Paediatric ARDS

Jenny Woodruff Nov 2021

 Original Definition
In 1994, the American-European Consensus Conference defined
“adult” or “acute” respiratory distress syndrome (ARDS) as:
• a severe form of acute lung injury (ALI)
• characterized by acute, noncardiogenic pulmonary edema with
bilateral pulmonary infiltrates on chest X-ray
• and a ratio of PaO2 to FIO2 of <200.

• (The term acute lung injury was adopted to describe patients with
PaO2/FIO2 <300 who otherwise meet the criteria for ARDS)
Berlin definition by
ARDS Definition Task
Force :
JAMA 2012
Proposed Mild/Mod /severe, got rid of ALI
• PALICC definition 2015
• Specific to paeds

• OI = (Fio2 × mean
airway pressure ×
100)/Pao2

• OSI = (Fio2 × mean

airway pressure ×
100)/Spo2.
Mnemonic !!
OI = Fix Me / Palicc
OSI = Fix Me / stat
Pathogenesis
Entholelial & Epithelial Injury
Alveolar-capillary barrier - two separate cellular linear barriers: the
vascular endothelium and the alveolar epithelium
During ARDS - influx of protein-rich oedema fluid into the air spaces
→increased permeability of the alveolar-capillary barrier
→pulmonary oedema = early phase of ARDS.
1. loss of epithelial integrity has numerous injury disrupts normal
epithelial fluid transport, and impedes the removal of oedema fluid
from the alveolar space.
2. Alveolar fluid clearance has been found to be impaired in the
majority of patients
3. Alveolar type II cell injury impedes surfactant production and
turnover, contributing to the characteristic surfactant abnormalities
4. Inflammatory cascade is activated with the release of numerous
mediators.
Phases
Exudative phase
• Lasts7-10 days
• alveolar macrophages secrete mediators →lead to accumulation of inflammatory
cells in the lung
• leading to pathologic vascular permeability, gaps in the alveolar epithelial
barrier, and necrosis of types I and II alveolar cells
• Intravascular coagulation in the alveolar capillaries leads to microthrombi
• The end result =
• pulmonary oedema,
• loss of surfactant and deposition of dead cells and debris along the alveoli
(hyaline membranes)
• which decrease pulmonary compliance and make gas exchange difficult
Phases
Proliferative phase
• Next two to three weeks
• Anti-inflammatory cytokines deactivate inciting neutrophils, which
then undergo apoptosis and phagocytosis
• Type II alveolar cells proliferate and differentiate into type I cells, re-
establishing the integrity of the epithelial lining.
• Alveolar ion channels and aquaporins are re-expressed, drawing fluid
out of the alveoli and into the pulmonary microcirculation and lung
lymphatics.
• Simultaneously, alveolar cells and macrophages remove debris from
the alveoli, and endothelial cells re-establish vascular integrity,
allowing the lungs to recover
Phases
Fibrotic phase
• Ongoing inflammation
• extensive basement membrane damage
• persistent oedema
• intra-alveolar and interstitial fibrosis, and microvascular damage
• Shear forces associated with mechanical ventilation may promote the
development of the fibrotic phase
• Although lung protective ventilation is thought to ameliorate this
effect.
• Progression to the fibrotic phase is associated with prolonged
mechanical ventilation and increased mortality
Risk Factors & Incidence (NB adult
info)
ARDSnet
classic trial
in adults
https://pubmed.ncbi.nlm.nih.gov/10793162/ Acute Respiratory Distress Syndrome Network, Brower RG,
Matthay MA, Morris A, Schoenfeld D, Thompson BT, Wheeler A. Ventilation with lower tidal volumes
as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.
N Engl J Med. 2000 May 4;342(18):1301-8. doi: 10.1056/NEJM200005043421801. PMID: 10793162.
 Treatment – PALICC 2015
• No outcome data on control vs assisted conventional mechanical ventilation
• If ventilated, in all patients: Use 5 – 8ml/kg tidal volumes
• Patient specific tidal volumes according to disease severity:
• “Tidal volumes should be 3–6 mL/kg predicted body weight for patients with poor
respiratory system compliance and closer to the physiologic range (5–8 mL/kg ideal
body weight) for patients with better preserved respiratory system compliance.
Weak agreement (84% agreement)
• We recommend an inspiratory plateau pressure limit of 28 cm H2O,
allowing for slightly higher plateau pressures (29–32 cm H2O) for patients
with increased chest wall elastance (i.e., reduced chest wall compliance).
(72% agreement)
 PEEP and recruitment manoevres
• We recommend moderately elevated levels of PEEP (10–15 cm H2O) titrated to the
observed oxygenation and hemodynamic response in patients with severe PARDS.
Weak agreement (88% agreement)
• We recommend that PEEP levels greater than 15 cm H2O may be needed for severe
PARDS, although attention should be paid to limiting the plateau pressure as
previously described. Strong agreement
• We recommend that markers of oxygen delivery, respiratory system compliance, and
hemodynamics should be closely monitored as PEEP is increased. Strong agreement
• We recommend careful recruitment maneuvers in the attempt to improve severe
oxygenation failure by slow incremental and decremental PEEP steps. Sustained
inflation maneuvers cannot be recommended due to lack of available data. Weak
agreement (88% agreement)
 PEEP – as per Rogers
• a logical strategy suggests stepwise escalation of PEEP in 3–5 cm
H2O increments, until arriving at the minimum PEEP that allows for
a PaO2 in the range of 55–80 mm Hg, with peripheral oxygen
saturation (SpO2) of 88%–95%, using an FIO2 of ≤0.5–0.6.
 HFOV
• HFOV recommended as alternative if plateau airway pressure
exceeds 28cm H2) in absence of clnical evidence of reduced chest
wall compliance ie consider for mod to severe PARDS
• In HFOV, we recommend that the optimal lung volume be achieved
by exploration of the potential for lung recruitment by a stepwise
increase and decrease of the Paw (continuous distending pressure)
under continuous monitoring of the oxygenation and Co2 response
as well as hemodynamic variables.
• Cuffed ETT recommended with conventional ventilation. Allow an
ETT Air leak during HFOV if needed for ventilation, if can keep Paw.
 Oxygenation targets
• We recommend that for mild PARDS with PEEP less than 10 cm H2O,
Spo2 should generally be maintained at 92– 97%. Weak agreement
(92% agreement)
• We recommend that after optimizing PEEP, lower Spo2 levels (in the
range of 88–92%) should be considered for those with PARDS with
PEEP at least 10 cm H2O. Strong agreement
• Insufficient data exist to recommend a lower Spo2 limit. Strong
agreement
• When Spo2 is less than 92%, monitoring of central venous saturation
and markers of oxygen delivery is recommended. Strong agreement
 pH / CO2 targets
• We recommend maintaining pH 7.15–7.30 within lung protective
strategy guidelines as previously described.
• There are insufficient data to recommend a lower limit for pH.
• Exceptions to permissive hypercapnia should include intracranial
hypertension, severe pulmonary hypertension, select congenital
heart disease lesions, hemodynamic instability, and significant
ventricular dysfunction. Weak agreement (92% agreement)
• 3.7.8 Bicarbonate supplementation is not routinely recommended.
Strong agreement
 Nitric Oxide
• Not for routine use. However may be considered with documented
pulmonary hypertension or severe RV dysfunction
• In severe PARDS may rescue or bridge to ECLS
• Assess its benefit as you start and serially and don’t continue to use
unless have seen it’s effective
 Prone positioning
• Cannot be recommended as routine, however should be considered
an option in cases of severe PARDS

