Pediatric ARDS is a common cause of respiratory failure in children. It is defined by acute onset hypoxemia that cannot be explained by cardiac failure, with bilateral lung opacities on chest imaging. Management involves controlling the underlying cause, lung protective ventilation with low tidal volumes, permissive hypercapnia, prone positioning, and consideration of recruitment maneuvers, HFOV, surfactant, inhaled nitric oxide, or ECMO in severe cases. Noninvasive ventilation may be tried initially for mild disease but intubation is often required for more severe pediatric ARDS. The goals of management are to maintain adequate oxygenation and ventilation while minimizing ventilator induced lung injury.

1. Pediatric ARDS
Dr Abhijeet Deshmukh
DNB pediatrics,
Fellow – PICU & NICU

2. Introduction
 ALI and ARDS are common causes of acute hypoxemic respiratory failure in
children.
 In 1967, Ashbaugh and colleagues described a syndrome of tachypnea, hypoxia,
and decreased pulmonary compliance in a series of 11 adults and one child with
respiratory failure.
 Adult respiratory distress syndrome - OLD
 Acute respiratory distress syndrome - NEW

3. Definition
 American- European Consensus Conference definition of ARDS. (1924)
Clinical feature Criteria
 Timing Acute onset
 Chest Xray Bilateral infiltrates
 Oxygenation Severe hypoxia on Oxygen therapy
 ALI PaO2 /FiO2 <300
 ARDS PaO2/FiO2<200
 Noncardiogenic origin pulmonary edema

4. The Berlin definition of ARDS (2012)
Clinical Feature Criteria
 Timing Within 1 week of a known clinical insult or new
worsening respiratory symptoms.
 Chest Imaging B/l opacities – not fully explained by effusions,
lobar/lung collapse, nodule
 Origin of edema Respiratory failure not fully explained d by cardiac
failure or fluid overload. Need objective assessment
(eg. Echo) to exclude hydrostatic eg. no risk factor
present.
 Oxygenation
 Mild =200 mm Hg< PaO2/FiO2<300mmHg with PEEP/CPAP>5 cm
 Mod.=100 mm Hg< PaO2/FiO2<200mmHg with PEEP>5 cm H2O
 Severe = PaO2/FiO2<100 mmHg with PEEP>5 cm H2O.

5. Common clinical conditions leading to ARDS
 Systemic Causes Direct Pulmonary Injury
• Sepsis Viral/Bacterial pneumonia
 Septic shock Aspiration pneumonia
 Hypovolemic shock Hydrocarbon/ smoke/noxious gas inhalation
 Pancreatitis Near drowning
 Burns Fungal pneumonia
 Cardiopulmonary bypass surfactant def.
 Fat embolism Ventilator induced lung injury
 Multiple organ major trauma Traumatic lung contusion
 Malaria
 Transfusion related ALI
 MODS
 Drug toxicity

6. Phases of ARDS
 Acute- Exudative, inflammatory ( 0-3 Days )
characterized by the acute development of decreased pulmonary compliance and
arterial hypoxemia.
 Subacute – Proliferative ( 4-10 days)
increased alveolar dead space and refractory pulmonary hypertension may develop
as a result of chronic inflammation and scarring of the alveolar-capillary unit.
 Chronic- Fibrosing alveolitis
( >10 days )

7. Pathogenesis
 Direct injury - regional consolidation , alveolar damage
 Indirect injury - pulmonary vascular congestion, interstitial edema, and less severe
alveolar involvement .
 Damage to capillary endothelium & alveolar epithelium disruption of normal
epithelial fluid transport, impaired reabsorption of edema fluid.
 Damage to Type I & Type II pneumatocytes Impaired surfactant production, re
epithelization & repair of damaged alveoli.

8.  Cytokine related inflammation
 Activated macrophages  chemotaxis & activated neutrophils
 VILI – increased pulmonary edema in uninjured & injured lung MOD
 Fibrotic stage (after 5-7 days) Fibrosing alveolitis - Initiated by IL 1, TNF &other
cytokines Alveoli filled with mesenchymal cells, collagen, new blood vessels,
 Resolution stage – Removal of Soluble proteins : by diffusion in between epithelial
cells & interstitium, Insoluble proteins : by endocytosis & phagocytosis by
macrophages.
- Type II cells – initiate re epithelization & repair of alveoli.

