation of the neonate: What is the evidence? NeoReviews
2009;10:e31-e35
Nasal-CPAP (nCPAP) is the most popular system for administering
continuous distending pressure to neonatal patients, but this technique
may fail due to several problems such as insufficiently applied pressure,
insufficient circuit flow, inappropriate prong size or placement, airway
obstruction from secretions, and a baby's open mouth creating a large leak
and lowering the pharyngeal pressure.1 In addition, severe nasal sk...
Nasal-CPAP (nCPAP) is the most popular system for administering
continuous distending pressure to neonatal patients, but this technique
may fail due to several problems such as insufficiently applied pressure,
insufficient circuit flow, inappropriate prong size or placement, airway
obstruction from secretions, and a baby's open mouth creating a large leak
and lowering the pharyngeal pressure.1 In addition, severe nasal skin
necrosis has been reported as a complication of this therapy.2 In this
case, nasal prongs have to be removed and a different patient-machine
interface is needed, possibly avoiding tracheal intubation.
To overcome this problem, Carlisle et al. report a novel method of oral
CPAP delivery in an extremely premature infant with severe nasal septum
erosion.3 However, previous work reported other interface solutions.4 The
helmet is one of the newest interfaces that can reduce several side
effects of NIV and improve tolerance in both adult and pediatric
patients.4
To improve the patient-ventilator interface, we developed a new device
(neonatal helmet CPAP) to administer CPAP in neonates.5 A previous short-
term physiological study showed that neonatal helmet CPAP was a feasible
method of supporting the breathing of preterm infants with better
tolerability compared with conventional nCPAP.5 Furthermore, this new
device allows the delivery of accurate nitric oxide levels, thus avoiding
NO2 accumulation.6
We are grateful to the authors for providing a new technique for
delivering CPAP to infants where nCPAP failed, however, the helmet-CPAP
system could be a further valid therapeutic option in these patients.
References
1. De Paoli AG, Morley C, Davis PG. Nasal CPAP for neonates: what do we
know in 2003 ? Arch Dis Child Fetal Neonatal Ed 2003;88:F168-F172
2. Robertson NJ, McCarthy LS, Hamilton PA, Moss ALH. Nasal deformities
resulting from flow driver continuous positive airway pressure. Arch Dis
Child 1996;75:F209-F212
3. Carlisle HR, Kamlin COF, Owen LS, Davis PG, Morley CJ. Oral continuous
positive airway pressure (CPAP) following nasal injury in a preterm
infant. Arch Dis Child Fetal Neonatal Ed 2010;95:F142-F143
4. Bellani G, Patroniti N, Greco M, Foti G, Pesenti A. The use of helmets
to deliver non-invasive continuous positive airway pressure in hypoxemic
acute respiratory failure. Minerva Anestesiol 2008;74:651-656
5. Trevisanuto D, Grazzina N, Doglioni N, Ferrarese P, Marzari F, Zanardo
V. A new device for the administration of continuous airway pressure in
preterm infants: comparison with a standard nasal CPAP system. Intensive
Care Med 2005;31:859-864
6. Trevisanuto D, Doglioni N, Micaglio M, Zanardo V. Feasibility of nitric
oxide administration by neonatal helmet-CPAP: a bench study. Paediatr
Anaesth 2007;17:851-855
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Dear Editor,
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Dear Editor,
It was with great interest that we read the article by Choong et al. - Remifentanil for endotracheal intubation in neonates: a randomised controlled trial. First of all, we would like to congratulate the authors for their relevant RCT. However, there are some aspects that should be pointed out. The premedication protocol for endotracheal intubation of this study includes many classes of drugs besid...
Nasal-CPAP (nCPAP) is the most popular system for administering continuous distending pressure to neonatal patients, but this technique may fail due to several problems such as insufficiently applied pressure, insufficient circuit flow, inappropriate prong size or placement, airway obstruction from secretions, and a baby's open mouth creating a large leak and lowering the pharyngeal pressure.1 In addition, severe nasal sk...
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