The letter written by Patole [1] on bullying in neonatal intensive
care units (NICU) is misleading if it is meant to refer to the Neonatal
Intensive Care Unit at The Townsville Hospital. In two years working as
Senior...
The letter written by Patole [1] on bullying in neonatal intensive
care units (NICU) is misleading if it is meant to refer to the Neonatal
Intensive Care Unit at The Townsville Hospital. In two years working as
Senior Registrar I have found this NICU to be an extremely pleasant place
to work and would highly recommend it to paediatric and neonatal trainees
in Australia and overseas.
Like many Australian NICUs we often employ foreign registrars who may have
difficulty adjusting to our Australian way of life where there is less
regard for rank and where we respect the expertise of our (mostly female)
nursing staff.
The routine posing of basic questions to medical and nursing staff on the
morning round is welcomed by most of us as educational. The atmosphere is
supportive and it is hard to imagine someone being upset that the group as
a whole is asked "What are six causes of hyperglycaemia in a preterm
neonate?". However it has been brought to our attention that some foreign
trained doctors do perceive this as bullying, which was never the
intention.
The key response to the implied charge of bullying of registrars in The
Townsville Hospital NICU (formerly Kirwan Hospital for Women NICU) is the
sentence in Dr Koh's letter on "Harmony in the NICU"[2] which states: "It is
tragic and disturbing when a small proportion of doctors interpret
reasonable efforts by both senior nurses and consultants to ensure optimal
care of the babies in NICU as bullying". It appears that to avoid being
labelled as bullies, we must not ask doctors to perform routine tasks of
caring for babies such as filling out pathology forms, reviewing
deteriorating babies and completing discharge summaries. Supobtimal
performance and laziness are not conducive to good relationships between
staff in the NICU.
I have recently conducted a survey of bullying in Australian NICUs. The
preliminary results show that 16% (5 of 32 NICU registrars) of anonymous
respondents to a questionnaire reported that they had felt bullied. The
mean severity of bullying was 2.2 on a scale where 0 was no bullying and 5
was extremely severe bullying.
Any doctor new to a unit can feel uncomfortable in a situation where the
"usual ward policy" is different to what they have previously encountered.
We all need to support our junior colleagues, but the bottom line must
surely be to provide the best care of the babies: any doctors refusing to
do this should seriously consider whether they should be working in a
NICU.
Donna Gandini FRACP
Department of Neonatalogy, The Townsville Hospital, QLD 4814 Australia
References
(1) Patole S. Bullying in neonatal intensive care units: free for all. Arch
Dis Child Fetal Neonatal Ed 2002; 86: F68-70.
(2) Koh THHG, Koh TS. Harmony in the NICU. Arch Dis Child Fetal Neonatal Ed
2002; 86: F68-70.
There is considerable interest surrounding echocardiography on the
neonatal unit as illustrated by the discussion that has followed Dr.
Katumba's recent article.[1] Unfortunately, as neonatologists we have
often tended to rely on anecdotal evidence to support the view that
echocardiography is a useful tool with which to diagnose and monitor
cardiac function in a Neonatal Intensive Care Unit (NICU)....
There is considerable interest surrounding echocardiography on the
neonatal unit as illustrated by the discussion that has followed Dr.
Katumba's recent article.[1] Unfortunately, as neonatologists we have
often tended to rely on anecdotal evidence to support the view that
echocardiography is a useful tool with which to diagnose and monitor
cardiac function in a Neonatal Intensive Care Unit (NICU).
There is very little published data which has been obtained
prospectively and systematically to inform us about who performs
echocardiography on the neonatal unit, why and when such scans are
performed, the range of echocardiographic findings and how they influence
clinical management.[2] A related issue is the reliability of
echocardiography in the hands of neonatologists, who have an interest (but
usually no formal training)in neonatal echocardiography. We believe these
are areas worthy of systematic study and where we hope to provide some
objective data in the near future.
Further information is essential before we can confidently state that
echocardiography is a useful and reliable tool in the hands of
neonatologists.
References
(1) Jasper Katumba-Lunyenya. Neonatal/Infant echocardiography the non
- cardiologist: a personal practice, past present and future. Arch Dis
Child Fetal Neonatal Ed 2002: 86: F55-57.
(2) Evans N. Echocardiography in neonatal intensive care unit in
Australia and New Zealand. J Paediatr Child Health 2000;36,169-71.
It is gratifying to read the experiences of Drs Katumba and McNamara,
which mirror my own exactly. In Australia and New Zealand, 40% of NICUs
now have their primary echocardiography service provided by a
neonatologist[1]. Like Dr Katumba, these neonatologists all stress the
importance of working in close association with a Paediatric Cardiology
Service. This reflects a general shift, which is the move of...
It is gratifying to read the experiences of Drs Katumba and McNamara,
which mirror my own exactly. In Australia and New Zealand, 40% of NICUs
now have their primary echocardiography service provided by a
neonatologist[1]. Like Dr Katumba, these neonatologists all stress the
importance of working in close association with a Paediatric Cardiology
Service. This reflects a general shift, which is the move of ultrasound
beyond its traditional boundaries of being a consultative diagnostic tool
to being an acute 'coal face' diagnostic tool. While there is resistence to
this change from some quarters, neonatology is not the only specialty
where this is happening. For me it is difficult to imagine practicing
without immediate access to ultrasound.
