@ Murdoch Children’s Research Institute, 2017

Management of Respiratory Disease in the Term Infant

David Tingay

1. Neonatal Research, Murdoch Children’s Research Institute, Melbourne

2. Neonatology, Royal Children’s Hospital

3. Dept of Paediatrics, University of Melbourne

2

Respiratory support of the term infant is more interesting

Aim for NIV as soon as practical

What is the pathophysiological process?

Homogeneous

Atelectasis

Normal Lung

Gas Trapping

In complex mixed regional lung pathophysiology

the correct approach is usually dictated by the

current primary problem – strategy needs

frequent re-evaluation.

CRS, RRSN

CRS N, RRS N

CRS N, RRS

P = positioning, VS = Volume Strategy; H = high, N = normal, L=low

HVS

Disease State? Mechanical State? Regional?

Cautious

HVS+P

LVS

N or

LVS+P

Ventilation

ApproachTi & Te

Short

Short

Normal

Long

Normal

- Long

Modality*

CMV/

HFOV

CMV/

HFOV

CMV

HFJV/

HFOV

HFJV/HFO

V/CMV

NVS

Hypoplasia CRS, RRS N

Where possible target VT not PIP

N or LVSShort HFJV

Heterogeneous

3

Ventilator settings for the term infant are not the same as the preterm

Tau = CRS x RRS

4

Time is an important factor in volume and oxygen change in the term infant

Tingay PhD 2008

Miedema et al ICM 2012

5

Kotecha et al Eur Respir J 2012

The Congenital Diaphragmatic Hernia lungRespiratory support for Bilateral Heterogeneous Hypoplasia

“…for many, the management of the newborn with CDH is more emotional than scientific.”

Glick, Irish & Holm Clin Perinatol 1996

“…unlike the other neonatal pulmonary diseases, CDH doesnot represent a recruitable lung and attempts to use a highmean airway pressure are likely to cause pulmonary damage”.

Bohn AJRCCM 2002

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CDH: Cardiac or respiratory disorder?

Adapted from Kinsella J Peds 2018

1. Conventional Ventilation

2. High frequency Oscillatory

Ventilation

3. High Frequency Jet

Ventilation

1. Inhaled Nitric Oxide

2. Sildenafil

3. Milnarone

4. PGE1

5. Other agents/ECMO

1. Milnarone

2. Adrenaline/Dobutamine

3. Noradrenaline

4. Steroids

5. ECMO

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Pulmonary

Hypoplasia Ventilator Induced InjuryVILI

CDH is not a static problem – understanding the baby

Poor Oxygenation

High CO2

Acid build UpLoss of lung elasticity “Large” lungs

Aggressive

Ventilation

Small Lungs

Surgery

1. Cautious use of pressure:

• Paw <15 cmH2O

• PEEP 4-6 cmH2O

• PIP <25 cmH2O

2. VT Target?

• VD & Alveolar VT unknown

What impact will my ventilator

settings have on RV and LV

Function?

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Different diagnoses but are they different diseases?

De Luca Lancet Rep 2017 Suppl Material

Term Blood Aspiration Preterm Pulmonary Haemorrhage Term Congenital Pneumonia

@ Murdoch Children’s Research Institute, 2017

The Montreux definition of Neonatal Acute Respiratory Distress SyndromeDiagnostic criteria for a ‘new’ neonatal disease

The Neonatal ARDS Collaborative Project (ESPNIC/ESPR)

D De Luca, AH van Kaam, DG Tingay, SE Courtney, O

Danhaive, VP Carnielli, LJ Zimmermann, MCJ Kneyber, P

Tissieres, J Brierley, G Conti, JJ Pillow, PC Rimensberger

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Biology of ARDS

Red circles/squares = proinflammatorymediators, ROS, proetases

Red shading = sits of ARDS-mediated cellular injury

Orange balls = intraalveolar plasma proteins

Phosplipase-driven surfactant dysfunction (sPLA2)

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Does Neonatal ARDS exist?

32 publications with term ‘neonatal ARDS’ from 1989

All with criteria that meet PALICC but occurred in perinatal period

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Proposed Pathophysiology of Neonatal ARDS

Aetiology

Direct injury to lung parenchyma

Extra pulmonary process

Perinatal or postnatal

Lung inflammation

Secondary surfactant dysfunction

Impaired compliance

Increased shunt

Alteration of local lung defences

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The Montreux definition

Oxygen impairment with decreased EEV needing Positive Pressure support to recruit alveoli

Respiratory failure not fully explained by lung oedema due to heart failure

0-44 weeks PMA or up to 4 weeks postnatal age

5 Criteria that must be met:

Timeframe: Acute onset (<7d) of known or suspected insult (including perinatal)

2. Exclusion: RDS, TTN, congenital anomalies and genetic disorders of surfactant dysfunction

3. Imaging confirmation: Diffuse bilateral irregular opacities on imaging (excludes primary RDS and focal events e.g. localised pneumonia and bronchiolitis)

4. Origin of Oedema: Not cardiac

5. Oxygenation defect based on OI

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Montreux Definition

Specific points:

Perinatal triggers allowed

Does not exclude preterm infants

Does not exclude infants managed with NIV

OI ideally defined using arterial blood gas but TcO2

allowed

SpO2 concentrations not to be used to asses oxygenation due to variable oxygen dissociation curve in neonates (eg SpO2/FiO2 ratio)

Preductal measures of oxygenation to account for co-morbidity of PPHN

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Different diagnoses same characteristics = same disease

De Luca Lancet Rep 2017 Suppl Material

Term Blood Aspiration Preterm Pulmonary

Haemorrhage

Term Congenital Pneumonia

1. Acute Onset 2. No RDS, TTN etc

3. Diffuse bilat irregular

opacities/infiltrates

5. Severe oxygenation deficit4. Oedema not cardiac*

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Summary

Term lung diseases are more diverse and requires greater understanding of

respiratory physiology

The concepts of respiratory support are the same as the preterm infant but

absolute values are not

Collectively diseases of the term infant are common but specific diseases are

rare relative to the preterm infant

A focus on pathophysiological processes rather than specific disease entity may

provide a better method of defining term lung disease

Opportunity to better evaluate new therapies and apply existing therapies

established in older populations