Management of Neonatal Respiratory Distress Syndrome

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Transcript Management of Neonatal Respiratory Distress Syndrome

Management of Neonatal
Respiratory Distress Syndrome
European Consensus Guidelines 2010 Update
Ola Didrik Saugstad, MD
Department of Pediatric Research
Oslo University Hospital, University of Oslo, Norway
Kiev, Nov 30th 2011
European Guidelines on RDS: 2010
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European panel of experts convened under
auspices of EAPM to develop evidence-based
guidelines on management of RDS. Supported
by an unrestricted educational grant from Chiesi
Farmaceutici but none of the panel members
received honoraria for their contributions.
HLH and CPS are consultants to Chiesi
ODS and VPC members of the Chiesi Advisory Board
European Consensus Guideline Panel
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Virgilio Carnielli
Gorm Griesen
Henry Halliday
Mikko Hallman
Eren Ozek
Richard Plavka
Ola Saugstad
Umberto Simeoni
Christian Speer
David Sweet
Ancona, Italy
Copenhagen, Denmark
Belfast, UK
Oulu, Finland
Istanbul, Turkey
Prague, Czech Republic
Oslo, Norway
Marseille, France
Wurzburg, Germany
Belfast, UK (Secretary)
Updated Guidelines: 2010
What is New?
Guidelines contain new evidence from recent
Cochrane reviews and the literature since 2007.
Many of the previous recommendations on
surfactant and CPAP are now more firmly
evidence-based. The section on delivery room
stabilisation has been considerably expanded.
New recommendations on delaying cord clamping
and a new section on avoiding or reducing
duration of mechanical ventilation, including
recommendations on caffeine therapy, nasal
ventilation, permissive hypercarbia and the role of
newer ventilator modalities. A new miscellaneous
section has also been added covering aspects of
RDS management that arise infrequently
Aims
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Discuss controversies in RDS
management
Examine the evidence for best practice
Develop consensus guidelines from
evidence available up to end of 2009
Publish the consensus recommendations
on management of RDS in 2010,
updating those of 2007
RDS - Definition
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Pulmonary insufficiency starting at birth
Mainly confirmed to preterm babies
Caused by lack of alveolar surfactant
Presents with respiratory distress
Development of respiratory failure
Natural course is death or recovery after 3-4 days
Classical X-Ray appearances
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Ground glass appearance
Air bronchograms
Chest radiograph before and after surfactant
RDS - Treatment
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Oxygen
CPAP
Mechanical ventilation
Surfactant replacement
Supportive Care
RDS – Aims of Management
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Maximise numbers of survivors
Minimise potential adverse effects of disease
or therapy
Many interventions have been studied in
randomised controlled clinical trials and
systematic reviews
Grades of Evidence and Levels of
Recommendation
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A = Meta-analysis or high quality RCT
B = Smaller RCT or systematic review of case/
control studies
C = Good quality case-control or cohort study
D = Case series or expert opinion
Modified from SIGN guidelines handbook
www.sign.ac.uk/guidelines/fulltext/50
European Guidelines on RDS: 2010
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Prenatal Care
Delivery Room Stabilisation
Surfactant Therapy
Oxygen Supplementation Beyond Stabilisation
Role of CPAP
Mechanical Ventilation (MV) Strategies
Avoiding or Reducing Duration of MV
Prophylactic Treatment for Sepsis
Supportive Care: thermal, fluid and nutrition,
tissue perfusion, ductus arteriosus
Miscellaneous Considerations
Management of RDS can be influenced
before birth
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Consider place of delivery
Role of infection in initiation of preterm labour
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Role of antenatal steroids
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Role of antibiotics?
Which steroid?
How many courses?
Who should get them?
Role of tocolytic agents
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Allow steroids to take effect or time to transfer
Prenatal Care Recommendations: 2010
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Mothers at high risk should be transferred to a perinatal
centre (C)
Single course of prenatal steroids should be given if
threatened preterm labour from 23 to 35 wk gestation
(A)
Antibiotics should be given to mothers with PPROM (A)
Consider short-term tocolytics to allow transfer in utero
or time to complete course of steroids (A)
Consider a second course of steroids if risk of RDS
outweighs uncertainty about long-term adverse effects
(D). Multiple pregnancy might be an example (C).