• Suctioning: maintain airway but be cautious to minimise

derecruitment
• Only use saline to suction if needed for thick secretions, not
routinely
• Chest physio insufficient data to be recommended
 Not recommended
• Surfactant
• High freq jet ventilation (unless big air leak possibly)
• High freq percussive ventilation (unless secretion induced lung
collapse cannot be otherwise resolved)
• Steroids as routine therapy
• DNAse outside of CF
 Rogers re steroids:
• Corticosteroids are intuitively appealing as an adjunct therapy for
ARDS but few data support their widespread use. Short courses of
high-dose corticosteroids administered early in ARDS have not
demonstrated an outcome benefit.
• A single study of methylprednisolone administration in 24 patients
with persistent ARDS reported a decrease in mortality when the
drug was initiated after 7 days. A multicenter, randomized
controlled trial published 8 years later found no mortality benefit
associated with the use of methylprednisolone as compared to
placebo in 180 patients with persistent ARDS.
 Non pulmonary therapies
• Minimal but effective sedation
• periodic assessments for extubation at least daily
• Withdraweal scores and sedation weaning

• Neuro musc block if needed if sedation inadequate

• Daily Roc holidays to review level of NMB and sedation
 Non pulmonary therapies
• Nutrition – enteral as per dietician

• Fluid management – goal directed. Aim to prevent positive balance

after initial resus and stabilization

• Transfusion threshold 7g/dl

Fluid management – single centre 2011 – 2019
• Of 723 children with ARDS, 132 died (18%). In unadjusted analysis, nonsurvivors had
higher cumulative fluid balance starting on day 3. In multivariable analysis, a positive
cumulative fluid balance on days 5 through 7 was associated with increased mortality.
Higher cumulative fluid balance on days 4 to 7 was associated with lower probability of
extubation.
• Elevated angiopoietin-2 on day 1 predicted early (within 3 d) fluid overload greater
than or equal to 10%, and elevated angiopoietin-2 on day 3 predicted late (between
days 4 and 7) fluid overload.