From this position, John Thompson and colleague's dismissal of serial
echocardiography in NICU because there is no evidence it improves outcomes
seems surprising. Using such an argument we would cease doing chest xrays,
blood tests, head ultrasounds, monitoring blood pressure or even clinical
examination, none of which have been rigorously tested or shown to improve
outcomes. We do them because they give us diagnostic information. While
serial echocardiography has not been proven to improve outcomes, it is a
powerful diagnostic tool that has gone a long way in improving our
understanding of newborn disease processes. Work by our group has defined,
in large cohorts of very preterm babies, an abnormal transitional
haemodynamic that includes a period of significant systemic hypoperfusion
that is significantly related to IVH [2], hyperkalaemia[3], abnormal
development at 3 years [4] and mortality [7]. We have also shown both how
limited clinical signs are in detecting this [5,6,7] and how limited our
current circulatory support strategies are in treating this abnormal
haemodynamic[8]. And yes, we have also shown that this abnormal
haemodynamic is probably partly due to immature myocardial function and
its reduced ability to respond to increases in afterload (not yet
published but will be in 2002 North American SPR abstracts).
It is exactly because neonatologists are acquiring echocardiographic
skills that rigorous serial study has been possible. This in turn has
highlighted many misconceptions of traditional thinking about newborn
haemodynamics. Through this better understanding may lie the key to
prevention of adverse outcomes in the babies we care for.
References.
(1) Evans N. Echocardiography in neonatal intensive care unit in Australia
and New Zealand. J Paediatr Child Health 2000;36,169-71
(2) Kluckow M, Evans N. Low superior vena cava flow and intraventricular
haemorrhage in preterm infants. Arch Dis in Child 2000;82: F188-194.
(3) 3. Kluckow M, Evans N. Low systemic blood flow and hyperkalaemia. J
Pediatr
2001;139:227-232
(4) Kluckow M, Evans N. High pulmonary blood flow, the duct and pulmonary
haemorrhage. J Pediatr 2000;137:68-72
(5) Hunt R, Evans N, Kluckow M, Reiger I. Low early superior vena cava flow
and neurodevelopment at 3 years. Pediatr Res 2001;49:336A (abstr)
(6) Kluckow M, Evans N. The relationship between cardiac output and blood
pressure in preterm infants requiring mechanical ventilation. J Pediatr
1996;129:506-512.
(7) Osborn DA, Evans N, Kluckow M. Accuracy of capillary refill time and
blood pressure for detecting low systemic blood flow in preterm babies.
Pediatr Res 2001;49:376A (abstr)
(8) Skelton R, Evans NJ, Smythe J. A blinded comparison of clinical and
echocardiographic evaluation of the preterm infant for patent ductus
arteriosus. J Paediatr Child Health 1994;30:406-11.
(9) Osborn DA, Kluckow M, Evans N. Randomised trial of dobutamine vs
dopamine in preterm infants with low systemic blood flow. J Pediatr 2002,
in press.
I read with great interest the article of Fang et al, who
investigated the relationship between mesenteric response to feeding and
feeding tolerance in preterm infants [1]. In a comparable population, we
reported that the significant increase in velocity in the superior
mesenteric artery after a first feed given during the first week of life
was not influenced by perinatal acute asphyxia, gesta...
I read with great interest the article of Fang et al, who
investigated the relationship between mesenteric response to feeding and
feeding tolerance in preterm infants [1]. In a comparable population, we
reported that the significant increase in velocity in the superior
mesenteric artery after a first feed given during the first week of life
was not influenced by perinatal acute asphyxia, gestational age,
intrauterine growth retardation, early post-natal respiratory distress or
hypotension [2]. In our small cohort, good tolerance to enteral feeds
during the first weeks of life was associated with a greater rise in end
diastolic velocity, which is close to the authors' observation of a
positive correlation between early tolerance to enteral feeds and a lower
index of vascular resistance after the test feed. Two questions
nevertheless seem important: Is a single Doppler measurement of superior
mesenteric artery blood flow sufficient to determine when to feed a "high
risk" preterm infant? And which criteria define the "high risk" infant? As
mentioned by Martinussen et al. [3], preterm infants require a systemic
circulatory adaptation to allow postprandial mesenteric hyperemia, with an
increase in cardiac output and a decrease in blood pressure. The
circumstances associated with hemodynamic instability, as in sepsis, or
elevated baseline cardiac output, as in ductal steal, could thus
compromise the circulatory response to feeding and lead to intolerance. In
our population, we tested numerous biodemographic and clinical factors
suggested by previous research [4], but also a more than 30% increase in
mesenteric diastolic velocity 30 min after a test feed of 4 ml/kg of human
milk, for their relationship to feeding tolerance during the first three
weeks of life. This multilinear regression analysis revealed the
significant positive influence of antenatal steroids and the negative
influences of significant ductus arteriosus, nosocomial infection, and
prolonged ventilatory dependency. The result of the mesenteric profile
after the test feed, however, was not included in the final model. We thus
believe that a single examination of superior mesenteric artery blood flow
velocities after a first feed at the third postnatal day - as suggested by
the authors - is probably insufficient to predict mean term feeding
tolerance and should instead be integrated into a more complete evaluation
of the patient's hemodynamic status. We personally recommend serial
evaluations in cases of ductus persistence or reopening and before enteral
feeding resumption after significant gut disease.
Gilles Cambonie
Neonatal Intensive Care Unit, Hôpital Arnaud de Villeneuve, University Hospital of Montpellier, France.
References
(1) Fang S, Kempley ST, Gamsu HR. Prediction of early tolerance to enteral
feeding in preterm infants by measurement of superior mesenteric artery
blood flow velocity. Arch Dis Child Fetal Neonatal Ed 2001; 85: F42-5.
(2) Cambonie G, Luc F, Montoya F, Sarda P, Rieu D. Mesenteric blood flow in
premature infants. Pediatr Res 1996; 40: 522 (A 46).
