Dr da Costa et al, and Dr Gatrad in his accompanying commentary [Arch
Dis Child Fetal Neonatal Ed 2002;86:F115-9], are mistaken in drawing
convulsions about Muslim families in relation to ‘do not resuscitate
orders’. Gatrad suggests doctors should receive training in ethical
issues of other cultures. Firstly, it is impossible to know the religious
or historical or personal background of every parent....
Dr da Costa et al, and Dr Gatrad in his accompanying commentary [Arch
Dis Child Fetal Neonatal Ed 2002;86:F115-9], are mistaken in drawing
convulsions about Muslim families in relation to ‘do not resuscitate
orders’. Gatrad suggests doctors should receive training in ethical
issues of other cultures. Firstly, it is impossible to know the religious
or historical or personal background of every parent. Secondly, Muslims
are not an homogenous group, just as Buddhists or Baptists are not. To
assume that because someone has a particular surname (e.g., Singh, a name
usually associate with Sikhism) or comes from a particular country (e.g.,
India, where many people are Hindus) or is of a particular religion (e.g.,
Catholicism, as there are lapsed Catholics, middle of the road Catholics,
and ardent Catholics) that they have a particular set of beliefs is very
unwise. Indeed, it is racist. For example, I have an evangelical
Christian faith, which is probably different in some respects from many
other evangelical Christians. What would my views be on ‘do not
resuscitate’ if faced with that for my children? Whatever they are, I
would be annoyed if my children’s medical attendants assumed that I had
the same views as all evangelical Christians.
Which raises a third point. Why are such issues only considered for
‘ethnic minority’ groups? I have yet to read a paper or hear a
presentation on cultural aspects for Methodists, Plymouth Brethren, born
again Christians, etc. In the end, though, it doesn’t matter, and neither
do da Costa et al’s or Gatrad’s views. It is important to treat the
families with respect, and listen to them.
I do not know the situation in Oman, where da Costa works, but in the
UK I think the pendulum has swung too far in terms of how we involve
parents in ‘end of life’ decisions. The parents’ views are important but
not determinative. Society, and the Courts, have devolved those decisions
to doctors. To ask parents to be involved in those decisions about their
own children is an unfair burden for them to carry, possibly for the rest
of their lives.
Nitric oxide (NO) is frequently used as a selective pulmonary
vasodilator in neonates. Since its metabolite, methaemoglobin can
potentially cause tissue hypoxia it is considered mandatory to measure
methaemoglobin levels when using NO. In an attempt to review and
rationalise our own practice of methaemoglobin measurement when using NO
we undertook a search of current literature and conducted a postal surv...
Nitric oxide (NO) is frequently used as a selective pulmonary
vasodilator in neonates. Since its metabolite, methaemoglobin can
potentially cause tissue hypoxia it is considered mandatory to measure
methaemoglobin levels when using NO. In an attempt to review and
rationalise our own practice of methaemoglobin measurement when using NO
we undertook a search of current literature and conducted a postal survey
of current practice.
38 questionnaires were sent to level II or III neonatal units in
England, Scotland and Wales. Of the 32 (84%) returned, 24 were from
centres using NO (63%). We asked about their timing for methaemoglobin
levels and what level was considered to warrant intervention. Our replies
found no standardised protocol for the timing of levels and no recognised
‘toxic’ level. The range of timings for levels was large varying from
every 4 hours to every 24 hours after starting NO therapy. Most hospitals
considered a methaemoglobin level of 4% needed a reduction in the dose of
NO and that levels of 5 to 7% required the NO to be stopped. All centres
agreed on the treatment of choice for toxic levels, ie, an infusion of
methylene blue, but there was no agreement on what level required
treating, quoted levels ranging from 5 to 15%.