Delivery Room Stabilisation
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Babies with RDS have difficulty maintaining FRC
and alveolar aeration.
Traditionally, many are resuscitated with bag &
mask using 100% oxygen and there is emerging
evidence that 100% oxygen may be harmful
Many are intubated for prophylactic surfactant
Uncontrolled tidal volumes are also detrimental to
the immature lung and early CPAP is being
advocated
Delayed clamping of the cord may confer benefits
Hypothermia should be avoided
Delivery Room Stabilisation –
Recommendations - 1
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If possible, delay cord clamping for at least 30-45 sec (A).
Oxygen should be controlled with a blender and the lowest
possible concentration should be used (~30%), provided
there is an adequate heart rate response (B).
30% oxygen to start and titrate using pulse oximetry but
note normal sats may be 40-60%, reaching 50-80% by 5
min but should be >85% by 10 min. Avoid hyperoxia (B).
If spontaneous breathing, stabilise with CPAP of 5-6 cm
water via mask or prongs (B). If breathing is insufficient
consider a sustained inflation rather than IPPV (B).
Ventilation with a T-piece device is preferable to a selfinflating or flow-inflating bag to generate PEEP (C).
Delivery Room Stabilisation –
Recommendations - 2
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If PPV is needed avoid excessive tidal volumes
and maintain PEEP (D).
Reserve intubation for babies not responding to
PPV or those requiring surfactant (D).
Verify correct position of the endotracheal tube
using colorimetric CO2 detection (D).
Plastic bags or occlusive wrapping under radiant
warmers should be used for babies < 28 weeks’
gestation (A).
Surfactant Therapy
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Surfactants have revolutionised respiratory
care over past 2 decades, and when given
prophylactically or as rescue therapy reduce
death and pulmonary airleaks in RDS
Many RCTs have been performed to
determine the best surfactant, and the
optimal timing of dosing and redosing
However, most trials were in the era of low
prenatal steroid and CPAP use
Surfactant Therapy – dosing and redosing
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At least 100 mg/kg phospholipid is required and
200 mg/kg may be better for established RDS
Administration by bolus results in better
distribution
Prophylaxis reduces mortality and air leaks, but
more babies end up being treated
Surfactant can be given whilst avoiding
mechanical ventilation using INSURE technique
A second (and occasionally a third) dose is
sometimes required
Surfactant Therapy - Recommendations
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Babies with or at high risk of RDS should be given a
natural surfactant preparation (A).
Prophylaxis for most babies < 26 weeks’ gestation.
Prophylaxis also if intubation required (A).
Early rescue for untreated babies if evidence of RDS
such as increasing oxygen requirement (A).
Poractant alfa 200 mg/kg is better than 100 mg/kg
(of poractant or beractant) for moderate to severe
RDS (B).
Consider early extubation to CPAP if stable (B).
A 2nd/ 3rd dose should be given if ongoing evidence
of RDS such as persistent oxygen or MV need (A).
Comparison of Animal Derived Surfactants
Surfacta
nt
Preparation/
Composition
Survanta Minced Bovine
Lung Extract/
(S)
DPPC, Palmitic
Acid,
Tripalmitin
Infasurf
(I)
Bovine Lung
Lavage/DPPC,
Cholesterol
Phospholi
pids
Plasma
logens
*mol %
SP- B
mg/ml
SP- C
mg/ml
Total <1mg/ml
84 %
1.5
0 - 1.3
(µg/µmol
PL)
1 – 20
(µg/µmol PL)
NA
95 %
0.9
0.26
0.44
0.45
0.55
(Alveofact)
Curosurf Minced Porcine
(C)
Lung
Extract/DPPC,
Polar lipids
99 %
3.8
(Liquid Gel
Chromatography)
* High Plasmalogen content is associated with lower BPD rate. Rudiger et al.