9. Host Immune response-Role of Cytokines

10. Clinical features
 Dyspnea, anxiety, agitation, increased WOB
 Hypoxemia refractory to supplemental O2 Hypercarbia Acidosis.
 Lung- scatter of normal alveoli along with various grades of severity of involvement
 Xray – B/l infiltrates – patchy, asymmetric, may associated pleural effusion
 In progressive fibrosing alv – persistant hypoxemia, decreasing compliance,
Pulmonary HT  Rt ventricular failure

11.  Initial phase – areas of normal lungs are more so PEEP works, Later (>5-7days)
abnormal lung increases so PEEP is less effective, PaCo2 increases.
 Fibroproliferative phase – slow recovery & ventilator dependency.
 Resolution phase – gradual recovery of hypoxemia, compliance, X ray resolution

12. Management
 Control of underlying disease/infection – Antibiotics
 Respiratory support :
 Basic ventilation strategies : Goal – maintain adequate oxygenation, minimize VILI,
 Lung protective strategies –
1. Avoid regional overinflation (Baby lung concept)
2. Avoid repeated opening/closing of alveoli (Open lung strategy)
3. Permissive hypercapnia
4. Permissive Hypoxemia

13.  Baby Lung concept :
 In most patients of ARDS, normally aerated tissue has dimension of 5-6 year old
child (300-500gm aerated tissue)
 Compliance is linearly related to baby lung quality i.e ARDS lung is not only stiff
but also small with nearly normal intrinsic elasticity in early phases
 This concept provides rationale for gentle ventilation d/t risk of VILI (at TV >8
ml/kg)

15.  Initiation of Ventilation
 ARDS Net trial – RCT 861 adult pt
 Traditional ventilation (Vt -12ml/kg & Ppeak – 50cmH2O) Vs Lung protective
ventilation (Tv 6,l/kg & Ppeak - < 30cm H2O)
 Result - Reduced mortality (31% vs 39.5), more vent free days, lower end organ
complications.

16. Initial Ventilator settings
 NIV – in very early and mild ARDS
 Mode – PRVC>PCV>VCV (HFOV when indicated)
 TV : <6ml/kg (adjusted acc to Pplat)
 Pplat <30 cm H2O
 Rate : 15 to 35
 I:E – 1:1 to 1:3
 PEEP & FiO2 is set acc to predetermined combinations (PEEP 5-24 ) FiO2 < 60%
 Oxygenation target : PaO2 : 55-80 mm Hg, SpO2 88-95%

17.  Start FiO2 of 100%, TV – 6ml/kg, PEEP -5  Subsequent titration to achieve desired
PaO2 at FiO2 <60% & Peak airway pressure 30-35cm H2O
 However in severe ARDS – SPO2 (85%) and PaO2 upto 60% is acceptable
 Maintain Hb at least 10g/dl
 PEEP : Improves oxygenation, Moves fluid from alveoli to interstitial space, recruit
small airways and alveoli, Increases FRC ( detrimental effects – barotrauma, dead
spacing, impaired venous return and impaired CO)
 Increase PEEP by 2-5 cm H2O every 5-10 breaths with closed watch on
hemodynamics

18.  Selection of PEEP :
 Higher PEEP & low FiO2 preferred
 Titration of PEEP and FiO2 according to lung recruitability shown in fig.

20. Ventilation with Lower VT vs. Traditional VT for
ALI and ARDS ( ARDS Net)

23.  pH GOAL: 7.30-7.45
 Acidosis Management: (pH < 7.30)
 If pH 7.15-7.30: Increase RR until pH > 7.30 or PaCO2 < 25 (Maximum set RR = 35).
 If pH < 7.15: Increase RR to 35.
 If pH remains < 7.15, VT may be increased in 1 ml/kg steps until pH > 7.15 (Pplat
target of 30 may be exceeded).
 May give NaHCO3
 Alkalosis Management: (pH > 7.45) Decrease vent rate if possible

24.  High FiO2 – Cellular toxicity, reabsorption atelectasis so keep <60%

25.  Open Lung strategy:
 Increased initial inflation pressure recruits collapsed alveoli which then require
minimal pressure to stay open.
 Early recruitment <72hrs – better response & maintain integrity of newly recruited
lung.
 Lung opens at 45cm H2O which then remains open even at 25cm H2O.