From the literature it would appear that neonates tolerate relatively high
methaemoglobin levels well. Normal blood levels of methaemoglobin have
been quoted as 0 to 1.9% for adults, 0 to 2.8% for term neonates and 0.08 to 4.7% for premature babies.[1] The higher level in neonates being due to
their immature enzymatic system and the fact that fetal haemoglobin is
more prone to oxidation. Furthermore, in a case where NO was inadvertently
given in extremely high concentrations, a neonatal methaemoglobin level of
13.4% was measured with no clinical deterioration and no other
intervention than stopping the NO therapy being required.[2]
Methaemoglobin has been shown to follow first order kinetics for both
its formation and metabolism with a time constant of 39 to 91 minutes. Peak
methaemoglobin levels occurred 3 to 5 hours after starting NO therapy after
which steady state concentrations were achieved.[3] From this data it would
seem appropriate to take a methaemoglobin levels 4 hours and 8 hours after
starting NO and then daily unless the dose is increased, when levels
should be re-measured at 4 and 8 hours after the change. Once the dose of
NO is being decreased levels should no longer be necessary.
Our survey has highlighted a lack of agreement for the safe use of
nitric oxide in neonates with regard to methaemoglbinaemia. The
pharmacokinetic data quoted was from healthy adults inhaling NO and
therefore may not be comparable to that of sick neonates. We therefore
feel this is an area that warrants further research and would be grateful
of other unit’s advice and experience in this area.
Dr RD Taylor*
Dr SA Calvert**
*Specialist Registrar anaesthetics Frenchay Hospital Bristol, UK
**Consultant Neonatologist
Neonatology Unit St George’s Health Care Trust London SW17 OQT, UK
References
(1) Bowman WC, Rand MJ. Methaemoglobinaemia. In: Textbook of
Pharmacology. Second edition. Blackwell Scientific publications.1984:21.45 – 48.
(2) Heal CA, Spencer SA. Methaemoglobinaemia with high dose nitric oxide administration. Acta Paediatr 1995;84:1318-19.
(3) Young JD, Dyar O, Xiong L, Howell S. Methaemoglobin production in normal adults inhaling low concentrations of nitric oxide. Intensive Care Med 1994;20:581-4.
I read with interest the report by Al-Dahhan and colleagues on the
beneficial effect of NaC1 supplementation of preterm infants during the
neonatal period on their later neurodevelopmental outcome. They found
better memory, learning, language and educational performances at the age
of 10-13 years in prematures who were given 4-5 mMol/day NaC2 when
compared to those not receiving NaC1 supplement.[1] In th...
I read with interest the report by Al-Dahhan and colleagues on the
beneficial effect of NaC1 supplementation of preterm infants during the
neonatal period on their later neurodevelopmental outcome. They found
better memory, learning, language and educational performances at the age
of 10-13 years in prematures who were given 4-5 mMol/day NaC2 when
compared to those not receiving NaC1 supplement.[1] In this regard, it is
relevant to mention our most recent findings describing a new aspect of
the relationship of neonatal sodium homeostasis to central nervous system
function. Namely, we demonstrated that hyponatraemia is one of the most
significant risk factors for development of sensorineural hearing
impairment detected by transient evoked otoacustic emission and confirmed
by auditory brainstem response.[2]
In addition, I consider their report raises an important clinical
issue, in that I regard their selection of list of references as
subjective and arbitrary. In particular, the work of our group in revealing
some major features of sodium homeostasis in premature has been ignored;
for example wasting, sodium depletion and hyponatraemia, [3,4,5] and the
first introduction of NaC1 supplementation in a dose of 3-5 mM/kg/day to
prevent sodium deprivation, to improve somatic stability and to avoid
untoward clinical consequences.[6]
Endre Sulyok MD
Professor & Chairman
County Children's Hospital, Institute of Health Promotion and Family Care
Faculty of Health Sciences, University of Pecs
H-7624 Pecs, POB 76, Hungary
References
(1) Al-Dahhan, Jannoun L, Haycock GB. Effect of salt supplementation of newborn premature infants on neurodevelopmental outcome at 10-13 years of
age. Arch Dis Child Fetal Neonatal Ed 2002;86:F120-F123.