Tracheal Aspirates with High Levels of
Plasmalogens Associated with Lower
BPD Rates
P<0.001
X
X
5
% DMAs on all Fatty Acids
X
X
• Aspirates were collected
4
prospectively from preterm
X
X
X
3
infants ≤32 wks GA intubated
X
within 1hr of birth
X
2
X
1
BPD
non BPD
Rüdiger M, et al. Critical Care Med. 2000;28:1572-1577
Comparison of Animal Derived Surfactants
Curosurf vs. Survanta (5 studies)
Trials (6-10)
Surfactant
N
Type
Patient
s
Results
Speer
1995
Curosurf vs.
Survanta
73
Tx
7001500 g
Curosurf: Lower FiO2, PIP
& MAP @ 12-24 h
Baroutis
2003
Curosurf vs.
Survanta vs.
Alveofact
80
Tx
< 2000 Curosurf: Fewer days on O2
& PPV; Decreased LOS
g
Ramanathan
2004
Curosurf vs.
Survanta
293
Tx
7501750 g
Curosurf: Lower FiO2,
Fewer doses, Decreased
Mortality < 32 wks
Malloy
2005
Curosurf vs.
Survanta
58
Tx
< 37
wks
Curosurf: Lower FiO2 up
to 48 h, Fewer doses, lower
volume
Fujii, 2010
Curosurf vs.
Survanta
52
Tx
< 30
wks
Curosurf: Faster weaning,
Less Air-Leaks, PDA & MV
Curosurf vs. Survanta – Rescue Trial (6)
Curosurf
(n= 33)
Survanta
(n = 40)
PIE
3%
10 %
PTX
6.1 %
12.5 %
IVH Total
21.2 %
35 %
3%
12.5 %
IVH Gr. III-IV
O2 @ 36 wks
12.5 %
PCA
Mortality
3%
No Difference in Death or BPD
11.4 %
12.5 %
Speer C et al. Arch Dis Child 1995; 72: F8-F13
Curosurf vs. Survanta – Rescue Trial
(6)
Changes in FiO2 , PIP & MAP
PIP & MAP
FiO2
Faster Weaning
Speer C et al. Arch Dis Child 1995; 72: F8-F13
FiO2 vs. Time curves after the first dose of Surfactant (n=293)
Trial #8
0.7
Faster
Weaning
0.65
0.6
Survanta
Curosurf 100
Curosurf 200
FiO2
0.55
0.5
0.45
0.4
0.35
* *
0.3
0.25
0.2
0
15’
Data : Mean  SEM *,* = p < 0.05
30’
2h
6h
Ramanathan R et al. AJP 21:109-119; 2004
% of Infants Requiring Additional Doses of Surfactant
#8
60
Fewer
Doses
49
41
Curosurf 100
Curosurf 200
Survanta 100
% Infants
40
*
27
20
20
15
8
0
1
4
0
2 Doses
* p < 0.05
3 Doses
4 Doses
36 % (C200) vs. 68 % (S100) received 2 or more doses
Curosurf vs. Survanta (n=50): (Rescue Trial
# 10)
Less Air Leaks & PDA with Curosurf
76
80
Beractant
70
P=
0.002
60
Poractant Alfa
50
50
%
40
P=
30
0.047
20 15
32
35
39
29
28
16
15 16
10
8
4 4
0
19
0
Air Leaks
PDA
PDALigation
BPD
ROP II-IV IVH II-IV
NEC
Mortality
Fujii AM et al. J Perinatol, 1-6; March 2010
Meta-analysis – Curosurf vs Survanta
Trials (6&8)*
OR
( 95 % C.I. )
PTX
0.54
0.19, 1.53
O2 @ 36 wks
1.03
0.61, 1.74
PDA
1.29
0.79, 2.08
Pulmonary Hge
1.01
0.32, 3.21
IVH Gr. I-II
1.39
0.65, 2.96
IVH GR.III-IV
0.65
0.28, 1.53
Neonatal
Mortality
0.35
0.13, 0.92
(* Speer et al. & *Ramanathan et al.) Halliday HL. Biol Neonate 2005;
Mortality of 3 different surfactants
Ramanthan et al Journal of Perinatology (2011), 1–7
Mortality of 3 different surfactants
Ramanthan et al Journal of Perinatology (2011), 1–7
Cost per patient: Curosurf vs. Survanta
2 000,00
Cost / Patient ($)
1 800,00
1 600,00
1 400,00
1 200,00
1 000,00
800,00
Survanta
Curosurf
 53% ($
950)
 46% ($
618)
 20% ($
220)
 20% ($
200)
600,00
400,00
200,00
0,00
Model 1 Model 2 Model 3 Model 4
Cost
Effective
Model 1: Speer et al (mean wt, single-use vial)
Model 2: Ramanathan et al. (mean wt, single-use vial)
Model 3: Ramanathan et al. (Actual wt, single-use vial) p=<0.01
Model 4: Ramanathan et al. (Actual wt, Survanta
p=0.018
as multi-use vial)
Marsh W, Smeeding J, York JM, Ramanathan R, Sekar K. JPPT 9:113-121; 2004
Surfactant for RDS: Evidence Based
Approach
1. Animal Derived Surfactants: Faster weaning of O2,
and MAP, Fewer air leaks, and Decreased Mortality
when compared to synthetic Surfactants.