(3) Martinussen M, Brubakk AM, Vik T, Yao AC. Mesenteric blood flow
velocity and its relation to transitional circulatory adaptation in
appropriate for gestational age preterm infants. Pediatr Res 1996; 39: 275
-80.
(4) Slagle TA, Gross SJ. Effect of early low-volume enteral substrate on
subsequent feeding tolerance in very low birth weight infants. J Pediatr
1988; 113: 526-31.
I would like to thank Dr Thomson and colleagues for their comments. I
need to clarify on an issue they picked upon which when quoted in
isolation gives the reader the wrong impression. They seem to suggest that
I am advising the reader that inappropriate referrals are “firmly refused”
out of hand. What I actually meant, if you read on, was that one should
refuse to see referrals from other colleagues w...
I would like to thank Dr Thomson and colleagues for their comments. I
need to clarify on an issue they picked upon which when quoted in
isolation gives the reader the wrong impression. They seem to suggest that
I am advising the reader that inappropriate referrals are “firmly refused”
out of hand. What I actually meant, if you read on, was that one should
refuse to see referrals from other colleagues which have not been properly
clinically assessed.
My colleagues have listened to me resulting in a dramatic drop in
numbers of innocent murmurs presenting to my clinic and to the two
outreach clinics run by two cardiologists, one from Oxford and the other
from the Brompton. They are, however, encouraged to refer for
echocardiography if in doubt.
I was a little disturbed by the statement made by Dr Thomson et al
that systolic dysfunction rarely causes hypotension in the neonate in
intensive care. I can not presume to comment on cause of hypotension in
bigger children in PICU, as I never scan this group of patients. There is,
however, no doubt that several authorities believe that poor myocardial
contractility together with "systemic steal" through the often silent
patent ductus arteriosus, and abnormal peripheral vasoregulation are the
three commonest contributors to hypotension in neonates especially the
extreme preterm during the first 24 to 72 hours of extrauterine life
[1-8]. Hypovolaemia, however, is the rarer cause of
hypotension in this setting. A D Gill and A M Weindling [2] recognised the
contribution of poor myocardial contractility to hypotension years ago.
There is a massive volume of authoritative literature to support the above
statements and the February 2001 issue of Seminars in Neonatology co-
edited by Nick Archer and Nick Evans covers this topic extensively as well
as providing a huge source of references. Dr Thomson et al do not give any
references to support his view and I am not personally aware, though I
stand to be corrected, of any such literature in the last few years.
Unlike in the adult and bigger child where it is easy to invasively
assess haemodynamic changes on the ICU, this is not as easily done in the
neonate and echocardiography provides a useful non-invasive tool for this
purpose on the NICU. The duct is also usually "silent" in the first three
to five days even when open and can only be diagnosed by echo. Recent
evidence suggests that ibuprofen is at least as effective as indomethacin
in closing the duct without the co-morbidity (decreased cerebral, renal
and gastrointestinal perfusion etc.) associated with indomethacin [9,10].
This would make medical closure of the duct much more acceptable even for
those paediatricians who have rightly so, hitherto, been worried about the
complications associated with indomethacin therapy.
If one accepts the fact that hypotension is associated with increased
morbidity and mortality [2] and that silent ducts can cause problems in
preterm neonates, then one can reasonably hope that "sequential
echocardiography"[7] during the first 72 hours, and later as necessary,
might reduce morbidity and mortality by improving assessment and
management of these problems.
Moreover Paediatricians and Neonatologists are already voting with
their feet and the Echo course at my tertiary centre is usually
oversubscribed by 100% because they are beginning to recognise usefulness
of echocardiography in neonatology.
I am pleased that the RCPCH SAC in Paediatric Cardiology is looking
at training paediatricians to develop the skills of cardiology but I
sincerely hope that the curriculum will include echocardiographic
assessment of the duct and hypotension in the sick preterm infant and its
impact on management. Not to include it will be a lost opportunity, which
I predict will only have to be redressed later because of the mounting
weight of evidence that echocardiography, is a very useful tool in this
setting.
References (1) Jasper Katumba-Lunyenya. Neonatal/Infant echocardiography the non-
cardiologist: a personal practice, past present and future. Arch Dis Child
Fetal Neonatal Ed 2002: 86: F55-57.
(2) AB Gill, AM Weinding. Echocardiographic assessment of cardiac
function in shocked very low birthweight infants. Arch Dis Child Fetal
Neonatal Ed 1993; 68: 17-21.
(3) Nick Evans. Diagnosis of patent Ductus arteriosus in the preterm
newborn. Arch Dis Child Fetal Neonatal Ed. 1993; 68: 58-63.
(4) Jon Skinner. Diagnosis of patent ductus arteriosus. Semin
Neonatology 2001; 6: 49-61.
(5) Evans N, Moorcroft J. Effect of patency of the ductus on blood
pressure in very preterm infants. Arch Dis Child 1992; 67: 1169-1173.
(6) David B Knight. The treatment of ductus arteriosus in preterm
infants. A review and overview of randomised trials. Semin Neonatal 2001;
6: 63-73.
(7) Martin Kluckow, Nick Evans. Low systemic blood flow in the preterm
infant. Semin Neonatal 2001; 6: 75-84.
(8) Istvan Seri. Circulatory support of the sick preterm infant. Semin
Neonatal 2001; 6: 85-95.
(9) B Van Overmeire et al. A comparison of Ibuprofen and Indomethacin
for closure of Patent Ductus Arteriosus. New England Journal of Medicine;
2000; 343:674-681.
(10) Jayesh Patel, Idris Roberts, Dennis Azzopardi, et al. Randomised
Double – Blind Controlled Trial Comparing the Effects of Ibuprofen with
Indomethacin on Cerebral Haemodynamics in Preterm Infants with Patent
Ductus Arteriousus. Paediatric Research 2000; 47: 36-42.