(2) Ertl T, Hadzsiev K, Vincze O, Pytel J, Szabó T, Sulyok E. Hyponatraemia and sensorineural hearing loss in preterm infants.
Biol Neonate 2001;79:109-12.
(3)Sulyok E.
The relationship between electrolyte and acid-base balance in the premature infant during early postnatal life.
Biol Neonate 1971;17:227-37.
(4) Sulyok E, Heim T, Soltész G, Jászai V.
The influence of maturity on renal control of acidosis in newborn infants.
Biol Neonate 1972;21:418-35.
(5) Sulyok E.
Sodium homeostasis in preterm infants.
Lancet, 1975;I:930 (letter).
(6) Sulyok E, Németh M, Tényi I, Csaba IF, Varga L, Varga F.
Relationship between the postnatal development of the renin-angiotensin-aldosterone system and
electrolyte and acid-base status of the NaCl supplemented premature infants.
In: The Kidney during Development Morphology and Function. Edited by Spitzer A.
Masson Publishing, New York 1982;273-281.*
*This paper was presented in 1980 in the First International Workshop on Developmental Renal
Physiology organized by A. Spitzer in New York
Me thinks Professor Sulyok doth protest too much. His early,
pioneering work on electrolyte balance in the newborn is well known (and
extensively cited in an earlier review of the subject co-authored by
myself.[1] In this, inter alia, his study of the effect of salt
supplementation on the renin-angiotensin-aldosterone system [2] is quoted in
support of the hypothesis that hyponatraemia in premature infant...
Me thinks Professor Sulyok doth protest too much. His early,
pioneering work on electrolyte balance in the newborn is well known (and
extensively cited in an earlier review of the subject co-authored by
myself.[1] In this, inter alia, his study of the effect of salt
supplementation on the renin-angiotensin-aldosterone system [2] is quoted in
support of the hypothesis that hyponatraemia in premature infants is due
to salt depletion rather than water retention). The reason these papers
were not cited in the present paper is that they are not relevant to it.
The paper is not a historical or general review of hyponatraemia in the
newborn but the results of a study specifically designed to examine
neurodevelopmental outcome in two particular groups of infants previously
studied by ourselves.[3-5] His recent study of hyponatraemia and
sensorineural deafness in preterm infants[6] had not been published when our
paper was submitted to the Archives, although we would certainly have
referred to it if it had been.
GEORGE HAYCOCK
References
(1) Haycock GB, Aperia A. Salt and the newborn kidney. Pediatr Nephrol 1991;5:65-70.
(2) Sulyok E, Németh M, Tényi I, Csaba IF, Varga L, Varga F. Relationship between the postnatal development of the renin-angiotensin-aldosterone system and the electrolyte and acid-base status in the sodium chloride supplemented premature infant. Acta Paediatr Acad Sci Hung 1981;22:109-21.
(3) Al-Dahhan J, Haycock GB, Chantler C, Stimmler L. Sodium homeostasis in term and preterm neonates. I. Renal aspects. Arch Dis Child 1983;58:335-42.
(4) Al-Dahhan J, Haycock GB, Chantler C, Stimmler L. Sodium homeostasis in term and preterm neonates.II. Gastrointestinal aspects. Arch Dis Child 1983;58:343-5.
(5) Al-Dahhan J, Haycock GB, Nichol B, Chantler C, Stimmler L. Sodium homeostasis in term and preterm neonates. III. The effect of salt supplementation. Arch Dis Child 1984;59:945-50.
(6) Ertl T, Hadzsiev K, Vincze O, Pytel J, Szabo I, Sulyok E. Hyponatremia and sensorineural hearing loss in preterm infants. Biol Neonate 2001;79:109-12.
I read with great interest the article by Shulman.[1] Indeed, orally
administered insulin may have a positive effect on gut maturation and
mucosal enzyme expression in preterm infants. We have recently
demonstrated that human milk is rich in insulin (mean = 60.2 micro U/ml),
and that insulin is barely detected in infant formulas.[2] Moreover, we
have hypothesized that insulin content of human milk may ha...