2. Among Animal Derived Surfactants, Porcine
surfactant, Curosurf provides Faster Weaning,
Rapid Extubation, Less PDA, Survival Advantage &
Cost-effectiveness when compared to Bovine
surfactants, Survanta or Infasurf
3. Best Timing: < 60 minutes of Age
Why Poractant Alfa (Curosurf)?
1. Highest amount of
Phospholipids
2. Phosphotidylcholine
molecular species closely
resembles human
surfactant
3. Highest amount of SP-B
4. Highest amount of
Plasmalogens
5. Highest amount of PUFA
in a smaller volume and
Lowering Surface Tension
& Better antiinflammatory effects
Better interaction with
SP-B
Rapid adsorption of
Phospholipids
Highest anti-oxidant
activity
Rapid distribution and
less reflux
Guidelines for Surfactant Treatment of RDS
< 28 wk
29-31 wk
> 32 wk
NIPPV in DR, Early
Rescue (<30’) in DR or
NICU with 200 mg/kg
of Poractant Alfa
Early CPAP/NIPPV
Surfactant if
intubated for
resuscitation
Observe
CPAP/NIPPV if
respiratory
distress
Extubate to NIPPV as
soon as possible (> 24
wk).
•Start Caffeine
Early Rescue with
100-200 mg/kg if FiO2
> 0.30 + white CXR.
•Start Caffeine
Delayed Rescue with
100 mg/kg if FiO2 >
0.40
+ white CXR
•Caffeine if
symptomatic
Redosing:
FiO2 > 0.30
How soon: 2-12 hrs
Redosing:
FiO2 > 0.35
How soon: 12 hrs
Redosing:
FiO2 > 0.40
How soon: 12 hrs
Oxygen supplementation beyond
stabilisation
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Currently no firm evidence to guide optimal
oxygen saturations in NICU
Suggestions to target between 85% and 93%
and not exceed 95% to reduce ROP and BPD
Long-term neuro-developmental outcomes are
unknown
Hyperoxia can occur following surfactant therapy
Fluctuations in oxygen saturations may also
increase the risk of ROP
Optimal saturation targets currently being
studied in BOOST-II, COT and SUPPORT
Oxygen supplementation beyond
stabilisation
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In oxygen, saturations should be maintained
at all times between 85 and 93% (D).
After surfactant, avoid a hyperoxic peak,
which is associated with IVH, by rapid
reduction in oxygen (C).
Avoid fluctuations in oxygen saturations in
the postnatal period (D).
What is new and why this topic?
Stabilisation/Resuscitation:
How to titrate FiO2 if oxygen is needed?
Optimal FiO2 for preterm infants is not known
Oxygen saturation beyond the DR in ELBWI:
New data on mortality has created uncertainty of safety
A too low SpO2 reduces ROP and BPD but increases mortality
Consequences for clinical practice
Previous reccommendations of SpO2 targets should perhap be changed
Should we resuscitate extremely low
birth weight infants with a low FiO2?