We read the article by Kumar et al[1] with interest especially in light
of the changing profiles of NICU practices as applicable to a developing
nation with limited resources and lack of uniform parameters for
antibiotic usage, resulting in the emergence of drug resistant strains.
However, the utility of a rapid diagnostic system has to be viewed in the
light of its universal applicability. The cost of s...
We read the article by Kumar et al[1] with interest especially in light
of the changing profiles of NICU practices as applicable to a developing
nation with limited resources and lack of uniform parameters for
antibiotic usage, resulting in the emergence of drug resistant strains.
However, the utility of a rapid diagnostic system has to be viewed in the
light of its universal applicability. The cost of setup and subsequent
maintenance of a rapid culture system like BacT/Alert needs to be looked
into vis a vis the traditional culture methodologies, which still are high
yield relative to their low cost and results are available within 48-72
hours. Appearance of a growth itself can be taken as a decision tool for
continuation of antibiotics pending the subculturing process in an
appropriate clinical scenario. Automation has its advantages but need for
calibration and standardization should not be ignored. Possibilities of
false positive signals do remain and in a scenario of frequent power
failures the performance of such a system may be far from ideal and can
lead to potentially disastrous decisions.
Authors emphasise that the clinical status of the neonate still
remains the most important factor in deciding the management of neonatal
sepsis and therefore, a symptomatic neonate will continue to get
antibiotics even in the absence of laboratory support, for a duration, if
the clinical condition so demands. In asymptomatic neonates, there is need
to have more clear guidelines about the duration of therapy once the
antibiotics were started initially, may be based upon either
symptomatology or high perinatal risk scores. In this study, the authors
have not spelt out the clinical or laboratory criteria utilized after
negative blood culture results at 36 hours, so as to consider presence or
absence of sepsis and to justify continuation or discontinuation of
antibiotics beyond 36 hours, awaiting the final culture report at 72
hours. It will be pertinent for the practice that between 36 and 72 hours
period, the decisions about antibiotic therapy should not be based on
negative culture test at 36 hours alone but must additionally utilize the
rapid diagnostic tests (RDT), like use of IL-6 and C-reactive protein or
TNF alpha. These RDTs have good cumulative accuracies for the diagnosis
and exclusion of sepsis. [2,3] RDTs negativity after 36 hours, in culture
negatives will give additional strength to decision of stopping of
antibiotics. If these RDTs remain positive at 36 hours in culture
negatives, then it will be justified to continue antibiotics till the
final blood culture report becomes available at 72 hours and decision
about antibiotic continuation taken accordingly. Therefore, it will be
interesting to have information from the current study, on clinical
condition and RDTs status of neonates, after obtaining 36 hours report of
culture till 72 hours of life and final decisions about use of
antibiotics. A rapid diagnostic blood culture system is likely to be most
relevant in a clinical scenario of high perinatal sepsis risk score
dictating use of antibiotics [4], asymptomatic neonate and with early
negative RDT. An early negative blood culture result at 36 hours then
could be the gold standard proof for absence of sepsis and mandating
discontinuation of antibiotics in this subset of neonates.
Lastly the study in its retrospective design has limitations of
applicability. There appears to be a bias towards LBW/prematures in the
study, as data regarding term/AGA babies is not available in this study.
The definitive pathogens in term babies are likely to be different and
there may not be predominance of coagulase negative staphylococcus in
them.
References:
(1) Kumar Y, Qunibi M, Neal TJ, Yoxall CW Time to positivity of neonatal
blood cultures. Arch Dis Child Fetal Neonatal Ed 2001 Nov;85(3):F182-6
(2) Ng PC, Cheng SH, Chui KM, Fok TF, Wong MY, Wong W, Wong RP, Cheung
KL.Diagnosis of late onset neonatal sepsis with cytokines, adhesion
molecule, and C-reactive protein in preterm very low birthweight infants.
Arch Dis Child Fetal Neonatal Ed 1997 Nov;77(3):F221-7)
(3) Philip AG, Mills PC Use of C-reactive protein in minimizing antibiotic
exposure: experience with infants initially admitted to a well-baby
nursery. Pediatrics 2000 Jul;106(1):E4
(4) Singh M, Narang A, Bhakoo ON Predictive perinatal score in the
diagnosis of neonatal sepsis J Trop Pediatr 1994 Dec;40(6):365-8
Dr Katumba-Lunyenya rightly recognises that management of common
cardiological problems in neonates is beyond the resource provision for
congenital heart disease specialists in the UK. The author also realises
that along with the echocardiographic skills come the “innappropriate
referrals”. Sadly there is no doubt that the increased reliance on
investigations of all types (particularly the echocardi...
Dr Katumba-Lunyenya rightly recognises that management of common
cardiological problems in neonates is beyond the resource provision for
congenital heart disease specialists in the UK. The author also realises
that along with the echocardiographic skills come the “innappropriate
referrals”. Sadly there is no doubt that the increased reliance on
investigations of all types (particularly the echocardiogram) has been
mirrored by a decline in cardiac clinical skills amongst paediatricians of
all grades.
In some of our outpatient clinics (Yorkshire heart centre) over 50% of new
referrals from specialist paediatric staff are innocent murmurs. Our data
support the view that these referrals (described as innappropriate by the
author) are increasing from both District and Teaching hospitals and that
a high proportion come from junior doctors, the patient having been
examined only once (during an intercurrent illness) and often not seen by
a consultant. If we were to follow the authors advice we would be “firmly
refusing” hundreds of referrals. Similar problems arise on neonatal
intensive care units, and whilst the echocardiogram can be a powerful
diagnostic tool in this setting, there is no evidence base to suggest that
serial echocardiography improves outcome in neonates. Systolic dysfunction
is rarely a cause of hypotension in children or neonates on intensive care
units and ultrasound is of very limited value in the assessment of
ventricular filling in this setting.