I read with great interest the article by Shulman.[1] Indeed, orally
administered insulin may have a positive effect on gut maturation and
mucosal enzyme expression in preterm infants. We have recently
demonstrated that human milk is rich in insulin (mean = 60.2 micro U/ml),
and that insulin is barely detected in infant formulas.[2] Moreover, we
have hypothesized that insulin content of human milk may have an important
role in the primary prevention of type 1 diabetes, by inducing active
cellular machanisms that suppress the development of autoimmune diabetes,
and by reducing intestinal transmission of 'triggering' dietary peptides.[3]
We suggest to add human insulin to infant formulas in a concentration
similar to insulin concentration present in human milk. This addition may
lead to the following beneficial effects: It will make infant formula
similar to human milk; it may fasten gut maturation; and it may protect
from the development of type 1 diabetes.
References
(1) Shulman RJ. Effect of interal administration of insulin on
itestinal development and feeding tolerance in preterm infants: a pilot
study. Arch Dis Child Fetal Neonatal Ed 2002;86:F131-3.
(2) Shehadeh N, Gelertner L, Blazer S, Perlman R, Solovachik L, Etzioni
A. Importance of insulin content in infant diet: suggestion for a new
infant formula. Acta Pediatr 2001;90:93-5.
(3) Shehadeh N, Shamir R, Berant M, Etzioni A. Insulin in human milk
and the prevention of type 1 diabetes. Pediatric Diabetes 2001;2:175-7.
I am familiar with the work of Dr Shehadeh et al. There may indeed
be a place for insulin in infant formula. However, before such a step is
taken, I believe that it is imperative that appropriate prospective
studies be done, including safety monitoring. Although our human pilot
study and animal studies suggest there may be a benefical effect of oral
insulin, much more work needs to be done...
I am familiar with the work of Dr Shehadeh et al. There may indeed
be a place for insulin in infant formula. However, before such a step is
taken, I believe that it is imperative that appropriate prospective
studies be done, including safety monitoring. Although our human pilot
study and animal studies suggest there may be a benefical effect of oral
insulin, much more work needs to be done and recommending its use now is,
to my mind, not appropriate. [1]
Reference
(1) RJ Shulman. Effect of enteral administration of insulin on intestinal development and feeding tolerance in preterm infants: a pilot study. Arch Dis Child Fetal Neonatal Ed. 2002;86:F131-3.
We thank Dr Bissenden for his comments regarding our paper.[1] We
would
suggest that injury to the phrenic nerve is an unusual complication of
chest tube placement in neonates because chest tubes are usually inserted
to drain a pneumothorax (rather than a pleural effusion as in the case we
describe [1]) and hence sited so that the tip lies anteriorally where it
most effectively drains air. Phrenic ner...
We thank Dr Bissenden for his comments regarding our paper.[1] We
would
suggest that injury to the phrenic nerve is an unusual complication of
chest tube placement in neonates because chest tubes are usually inserted
to drain a pneumothorax (rather than a pleural effusion as in the case we
describe [1]) and hence sited so that the tip lies anteriorally where it
most effectively drains air. Phrenic nerve injury is most likely to occur
if the drain is placed deep in the chest where the phrenic nerve runs over
the mediastinium.
Reference
(1) O. Williams, A Greenough, N Mustafa, S Naugen and GR
Rafferty. Extubation failure due to phrenic nerve injury. Arch Dis Child Fetal Neonatal Ed 2003:88:72-73.
In a recent issue of the journal, Ng et al.
described the endoscopic view of an
congenital epiglottic cyst. We report the recently discovered antenatal vallecular cyst (VC). [1]
The incidence of VC is low.[2] We discovered this case of
congenital VC at 25 weeks of gestation, diagnosed on routine
ultrasound survey for polyhydramnios. An axial scan of the
oropharyngeal region showed a cystic mas...