26.  Recruitment Maneuvers (RMs)
 Grasso et al (22patients) – PEEP 40cm for 40 sec. If lung is recruitable –
improvement in lung & Chest compliance by 175%, Improved SpO2 & PaO2 within
2 min.
 Patients with non recruitable lungs – little response/deterioration inSpO2, PaO2/
hemodynamics. Indication for HFOV

27. Recruitment maneuvers in ARDS

29. Prone Position
1) to improve oxygenation;
2)to improve respiratory mechanics;
3) to homogenize the pleural pressure gradient, the alveolar inflation and the
ventilation distribution;
4) to increase lung volume and reduce
the amount of atelectatic regions;
5) to facilitate the drainage of secretions; and
6) to reduce ventilator-associated lung injury

31. Physiological effects of prone positioning
 Effects on oxygenation :
- Alveolar dimensions depend on the
transpulmonary pressure (Ptrans pulm = Palv-Ppl)
- Since PA is more negative in nondependent lung regions,
transpulmonary pressure is greater in the nondependent,
compared to the dependent areas.

32.  Ptp depends upon
- Lung weight
- Cardiac mass.
- Cephalic displacement of the abdomen
- Regional lung and chest wall mechanical properties
and shape.
(Thoracic shape is more similar to a triangle
in the supine position (apex on top) allows the formation of more
extensive atelectasis than a rectangular thoracic shape)

33.  Permissive Hypercapnia
 As far as pH is maintained >7.15 ( PaCO2 is accepted upto 80mm Hg)
 But in septic patient , correct acidosis to improve outcome.
 Hypothesis – Hypercapneic acidosis is beneficial as it downregulates inflammatory
cell activity and xanthine oxidase activity thus reducing oxidative stress.
 C/I in Traumatic brain injury & Cardiac dysfunction

34.  Stepwise treatment of Hypoxemia
 PIP/PEEP titration
 Prone position
 HFOV
 Surfactant
 Inhaled NO
 Corticosteroids
 ECMO

35.  HFOV
 Introduced by Lunkenheimer 1972
 Expiration and Inspiration active process
 VT 1-3ml/kg ,freq 100 - 2400/min
 Prevents air trapping,over distension and CVS depression
 Applied for severe ARDS
 better oxygenation
 Early institution may be beneficial

36.  Considered in pts requiring high Pressures
 FiO2 req >60%
 Failure to improve oxygenation index within 24-48hrs
 Non responders to HFOV have high mortality.

37.  Surfactant:
RCTs and retrospective studies :
rapid and sustained improvement in oxygenation, faster weaning, shorter ICU stay
but no difference in mortality.

38.  NO
 Useful in Pulmonary HT in ARDS
 Improves short term oxygenation in ARDS
 Little impact on long term oxygenation and mortality

39.  ECMO
 To support oxygenation while lung healing takes place
 Retrospective studies – survival in critically ill ARDS pts

40. Noninvasive Support Ventilation
Management.(PARDS)
 NPPV - reduce atelectasis, and potentially unloads fatigued respiratory muscles,
preserving the child's natural airway and airway clearance mechanisms.
 avoids complications of invasive therapies as well as the need for sedation or
muscle relaxation
 NPPV provides a continuous level of positive expiratory pressure - maintains small
airway patency, increase end-expiratory lung volumes, and improve pulmonary
compliance, reducing the change in alveolar pressure needed to initiate inspiration.
 With bilevel support, the additional inspiratory pressure can help raise tidal
volumes and support fatigued respiratory muscles - improve work of breathing,
dyspnea, and gas exchange until the underlying disease process improves.

41.  NPPV be considered early in disease in children at risk for PARDS to improve gas
exchange, decrease work of breathing, and potentially avoid complications of
invasive ventilation
 children with immunodeficiency – more benefit
 not recommended for children with severe disease

42. NIPPV for the Treatment of ARDS -studies

43.  Children with more severe PARDS, however, are significantly more likely to require
intubation despite the use of NPPV.
 the median frequency of NPPV failure in those children with more mild PARDS was
21%

44. Role of High-flow Nasal Cannula (PARDS)
 provides improved oxygenation and reduced dead space by "washing out" of
nasopharyngeal CO2, thereby increasing effective ventilation.
 HFNC generates a modest degree of positive pressure, thereby reducing upper
airways resistance and reducing work of breathing.
 level of positive pressure generated by currently available HFNC systems is
unknown, but it is thought to be less than that provided by NPPV.

45. Approach to Diagnosis
 Essential Laboratory Tests
 ABG - PaO2 and PaO2/FiO2 ratio.
 CXR
 Acute progressive hypoxemic respiratory failuare.
 Occasionaly –
 2DEcho and CT Chest
 Additional tests –
CBC, Lactate, bld c/s, ET secretion C/S, S. Electrolytes
 Valuable test in severe hypoxemia
ScvO2
 Noninvasive monitoring of systemic oxygenation
SPO2 and End tidal CO2 capnography.

46. Summary – Management strategy of ARDS

49. Thank You!!!