The RCP SAC in Paediatric Cardiology recognises the implications of
increasing demands on paediatric cardiac services. With the Royal College
of Paediatrics and Child Health a working party has been established to
develop a curriculum of training for paediatricians with a special
expertise in paediatric cardiology to increase the opportunities for
paediatricians to develop clinical skills in cardiology (of which
echocardiography is just one) relevant to the management of these
patients.
Dr John Thomson
Specialist registrar and trainee representative SAC Paediatric Cardiology
Dr John Gibbs
Consultant paediatric cardiologist and secretary SAC Paediatric Cardiology
Both Yorkshire heart centre, Leeds general infirmary NHS Trust.
Dr Sue Hobbins
Consultant Paediatrician with special expertise in Paediatric Cardiology
and RCPCH representative on SAC in paediatric cardiology.
Bromley Hospitals NHS Trust.
I would like to thank Dr McNamara for his useful comments about my
paper. It is quite clear from his letter, however, that his degree of
development of the skill of echocardiography is way beyond that required
by a neonatologist. This needs to be emphasised lest neonatologists are
put off for fear of having to go for formal retraining to achieve the
obviously very advanced level of scanning like D...
I would like to thank Dr McNamara for his useful comments about my
paper. It is quite clear from his letter, however, that his degree of
development of the skill of echocardiography is way beyond that required
by a neonatologist. This needs to be emphasised lest neonatologists are
put off for fear of having to go for formal retraining to achieve the
obviously very advanced level of scanning like Dr McNamara’s. He lists
“novel echocardiographic methods” like acoustic quantification, three
dimensional echo, and tissue Doppler [2] in his repertoire. These are not
standard echocadiographical techniques even for the paediatric
cardiologist in the UK and the neonatologist need not worry about the cost
to acquire such equipment nor the expertise to use it. One does not need
such a sophisticated machine to scan neonates, and for less than £50,000-
00 one can acquire a respectable 2D machine with colour and Doppler [1]
that will do all that is required for good up-to-date neonatal
cardiological studies. Some very good short Echocardiography courses are
available in the UK for the non-cardiologist and if these are followed by
frequent scanning using the disciplined method of “sequential chamber
localisation”[3], then one will soon make progress. Like Dr McNamara I
found that frequent scanning enhanced my skills during the earlier days.
I agree with Dr McNamara about the need to recognise one’s
limitations and the need to involve the paediatric cardiologist early.
This is mentioned several times in my article. The availability of
Telemedicine makes it even easier to consult [1,4,5,6]. A recent
experience on our unit demonstrates this very well, as described below.
After a very long and tiring joint cardiology clinic with a
paediatric cardiologist from a tertiary centre, I tried to sneak into my
office at about 1830hrs without being noticed as I was not on call that
night. This was wishful thinking, however, as my presence got noticed by
one of our Senior Staff Nurses who immediately made off very rapidly in
the opposite direction. She returned just as rapidly with a Staff Grade
Paediatrician, an SHO, and two Medical Students in tow. Breathlessly she
pronounced that they had a “blue baby” and could I have a look. The senior
on call that night was on his way in and I knew that he would not mind my
intrusion, as he could not scan. I soon discovered the atretic pulmonary
artery, intact ventricular septum and the barely patent ductus arteriosus.
I was ordering a prostin (Dinoprostone) infusion when my deeply relieved
colleague walked in. I made video recording of my findings and left for
home. My colleague subsequently transmitted the pictures to the paediatric
cardiologist via telelink at the tertiary centre. In the event the infant
was saturating normally on self-ventilation in air, had normal gases and
blood pressure by the time of transmission. During the ensuing discussion
with the cardiologist the diagnosis was confirmed and it was agreed that
the infant be transferred electively the following morning. Telemedicine
will enhance the safety of this skill being performed by the non-
cardiologist because of the ease of consultation. Availability of this
facility should go a long way towards satisfying even the most hardened
doubters.
Dr McNamara also revisits the issue of “working in the dark” while
managing neonatal haemodynamic problems. I do not think that
neonatologists can resist, or indeed continue to denigrate the acquisition
of echocardiographic skills for much longer. The case for acquiring the
skill by at least one in-house neonatologist at NICUs that manage the very
preterm neonate is overwhelming.
I am encouraged to hear that neonatologists form other parts of the
world, like Dr McNamara originally from Belfast and now in Toronto,
Canada, are developing this skill which can only be good for the neonate.
Jasper Katumba-Lunyenya
Paediatrician
References (1) Katumba-Lunyenya JL. Neonatal/infant echocardiography by the non-
cardiologist: a personal practice, past, present, and future. Arc Dis
Child Fetal Neonatal Ed 2002:86 F55-F57.
(2) Patrick J McNamara. The Forgotten Organ on NICU. ELetters ADC 7th
February 02.
(3) Skinner J, Alverson D, Hunter S: Echocardiography for the
neonatologist. Edinburgh: Churchill-Livingstone, 2000:174-9.
(4) Casey FA. Telemedicine in paediatric cardiology. Arch Dis Child
1999; 80:497-9.
(5) Rundolph GR, Hagler DJ, Khanderina BK, et al. Remote telemedical
interpretation of neonatal echocardiograms: impact on clinical management
in a primary setting. J Am Coll Cardiol 1999; 34:241-5.