In a recent issue of the journal, Ng et al.
described the endoscopic view of an
congenital epiglottic cyst. We report the recently discovered antenatal vallecular cyst (VC). [1]
The incidence of VC is low.[2] We discovered this case of
congenital VC at 25 weeks of gestation, diagnosed on routine
ultrasound survey for polyhydramnios. An axial scan of the
oropharyngeal region showed a cystic mass (35 x 30 mm) that
appeared to be intimately attached to the base of the tongue,
and a colour Doppler study showed that there was no
neovasularisation. A diagnosis of VC was
suggested. At 33 weeks, on the basis of an important
polyhydramios, a caesarean section was carried out. Just after birth, the baby could not cry. The cyst was partly
drained with a syringe and the airway was stabilised with
intubation. Marsupialisation of the VC using nasotracheal
intubation was performed on the 10th of life.
An awareness of the existence of VCs is important because they
can cause upper airway obstruction.[3] The widespread use of
prenatal ultrasound can lead to an earlier diagnosis of a VC and
allows for appropriate counselling and preparation at
delivery and for the proper preparation of staff and
equipment in the management of these neonates.[4,5] It allows the obstetrician to collaborate with the neonatologist,
paediatric surgeon, and paediatric otolaryngologist in order to
plan for perinatal management. It also allows an explanation to
be given to the parents, the time and place of delivery to
be decided, and planning for resuscitative efforts to be
organised in advance.
References
(1) Ng SK , Abdullah VJ, van Hasselt CA. Congenital epiglottic cyst. Arch Dis Child Fetal Neonatal Ed 2002;86:F134.
(2) Amagasu M, Lee D, Bluestone CD. Imaging quiz case
one. Vallecular cyst. Arch Otolaryngol Head Neck 1999;125:592-5.
(3) Myer CM. Vallecular cyst in the newborn. Ear Nose
Throat J 1988;67:122-4.
(4) Gluckman PG, Chu TW, Van Hasselt CA. Neonatal
vallecular cysts and failure to thrive. J Laryngol Otol 1992;106:448-9.
(5) Oluwole M. Congenital vallecular cyst: a cause of
failure to thrive. Br J Clin Pract 1996 Apr-May;50(3):170.
The paper by Wardle et al brings the interesting concept of use of
peripheral fractional oxygen extraction to guide the blood transfusion in
preterm infants in clinical practice[1]. The clinical dilemma of deciding
when to and when not to transfuse preterm neonates is always a major
topic of debate amongst professionals involved in caring preterm neonates.
There is a great deal of variation among...
The paper by Wardle et al brings the interesting concept of use of
peripheral fractional oxygen extraction to guide the blood transfusion in
preterm infants in clinical practice[1]. The clinical dilemma of deciding
when to and when not to transfuse preterm neonates is always a major
topic of debate amongst professionals involved in caring preterm neonates.
There is a great deal of variation amongst Neonatologists about the cut
off of hemoglobin or hematocrit levels to be used for transfusions in
preterm babies. There are not many randomised studies in literature to
address this issue, and of the few we know, they have either
methodological limitations or are not published in their full form [2,3,4,5,6].
Therefore, as Wardle et al state, there is no doubt that we need
more studies to produce evidence-based guidelines for blood transfusion in
preterm neonates[1]. These studies should not only look at number of
transfusions, acute mortality and morbidity but also developmental
outcomes at 2-3 years of age.
Can a more serious consideration of physiologic basis assist us in
deciding us about when to transfuse? These might have postulated benefits
in terms of oxygen delivery to the tissues[7].
The risks and benefits of
transfusion include those of maintaining a high or low hemoglobin and some
additional risks and benefits of the transfusion itself. A high hemoglobin
level, maintained by frequent transfusion, enhances arterial oxygen
content and oxygen transport to the tissues. But this is usually far in
excess of need, and so oxygen delivery (equal to oxygen uptake or
consumption) is not limited by hemoglobin content. However, in chronic
ischemic or hypoxic hypoxia, where oxygen delivery may be limited by
oxygen transport, a high hemoglobin may be required to maintain oxygen
delivery to the tissues. Expected consequences of chronic anemic hypoxia
might be thought to be poor growth or impaired neurodevelopmental outcome.
