Pediatric ARDS - Aetiopathogenesis, trials and ventilation strategies

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!!!