High (90% Vs low (30%) FiO2 Resuscitating ELBWIs
Raquel E et al Pediatrics May 2008
Heart rate in ELBWI (< 28 w) resuscitated with high or low O2 aiming at SaO2 of 85%
200
low FiO2
beats per min
High FiO2
150
100
50
0
3
6
9
12
15
min after birth
Raque l E e t al Pe diatrics M ay 2008
SpO2 in extremely low gestational age neonates
120
SpO2 (%)
100
80
60
40
20
0
0
5
10
15
20
Time after birth (min)
Hox group (n=41)
Lox group (n=37)
Vento et al, Pediatrics 2009
25
30
35
Isofurans
**
ng/mg creatinine
50
40
**
30
20
10
0
da y 1
da y 7
How could SpO2 centiles be used to inform decision
making in the DR?
100
90
80
70
60
50
40
30
20
10
Suggested level for administration of oxygen
0
0
1
2
3
4
5
6
7
8
9
Minutes after birth
10th
25th
50th
75th
90th
Dawson, Vento, Finer, Rich, Saugstad, Morley, Davis J Pediatrics 2011
10
TRANSITIONAL OXYGEN TRACKING SYSTEM
Allowing to individualize FiO2 avoiding hyper/hypoxia
50%
10%
Rich W et al non published data 2010
High or Low Saturation for ELBWIs?
Effect on BPD and ROP
At least 9 studies have been published
investigating the effect on BPD and ROP of
low or high oxygen saturation in VLBWI or
ELBWIS.
Of these 3 only are randomized
Studies regarding high or low SpO2 targets in VLBWI or ELBWIs – Characterisation of Studies
Study
GA w/BW g
Study design High SaO2
Low SaO2
STOP ROP 2000
Mean 25.4 w
Randomized
96-99
89-94
Tin 2001
<28 weeks
Observational
88-98
70-90
Sun 2002
500-1000gr
Survey
>95
≤ 95
BOOST 1 2003
<30 weeks
Randomized
95-98
91-94
Chow 2003
500-1500 gr
Observational
90-98
85-93
VanderVeen 2006
≤28 weeks
≤ 1250 gr
Historical
control
87-97
85-93
Deulofeut 2006
≤ 1250 gr
Historical
control
92-100
85-93
Noori 2009
< 1000 gr
Historical
control
89-94
83-89
SUPPORT 2010
24-28 weeks
Randomized
91-95
85-89
Saugstad and Aune, Neonatology 2010;100:1-8.
BPD and SpO2
Relative Risk
(95% CI)
Study
Randomized trials
STOP ROP, 2000
0.64 ( 0.40, 1.03)
Askie, 2003
0.71 ( 0.59, 0.86)
Support, 2010
0.91 ( 0.79, 1.05)
Subtotal
0.79 ( 0.64, 0.97)
Observational studies
Tin, 2001
0.40 ( 0.22, 0.69)
Sun, 2002
0.66 ( 0.57, 0.76)
Deulofeut, 2006
0.69 ( 0.55, 0.85)
Noori, 2009
1.04 ( 0.79, 1.36)
Subtotal
0.70 ( 0.54, 0.91)
Overall
0.74 ( 0.63, 0.87)
.2
.5
1
Relative Risk
2
Saugstad and Aune, Neonatology 2010;100:1-8.
ROP and SpO2
Relative Risk
(95% CI)
Study
Randomized trials
Support, 2010
0.48 ( 0.34, 0.68)
Subtotal
0.48 ( 0.34, 0.68)
Observational studies
Tin, 2001
0.40 ( 0.22, 0.69)
Sun, 2002
0.66 ( 0.57, 0.76)
Chow, 2003
0.22 ( 0.05, 0.85)
Deulefeut, 2006
0.64 ( 0.27, 1.46)
VanderVeen, 2006
0.32 ( 0.12, 0.80)
Noori, 2009
0.28 ( 0.18, 0.42)
Subtotal
0.42 ( 0.27, 0.65)
Overall
0.44 ( 0.31, 0.61)
.03
.1
.25
.5
1
Relative Risk
2
Saugstad and Aune, Neonatology 2010;100:1-8.