On the other hand, if allowing the hemoglobin to fall to lower levels has
no critical or limiting effects on oxygen delivery, growth and development
will continue unimpaired without the potential adverse effects of blood
transfusion, such as transfusion-borne infection or iron overload. Even
further complicating these physiologic considerations is the decrease in
oxygen affinity of hemoglobin with postnatal age, which increases the
ability of the blood to deliver oxygen, and the effect of transfusion of
adult hemoglobin, which enhances this effect.
While reading the paper by Wardle et al raised several questions in
my mind.
(1) In the abstract of article it is stated that the primary outcome
measures were number of transfusion received, rate of weight gain, and
postmenstrual age at discharge. In contradiction to this in the main
methodology details of article authors state single primary outcome
measure as, “number of transfusions received after randomization”, and all
other were secondary outcome measures.
(2) The first criterion stated in Group 1 (Conventional Group) for
transfusion, “ transfused at Hb of 140g/L if inspired oxygen concentration
>0.35 or mean airway pressure >6 cm of water” appears liberal.
(3) It is stated that one of the transfusion criterion set for Group 2
(NIRS Group), “ transfused at FOE >0.47”. In “blinding” paragraph it is
stated that, “forearm FOE measurements were made on all infants in both
groups, these results were only available to researchers and not to the
clinical team”. This statement implies that clinicians were not aware or
notified of the FOE values even in “NIRS Group”.
(4) The frequency of Hb measurement by authors is described as, “daily in
first week of monitoring, then about 4 times a week until the infant was
30 weeks postconceptional age, and then about twice a week”. Going through
the paper it is evident that these infants were enrolled in to study when
they were not ventilated or ventilated with FIO2 <_40 and="and" the="the" postnatal="postnatal" median="median" age="age" at="at" randomization="randomization" was="was" _5days.="_5days." taking="taking" these="these" two="two" facts="facts" in="in" to="to" account="account" i="i" think="think" frequency="frequency" of="of" hb="hb" monitoring="monitoring" during="during" study="study" very="very" frequent="frequent" contributing="contributing" excess="excess" iatrogenic="iatrogenic" blood="blood" loss.br="loss.br"/>
(5) In the footnote of Table 1, it is mentioned that the results are
given as “median (range)”. For example, birthweight in grams in NIRS group
1200 (range1004-1373). The reader will interpret this as the baby in this
group with lowest weight at 1004 gram. But as you go through the table
later it is mentioned that 9 infants were £ 1000 gram. It is left to the
poor reader to make a serious thoughtful effort to interpret this “range”
in reality means ‘interquartile range”.
(6) In discussion authors state that many infants in NIRS group were
transfused on by clinicians because of low Hb or clinical symptoms, even
though FOE was not >0.47. Authors state that these clinical symptoms
could have been due to clinical reasons other than anemia such as
infection. It would have been useful if authors had given us some data
about infection rate differences in two groups knowing that this is a
prospective study.
References
(1) Wardle SP, Garr R, Yoxall CW, Weindling AM. A pilot randomised
controlled trial of peripheral fractional oxygen extraction to guide blood
transfusions in preterm infants. Arch Dis Child Fetal Neonatal Ed 2002;
86:F22-27.
(2) Blank JP, Sheagren TG, Vajaria J, Mangurten HH, Benawra RS,
Puppala BL. The role of RBC transfusion in the premature infant.
Am.J.Dis.Child. 1984; 138:831-833.
(3) Ransome OJ, Moosa EA, Mothebe FM, Spector I. Are regular 'top-up'
transfusions necessary in otherwise well, growing premature infants? S Afr
Med J. 1989; 75:165-166.