(6) Mulholland HC, Casey F, Brown D, et al. Application of a low cost
telemdicine link to the diagnosis of congenital heart defects by remote
consultation. Heart 1999; 82:217-21.
The personal experience by Katumba-Lunyenya echoes the views and
experiences of many contemporary neonatologists who recognize the
importance of routine echocardiography as an integral part of neonatal
intensive care [1]. Oftentimes the importance of routine echocardiography in
the management of the sick preterm or term infant is underestimated. The
echocardiographic needs of a large neonatal intensive c...
The personal experience by Katumba-Lunyenya echoes the views and
experiences of many contemporary neonatologists who recognize the
importance of routine echocardiography as an integral part of neonatal
intensive care [1]. Oftentimes the importance of routine echocardiography in
the management of the sick preterm or term infant is underestimated. The
echocardiographic needs of a large neonatal intensive care unit could
potentially cripple any cardiology service. Some neonatologists continue
to "work in the dark" when confronted with common problems such as
hypotension, pulmonary hypertension and the silent ductus arteriosus. The
impact of a hemodynamically significant patent ductus arteriosus (PDA) on
blood pressure and consequently cerebral and systemic perfusion is well-
recognized [2,3]. In very low birth weight infants the characteristic signs
of a clinically significant PDA on which may neonatologists rely, such as
bounding pulses and wide pulse pressure, are unreliable as the immature
heart is not able to compensate for the large left to right shunt by
maintaining systolic blood pressure [3]. Without serial echocardiography in
the early perinatal period therapeutic intervention is often delayed until
the appearance of a murmur by which time the effects of systemic
hypoperfusion include necrotizing enterocolitis [4], ischaemic cerebral
white matter disease and intraventricular hemorrhage have occurred [5]. A
targeted approach to the management of the ductus arteriosus based on the
early identification of suitable echocardiographic markers may minimise
complications. This article also highlights the importance of regular
echocardiography in the management of the "blue baby" which commonly leads
to misdiagnosis and inappropriate therapeutic intervention when
conventional methods are used. The benefits are twofold; by
differentiating duct dependant cyanotic heart disease from persistent
pulmonary hypertension of the newborn and when the latter is diagnosed by
monitoring pulmonary pressure and left ventricular function and gauging
the response to therapeutic interventions such as inotropes and Nitric
Oxide. Routine screening for the ductus arteriosus, monitoring pulmonary
pressure and ventricular function, tracking central venous and arterial
line position and diagnosing pericardial effusions before the onset of
catastrophic haemodynamic collapse in high-risk neonates would impose a
great burden on paediatric cardiology resources leading one to conclude
that they would be best performed by a neonatologist with a dedicated
interest in perinatal cardiology and skilled in echocardiographic methods.
One must tread with caution however and recognise our limitations
particularly with respect to the management of complex structural heart
lesions. Katumba-Lunyenyaa tabulates a comprehensive list of cardiac
lesions diagnosed at his institution which deserves credit however it must
be stressed that all neonates with potential structural cardiac problems
need urgent referral to a paediatric cardiologist for appropriate
investigation and counselling. It is vitally important that the role and
expertise of the paediatric cardiologist remains paramount to the
management of these patients.
Pediatric cardiologists in the past have raised great concerns that
in the wrong hands this "tool" may be potentially dangerous and without
appropriate training and supervision this may indeed be the case. I can
share a personal experience of a 3-day-old term infant of a diabetic
mother who presented on day 3 of life with respiratory distress and
cardiomegaly on chest x-ray. I performed an echocardiogram, which revealed
a large PDA, perimembranous ventricular septal defect (VSD) and postductal
coarctation of the descending aorta. The child was referred to the
regional pediatric cardiology center that diagnosed a PDA with a
perimembranous VSD and recommended treatment with diuretics and an ACE
inhibitor. The clinical course deteriorated over the ensuing 3-4 days and
when the patient needed to be intubated for cardiorespiratory support the
child was referred back to the tertiary cardiac center. A decision was
made to perform ductal ligation however following the procedure the child
became profoundly hypotensive and when further exploratory surgery was
performed a coarctation of the aorta was diagnosed. Postoperatively the
patient developed multiorgan failure and eventually died. I share this
case with your readers not to criticize the management by the tertiary
cardiac center but to highlight the valuable contribution a neonatologist
competent in echocardiography has to the management of sick newborns. My
personal associations with echocardiography began as a senior house
officer at Royal Maternity hospital, Belfast in 1995 and over the last
seven years my skills have improved under the supervision of several
neonatologists, pediatric cardiologists and echocardiography technicians
who have helped me achieve my level of competency. Like Dr Katumba-
Lunyenya it took me time to successfully reach the point where I could
obtain clear reproducible images and confidently recognize normal cardiac
anatomy. However since negotiating that steep part of the learning curve
I have accumulated a portfolio of diverse cardiac abnormalities by
regularly (oftentimes 10-20 scans per week) performing detailed heart
scans on suitable patients. It has often been said in the centers I have
worked that "I am attached by an umbilical cord to the echo-machine". My
enthusiasm and desire to stress the importance of regular echocardiography
and develop the role of the neonatologist as a competent echocardiographer
has led me to cross the Atlantic to further my knowledge and skills. I am
currently working as a research fellow in collaboration with the
paediatric cardiologists at the Hospital for Sick Children, Toronto,
Canada and using novel echocardiographic methods such as acoustic
quantification, three-dimenisonal echocardiography and Tissue Doppler
imaging to assess ventricular function in neonates.