• Conclusion:
• Fluid overload after day 4 of acute respiratory distress syndrome, but not before, was
associated with worse outcomes. Higher angiopoietin-2 predicted subsequent fluid
overload. Our results suggest that future interventions aimed at managing fluid
overload may have differential efficacy depending on when in the time-course of acute
respiratory distress syndrome they are initiated.
• Black, Thomas,
Yehya , PCCM 2021

• Timing and Clinical

Significant of Fluid
overload in PARDS
 Monitoring
• Exhaled TV
• Inspiratory pressure: based on peak pressure in pressure regulated
• modes and plateau pressure during ventilation in volume-control modes.
It should be interpreted with caution in patients with suspected abnormal
chest wall compliance or with spontaneous breathing. Strong agreement
• Monitoring of Fio2, Spo2 and/or Pao2, Paw, and PEEP is recommended to
detect PARDS, to assess PARDS severity, and to guide the management of
oxygenation failure.

• Arterial line
• Echo : In patients with suspected cardiac dysfunction,
echocardiography is recommended for noninvasive evaluation of
both left and right ventricular function, the preload status, and
pulmonary arterial pressures. Strong agreement
 ECMO criteria as per Palicc
• It is not possible to apply strict criteria for the selection
• of children who will benefit from ECMO in PARDS. We recommend
that children with severe PARDS should be considered
• for ECMO when lung protective strategies result in
• inadequate gas exchange. Strong agreement
 ECMO criteria – paeds 2013 national standards
/ commissioning:
2.4.1 Referral criteria, sources and routes
All providers use the nationally agreed ECMO referral criteria (for more information, please refer to the service
standards):
• oxygenation index (OI) >40
• weight > 2kgs
• reversible lung disease
• no lethal congenital anomalies
• no irreversible central nervous system injury
• no major immunodeficiency
• anticoagulation is not contraindicated.
Variations to these criteria may be made on clinical assessment of the individual patient.
The technical success of neonatal ECMO led to the increased use of ECMO in the paediatric population. The paediatric
age group is more heterogeneous. Indications for paediatric ECMO include:
• inadequate oxygenation despite appropriate ventilation
• air leak syndrome
• older children OI >25 or Acute deterioration
• large airway disease / disruption making ventilation impossible
• refractory septic shock
• the need for high pressure ventilation in the face of a persistent air leak.
 Now OI >25 is more standard eg CATS
guideline for ECMO referral
ECMO may be considered for children with the following Criteria for ECMO referral:
conditions:  Failure to respond to maximal conventional treatment
Respiratory or cardio-respiratory failure resulting from:  Disease is thought to be reversible (unless bridge-to-
 Meconium aspiration syndrome transplant)
 Persistent pulmonary hypertension of the newborn  <14 days of high pressure ventilation
 Pneumonia  Weight > 2.0 kg
 Sepsis  Newborn > 34 weeks gestation
 ARDS  Oxygenation index >25
 Congenital diaphragmatic hernia with severe  Severe barotrauma (PIE, chest drains)
barotrauma/air leak  No contraindication to systemic anticoagulation (intracranial
 Paediatric cardiac patients requiring assessment by the haemorrhage)
Heart Failure / Transplant teams  No lethal congenital abnormalities
 No irreversible organ dysfunction including neurological
injury
 No major immunodeficiency
 Resources / References
• Zimmerman
• ARDSnet trial
• https://pubmed.ncbi.nlm.nih.gov/10793162/ Acute Respiratory Distress Syndrome Network, Brower RG,
Matthay MA, Morris A, Schoenfeld D, Thompson BT, Wheeler A. Ventilation with lower tidal volumes
as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.
N Engl J Med. 2000 May 4;342(18):1301-8. doi: 10.1056/NEJM200005043421801. PMID: 10793162.

• Palicc statement: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5253180/

• ECMO criteria: https://
www.england.nhs.uk/wp-content/uploads/2013/06/e07-ecmo.pdf
• CATS ECMO criteria https://
cats.nhs.uk/wp-content/uploads/guideline-ecmo.pdf
• Happy to answer any questions