(4) Connelly RJ, Stone SH, Whyte RK. Early vs. late red cell transfusion in
low birth weight infants. Pediatr Res 1998; 43: 170A.
(5) Bell EF, Strauss RG, Widness JA, Mahoney LT, Mock DM, Seward VJ, et al.
Choice of hematocrit threshold for erythrocyte transfusion in preterm
infants. Pediatric Res.2000; 47:389A.
(6) Bifano EM, Bode MM, D’Eugenio DB. Prospective randomized trial of high
vs. low hematocrit in ELBW Infants: One-year growth and neurodevelopmental
outcome. Pediatr Res 2002; 51:325A.
(7) Andersen C. Critical haemoglobin thresholds in premature infants. Arch
Dis Child Fetal Neonatal Ed. 2001; 84:F146-148.
Walker et al.[1] have highlighted the diversity in practice in the management of sick neonates with established meconium aspiration syndrome (MAS) and refractory pulmonary hypertension. We report our experience with five infants, among 1419 neonatal admissions, who required transfer for ECMO support between 1998-2002.
Table 1 gives the summary of the cases. Infant 2 developed progressive respiratory...
Walker et al.[1] have highlighted the diversity in practice in the management of sick neonates with established meconium aspiration syndrome (MAS) and refractory pulmonary hypertension. We report our experience with five infants, among 1419 neonatal admissions, who required transfer for ECMO support between 1998-2002.
Table 1 gives the summary of the cases. Infant 2 developed progressive respiratory distress at 18 hours of age and died after 4 days on ECMO. Infant 3 with congenital diaphragmatic hernia (CDH) had a mean pH of 7.24 (range 7.13-7.3) prior to transfer and showed a poor response to Tolazoline and Magnesium sulphate therapy. He received Inhaled Nitric Oxide (iNO) following transfer and was on ECMO support for 4 days prior to surgery. Infant 5 developed progressive respiratory distress with the clinical and radiological evidence of severe Surfactant Deficiency Lung Disease (SDLD). Progressive hypoxaemia and metabolic acidosis were unresponsive to alkali therapy and administration of iNO (portable iNO) brought some improvement. All infants received surfactant and required inotrope support before and during transport. All infants had normal core temperature and blood pressure at transfer. Oxygenation Index >40 is considered a clear evidence of inadequate oxygenation.[2] In our infants (OI >40) transfer for ECMO was considered when hypoxaemia showed poor response to conventional ventilation. Most district general hospitals have no access to iNO or HFOV. Faced with a sick infant with persistent hypoxaemia , there are limited options for further treatment. We would like to support the recommendation that in these infants ECMO should be considered early and would like to add that adequate attention should be given to inotrope support, acid base balance and maintenance of normothermia prior to the arrival of transport team.
Table 1 Summary of events prior to E.C.M.O transfer and immediate outcome
Characteristics
Infant 1
Infant 2
Infant 3
Infant 4
Infant 5
Diagnosis
MAS
GBS infection
CDH
MAS
PPHN
Sex
Male
Male
Female
Male
Male
Birth Weight (g)
3720
3540
4100
2950
3100
Mode of Delivery
N
N
LSCS
LSCS
LSCS
Age at intubation (h)
1
20
Birth
2
25
Oxygenation Index (OI)
43
40.6
44.9
40.8
54.1
pH
7.33
7.43
7.22
7.39
7.27
PCO2
5.34
3.1
4.87
4.33
5.4
Age at transfer (h)
7
36
9
12
39
Duration of ECMO (d)
3
4
5
3
4
Outcome
Survived
Died
Survived
Survived
Survived
Footnote
MAS- Meconium Aspiration Syndrome
GBS- Group B Streptococcus
CDH- Congenital Diaphragmatic Hernia
PPHN- Persistent Pulmonary Hypertension of Newborn
LSCS- Lower Segment Caesarean Section
References
(1) Walker GM, Coutts JAP, Skeoch C, Davis CF. Paediatricians’ perception of the use of extracorporeal membrane oxygenation to treat meconium aspiration syndrome. Arch Dis Child Fetal Neonatal Ed 2003;88:F70-F71
(2) Field D. Management of persistent pulmonary hypertension of the newborn. Current Paediatrics (Mini-symposium: Neonatology) 1997;7:73-77.