I firmly believe that the role of the modern neonatologist, armed
with his/her comprehensive knowledge of the individualistic clinical
problems of each patient and the additional benefits of experience in
neonatal echocardiography, potentially compliments the role of the
pediatric cardiologist in a neonatal intensive care setting. My views and
experiences are stereotypical of a new generation of neonatologists who
recognize the importance of routine neonatal echocardiography and also the
lack of appropriate consideration for cardiac related problems in the
newborn period. Unfortunately the heart is oftentimes the "forgotten
organ" with current research interests concentrating on brain, lungs and
bowel disease. The time has come to reconsider the training needs of
physicians interested in neonatal medicine to address these fundamentally
important issues. All specialist registrars should be given the
opportunity to spend a predetermined period of time in a formal training
programme under the supervision of experienced pediatric cardiologists and
neonatologists with expertise in perinatal cardiology and
echocardiography. The programme should include focused teaching of
cardiovascular physiology and the transitional circulation, fetal
medicine, assessment of ventricular function and pulmonary hemodynamics,
identification of common structural heart defects as well as supervised
"hands-on" echocardiography. The longterm benefits to both patient care
and the evolving link between neonatology and pediatric cardiology will be
great.
References (1) Katumba-Lunyenya. Neonatal/infant echocardiography by the non-
cardiologist: a personal practice, past, present and future
(2) Ratner I, Perelmunter B, Toews W, Whitfield J. Association of low
systolic and diastolic blood pressure with significant patent ductus
arteriosus. Pediatrics 1985; 13:497-500
(3) Evans N, Moorcraft J. Effect of patency of the ductus arteriosus on
blood pressure in very preterm infants. Arch Dis Child 1992; 67:1169-1173.
(4) Ryder RW, Shelton JD, Guinan ME. Necrotising enterocolitis: A
prospective multicenter investigation. Am J Epidemiol 1980; 112:113-23
(5) Lipman B, Server GA, Brazy JE. Abnormal cerebral hemodynamics in
preterm infants with patent ductus arteriosus. J Pediatr 1982; 112:113-23
We have read with interest the article by Oddie et al [1] and
subsequent correspondence from Williams [2], Harding et al [3] about
weighing breast fed babies. With the ongoing shortage of midwives
throughout the UK, staffing levels on postnatal wards are low. We are
increasingly worried about the decline in support available to mothers
trying to establish lactation in the days immediately after delivery...
We have read with interest the article by Oddie et al [1] and
subsequent correspondence from Williams [2], Harding et al [3] about
weighing breast fed babies. With the ongoing shortage of midwives
throughout the UK, staffing levels on postnatal wards are low. We are
increasingly worried about the decline in support available to mothers
trying to establish lactation in the days immediately after delivery.
Early postnatal discharge from maternity units is now the norm, usually
within 24 hours of delivery, and by 48-72 hours after LSCS in our
hospital.
We report 3 breast fed term infants who have presented within the past 6
months with profound hypoglycaemia, neonatal convulsions and significant
dehydration which we attribute to undernutrition in the first 3 days after
birth.
All 3 infants have abnormal MRI changes compatible with white matter
infarction secondary to hypoglycaemia and all are showing signs of
significant neurodevelopmental delay within 6 months of birth. Neither the
mothers nor midwives recognised any worrying signs in the infants' pattern
of suckling, tone or state of alertness until the onset of convulsions (2
infants), and repeated cyanotic episodes (1 infant).
Case 1
A 4 day old infant (birth weight 4320g, OFC 37 cm) presented with a 48
hour history of poor feeding and jitteriness.The baby was severely
dehydrated with a weight loss of 18% since birth. Convulsions commenced
soon after presentation. Laboratory blood sugar was unrecordable, Hb 19.2
g/dl, Na 154 mmol/l, creatinine 116 umol/l, urea 27.8 umol/l. The baby had
been discharged from hospital at 7 hours of age after a spontaneous,
uncomplictaed vaginal delivery at term, and the baby was breast fed.
Emergency resuscitation was required and intensive care for 4 days. No
underlying infective or metabolic cause was identified, although insulin
levels were not measured at the time of presentation when the infant was
hypoglycaemic. Thrombophilia screen was normal. MRI scan of brain at 13
days of age revealed a widespread abnormal signal intensity throughout the
white matter consistent with parasagittal infarction, a pattern recognised
in hypoglycaemic brain injury. EEG at 3 weeks of age was abnormal and the
infant has required ongoing anti-convulsants for clinical seizures. OFC
has fallen from 90th to 25th centile by 2 months of age.
Case 2
An infant (birth weight 2550gm, OFC 33.5 cm) was transferred to NICU at 70
hours of age after a cyanotic episode on the postnatal ward. The baby had
been delivered by semi-emergency LSCS because of growth restriction and
CTG signs consistent with placental insufficency at 39 weeks gestation,
but was in good condition at birth (Apgar scores 8 @ 1;10 @ 5 mins).
Laboratory blood glucose was unrecordable on admission to NICU.
Normoglycaemia was restored with an intravenous infusion of 10 % dextrose
(7 mg/kg/min). Weight loss of 12% since birth was documented on admission
to NICU. At 80 hours of age, a left sided focal convulsion occurred. No
infective or metabolic cause was identified apart from hypoglycaemia. The
baby had been breast fed. Cranial ultrasound on day 4 revealed a bright
echodensity in the caudothalamic notch. MRI scan of brain on day 5 showed
multiple haemorrhagic lesions in the white matter consistent with
hypoglycaemic brain injury. In addition there was a small infarct in the
right lentiform nucleus extending into the internal capsule. The aetiology
of the infarct is uncertain and the results of the thrombophilia screen
are awaited.