Avoidance of mechanical ventilation by
surfactant treatment of spontaneously
breathing preterm infants (AMV): an
open-label, randomised, controlled trial
Wolfgang Göpel, MD, Angela Kribs, MD, Andreas Ziegler, PhD, Reinhard Laux, MD,
Thomas Hoehn, MD, Christian Wieg, MD, Jens Siegel, MD, Stefan Avenarius, MD,
Axel von der Wense, MD, Matthias Vochem, MD, Peter Groneck, MD, Ursula Weller,
MD, Jens Möller, MD, Christoph Härtel, MD, Sebastian Haller, MD, Bernhard Roth,
MD, Egbert Herting, PhD and on behalf of the German Neonatal Network
The Lancet September 30, 2011
Terms and Conditions
Randomized studies
high or low SpO2 for ELBWI
• SUPPORT
• BOOST 2 (UK, Australia, New Zealand)
• COT
High 91-95 %
Low 85- 89%
Mortality at 36 weeks PMA in High or Low SpO2 - Support + BOOST 2
Stenson B et al, NEJM, April 28, 2011 p 1681
Summary
Postnatal oxygenation of ELBWIs
High SpO2
• Increases severe ROP and BPD
 Fluctuations should be avoided – especially first 5 days
 Should not exceed 95%
Low SpO2
• increases mortality
 Is a SpO2 at 85% too low ?
•
How to find the right balance of SpO2 between:
1) lowest mortality rate
2) lowest incidence of morbidity (BPD, ROP)?
•
•
Randomized controlled trials are needed and one more large study is underway
However, new studies would probably be needed
SpO2 85-89% Vs 91-95 %
BPD 25%
ROP 50%
Mortality
20%
What is the ”right” balance between mortality and morbidity?
SpO2
?
89-93% ??
91-95 % ??
Oxygen saturation in ELBWIs revisited
Updated recommendations
“This means that SpO2 of ELBWIs should not be targeted at
85-89 % until further data become available”.
“This recommendation may be controversial knowing that even if
mortality is slightly reduced it may lead to considerably higher
rates of severe ROP and BPD”.
“The SpO2 targets describing the optimal balance between
mortality on one hand and complications such as ROP and BPD
on the other is therefore presently not known”.
“In fact, it may take several years until more precise information is
available to guide clinical practice”.
Saugstad, Halliday, Speer, Neonatology, October 2011 (editorial)
Conclusions
•It is best to initiate resusctiation of term babies
with air
•The optimal FiO2 for resuscitation of ELGANs is
not known. But do not use 100% oxygen, start low
with 21 or 30%
•Low SaO2 (85%) beyond the DR
probably reduces BPD and ROP
But may increase mortality
Do not target SaO2 between 85-89%
CPAP - Recommendations
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CPAP should be started from birth in all babies at
risk of RDS, such as those <30 wk not needing
MV, until clinical status can be assessed (D).
Short binasal prongs should be used rather than
a single prong and a pressure of at least 6 cm
water should be used (A).
CPAP with early rescue surfactant should be
considered in babies with RDS to reduce MV (A).
Mechanical Ventilation Recommendations
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MV should be used to support babies with
respiratory failure as this improves survival (A).
Avoid hypocarbia, as this is associated with
increased risks of BPD and PVL (B).
Settings of MV should be adjusted frequently
with the aim of maintaining optimum lung
volume (C).
Duration of MV should be minimised to reduce
injurious effect on the lung (B).
Avoiding or Reducing Duration of MV
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Clear links between MV and development of
BPD and neurological sequelae
Interventions to avoid or shorten MV include:
caffeine, CPAP or NIPPV with or without
surfactant, INSURE technique, permissive
hypercarbia and aggressive weaning with
early extubation
Avoiding or Reducing Duration of MV:
Recommendations: 2010
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Caffeine should be used to treat apnoea and
to facilitate weaning from MV (A). It should
also be considered for those at high risk of MV
(e.g. <1250 g on CPAP or NIPPV) (B).
CPAP or NIPPV should be used if possible to
avoid MV through an endotracheal tube (B).
Weaning from MV - reasonable to tolerate
moderate hypercarbia provided pH > 7.22 (D).