Dear Editor
Dr da Costa et al, and Dr Gatrad in his accompanying commentary [Arch Dis Child Fetal Neonatal Ed 2002;86:F115-9], are mistaken in drawing convulsions about Muslim families in relation to ‘do not resuscitate orders’. Gatrad suggests doctors should receive training in ethical issues of other cultures. Firstly, it is impossible to know the religious or historical or personal background of every parent....
Nitric oxide (NO) is frequently used as a selective pulmonary vasodilator in neonates. Since its metabolite, methaemoglobin can potentially cause tissue hypoxia it is considered mandatory to measure methaemoglobin levels when using NO. In an attempt to review and rationalise our own practice of methaemoglobin measurement when using NO we undertook a search of current literature and conducted a postal surv...
I read with interest the report by Al-Dahhan and colleagues on the beneficial effect of NaC1 supplementation of preterm infants during the neonatal period on their later neurodevelopmental outcome. They found better memory, learning, language and educational performances at the age of 10-13 years in prematures who were given 4-5 mMol/day NaC2 when compared to those not receiving NaC1 supplement.[1] In th...
Me thinks Professor Sulyok doth protest too much. His early, pioneering work on electrolyte balance in the newborn is well known (and extensively cited in an earlier review of the subject co-authored by myself.[1] In this, inter alia, his study of the effect of salt supplementation on the renin-angiotensin-aldosterone system [2] is quoted in support of the hypothesis that hyponatraemia in premature infant...
Dear Editor
I read with great interest the article by Shulman.[1] Indeed, orally administered insulin may have a positive effect on gut maturation and mucosal enzyme expression in preterm infants. We have recently demonstrated that human milk is rich in insulin (mean = 60.2 micro U/ml), and that insulin is barely detected in infant formulas.[2] Moreover, we have hypothesized that insulin content of human milk may ha...
To The Editor:
I am familiar with the work of Dr Shehadeh et al. There may indeed be a place for insulin in infant formula. However, before such a step is taken, I believe that it is imperative that appropriate prospective studies be done, including safety monitoring. Although our human pilot study and animal studies suggest there may be a benefical effect of oral insulin, much more work needs to be done...
Dear Editor
We thank Dr Bissenden for his comments regarding our paper.[1] We would suggest that injury to the phrenic nerve is an unusual complication of chest tube placement in neonates because chest tubes are usually inserted to drain a pneumothorax (rather than a pleural effusion as in the case we describe [1]) and hence sited so that the tip lies anteriorally where it most effectively drains air. Phrenic ner...
Dear Editor
In a recent issue of the journal, Ng et al. described the endoscopic view of an congenital epiglottic cyst. We report the recently discovered antenatal vallecular cyst (VC). [1] The incidence of VC is low.[2] We discovered this case of congenital VC at 25 weeks of gestation, diagnosed on routine ultrasound survey for polyhydramnios. An axial scan of the oropharyngeal region showed a cystic mas...
Dear Editor
The paper by Wardle et al brings the interesting concept of use of peripheral fractional oxygen extraction to guide the blood transfusion in preterm infants in clinical practice[1]. The clinical dilemma of deciding when to and when not to transfuse preterm neonates is always a major topic of debate amongst professionals involved in caring preterm neonates. There is a great deal of variation among...
Walker et al.[1] have highlighted the diversity in practice in the management of sick neonates with established meconium aspiration syndrome (MAS) and refractory pulmonary hypertension. We report our experience with five infants, among 1419 neonatal admissions, who required transfer for ECMO support between 1998-2002.
Table 1 gives the summary of the cases. Infant 2 developed progressive respiratory...
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