Case 3
A 60 hour old infant (birth weight 2760g, OFC 31.7 cm) was admitted with
lethargy, poor feeding and convulsions within 9 hours of discharge home
from the postnatal ward. He had been born by semi-elective LSCS because of
failing fetal growth and oligohydramnios. No resuscitation was required at
birth. Apgar scores were 9 @ 1;10 @ 5mins. He was breast fed. Laboratory
blood sugar was unrecordable on readmission. An intravenous infusion of
glucose at 13 mg/kg/min restored normoglycaemia. Weight loss of 6% from
birth was documented. Infection, metabolic and thrombophilia screen
revealed no other abnormality. MRI scan of brain at 11 days of age showed
posterior and temporal white matter infarction consistent with
hypoglycaemic brain injury. OFC has fallen from 10th to well below 3rd
centile by 7 months of age and he has significant neurodevelopment delay.
These 3 infants presented with significant hypoglycaemia within 4
days of birth and all have abnormal MRI scans consistent with
hypoglycaemic brain injury. Transient hyperinsulinaemia was not excluded
in any of the infants as insulin levels were not measured at the time of
initial presentation with hypoglycaemia.The glucose requirement to restore
normoglycaemia was not particularly high, however, and as there was no
recurrence of hypoglycaemia in any of the infants after commencing the
infusion of glucose, transient hyperinsulinaemia seems unlikely. Two
infants (cases 2 and 3) were delivered by LSCS because of signs of
placental insufficiency, and therefore may have been at risk of
hypoglycaemia, but as they were in good condition at birth and birthweight
was not <10th centile, the mothers and infants all received "normal"
postnatal care. The reason for the hypoglycaemia in case 1 is unclear. The
mother showed no overt signs of gestational diabetes, and transient
hyperinsulinaemia remains a possible explanation. No other underlying
pathology in the infants was demonstrated. All infants are showing signs
of neurodevelopmental delay and feeding problems and two have developed
microcephaly. Because of the concomitant weight loss (> 12 % in cases 1
and 2), we have concluded that undernutrition whilst attempting to
establish lactation is the most likely cause of the hypoglycaemia.
We are painfully aware that there is a low midwife/ mother ratio on
our postnatal ward and that mothers may not always be able to receive
optimal supervision and support whilst attempting to establish lactation.
The use of lay breast counsellers and appropriately trained health care
assistants to support breast feeding mothers, particularly primipara and
mothers who may benefit from additional support after LSCS, is being
explored. We support the view of Williams that experienced midwives can
assess the establishment of lactation and clinical hydration of the baby
by observation of feeding pattern and other clinical signs without having
to resort to early weighing. However, there is a national shortage of
midwives and we believe that very few maternity units have sufficient
midwives to provide optimal support for all mothers to establish
successful lactation. Discussion with other paediatric colleagues suggests
that they are also seeing a resurgence of dehydration and hypoglycaemia in
a small number of breast fed term infants.
Healthy term breast fed babies have been shown to tolerate
asymptomatic hypoglycaemia during early lactation (4), but infants at risk
of hypoglycaemia because of fetal undernutrition may require additional
feeding or glucose intake in the first few days after birth. Birth weight
<10th centile is commonly used to identify babies who might benefit
from routine blood glucose monitoring in the first few days after birth,
but it is only a crude indicator of which babies may be at risk of
hypoglycaemia, particularly if postnatal nutrition is inadequate. Clear
guidelines for health care workers about the clinical assessment of
adequacy of breast feeds to include observation of suckling pattern, state
of alertness, frequency of stools and wet nappies, particularly after 12
hours of age, may help to prevent dehydration and hypoglycaemia. We would
not dismiss the potential benefit of weighing some, but not all, breast
fed babies on 2nd or 3rd day after birth, as this may identify babies with
significant weight loss before more serious symptoms develop. The
challenge remains to prevent serious complications in a minority of
potentially vulnerable infants without undermining the establishment of
successful breast feeding for the majority of normal term infants.
R Thomas
F Isaza
W Hyer
References
(1) Oddie S, Richmond S, Coulthard M. Hypernatraemic dehydration and breast
feeding: a population study. Arch Dis Child 2001;85: 318-320.
(2) Williams A . Weighing breast fed babies. Arch Dis Child Fetal Neonatal
Ed 2001;86:F69.
(3) Harding D, Cairns P, Gupta S, et al. Hypernatraemia: why bother
weighing breast fed babies? Arch Dis Child Fetal Neonatal Ed 2000;85:145.
(4) Hawdon J, Ward Platt M P, Aynsley-Green A. Patterns of metabolic
adaptation for preterm and term infants in the first neonatal week. Arch
Dis Child 1992;67:357-365.
NB This letter is also in response to Dr Koh's letter on the same topic (click link for access):
http://adc.bmjjournals.com/cgi/content/full/fetalneonatal;86/1/F68-a
Dear Editor
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There is considerable interest surrounding echocardiography on the neonatal unit as illustrated by the discussion that has followed Dr. Katumba's recent article.[1] Unfortunately, as neonatologists we have often tended to rely on anecdotal evidence to support the view that echocardiography is a useful tool with which to diagnose and monitor cardiac function in a Neonatal Intensive Care Unit (NICU)....
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Dear Editor
The personal experience by Katumba-Lunyenya echoes the views and experiences of many contemporary neonatologists who recognize the importance of routine echocardiography as an integral part of neonatal intensive care [1]. Oftentimes the importance of routine echocardiography in the management of the sick preterm or term infant is underestimated. The echocardiographic needs of a large neonatal intensive c...
Dear Editor
We have read with interest the article by Oddie et al [1] and subsequent correspondence from Williams [2], Harding et al [3] about weighing breast fed babies. With the ongoing shortage of midwives throughout the UK, staffing levels on postnatal wards are low. We are increasingly worried about the decline in support available to mothers trying to establish lactation in the days immediately after delivery...
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