Synchronised and targeted tidal volume
modes with aggressive weaning should be
used (B).
Prophylactic Treatment for Sepsis:
Recommendations: 2010


Antibiotics should be started in all babies with
RDS until sepsis is ruled out. Penicillin or
ampicillin with an aminoglycoside is
commonest but units need to develop local
protocols (D).
Protocols should also be developed for
antifungal prophylaxis in very preterm babies
based on local incidence and risk factors (D).
Supportive Care



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
Temperature Control
Fluid and Nutritional Management
Maintenance of Tissue Perfusion
Management of Persistent Ductus
Arteriosus
Support of the Family
Temperature Control




All efforts should be made to reduce heat loss
Use of polythene bags < 28 weeks reduces heat
loss and may improve survival
Incubators reduce insensible water losses
compared to radiant warmers
Servo-controlled temperature decreases mortality
Recommendation: 2010
 Maintain axillary temp 36.5 – 37.5 oC at all times
(C)
Very preterm
baby being
placed in a
plastic bag
Fluid and Nutrition Management:
Recommendations: 2010





Most babies should be started on 70-80 mL/kg/day and
nursed in high humidity (D).
Fluid and electrolyte therapy should be tailored
individually allowing a 2.5-4% daily weight loss (15%
total) over first 5 days (D).
Sodium intake should be restricted over first few days
and initiated after onset of diuresis with careful
monitoring of fluid and electrolyte levels (B).
Full parenteral nutrition can be started on day 1 (A).
May include protein 3.5 g/kg/day and lipid 3 g/kg/day in
10% dextrose.
Minimal enteral feeding should be started from the first
day (B). Early aggressive feeding is popular but level
A evidence is lacking.
Maintenance of Tissue Perfusion:
Recommendations: 2010






Treatment of hypotension is recommended when
confirmed by evidence of poor tissue perfusion (C).
Volume expansion with 10-20 mL/kg normal saline as
first line if myocardial dysfunction excluded (D).
Dopamine (2-10 ug/kg/min) if volume expansion fails (B).
Dobutamine (10-20 ug/kg/min) as first line and
epinephrine (0.01-0.5 ug/kg/min) if low systemic blood
flow and myocardial dysfunction need to be treated (D).
Hydrocortisone (1 mg/kg 8 hourly) in cases of refractory
hypotension when conventional therapy has failed (B).
Echo may help decisions when to start treatment for
hypotension and what drug to use (B).
Management of the Ductus Arteriosus


PDA may cause clinical problems for preterm
babies with RDS
Insufficient data on long-term outcomes when
treating PDA with indomethacin, ibuprofen or
surgical ligation. Treatment must be based on
individual assessment
Recommendations: 2010
 If decision to try to close PDA then indomethacin
or ibuprofen are equally effective (B).
 Pharmacological or surgical treatment of PDA
must be based on assessment of clinical signs
and echo findings suggesting poor tolerance of the
PDA (D).
Miscellaneous Considerations





Babies at or near term, especially if born by
elective caesarean section, can develop
severe RDS.
Some term babies with RDS may have genetic
disorders (SP-B or ABCA3 deficiency).
If pulmonary hypertension is present iNO may
help, otherwise not.
If pulmonary haemorrhage occurs surfactant
may help at least transiently.
Later surfactant therapy has not been shown
to reduce or modify course of BPD.
Miscellaneous Considerations:
Recommendations: 2010




Elective caesarean section in low risk
pregnancies should not be done < 39 wk (B).
Inhaled NO is not beneficial in management
of babies with RDS unless pulmonary
hypertension is present in near term infants
(A).
Surfactant improves oxygenation in babies
with pulmonary haemorrhages (C).
Surfactant cannot be recommended for
prevention of evolving BPD (C).
Summary – Management of RDS




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
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
Prenatal Care
Delivery Room Stabilisation
Surfactant, CPAP and Mechanical Ventilation
Temperature Control
Fluid Management
Nutritional Support
Management of PDA and Poor Tissue
Perfusion
Miscellaneous Considerations
Thank You