Pediatric ARDS Dr Abhijeet DeshmukhDNB pediatrics, Fellow – PICU & NICU

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

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

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.

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

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 )

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.

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.

Host Immune response-Role of Cytokines

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

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

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 hypercapnia4. Permissive Hypoxemia

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)

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.

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%

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

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

Ventilation with Lower VT vs. Traditional VT forALI and ARDS ( ARDS Net)

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

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

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.

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

Recruitment maneuvers in ARDS

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 reducethe amount of atelectatic regions; 5) to facilitate the drainage of secretions; and 6) to reduce ventilator-associated lung injury

Physiological effects of prone positioning

Effects on oxygenation :

- Alveolar dimensions depend on thetranspulmonary 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.

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 trianglein the supine position (apex on top) allows the formation of more

extensive atelectasis than a rectangular thoracic shape)

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

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

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

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

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

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

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

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.

 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

NIPPV for the Treatment of ARDS -studies

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% 

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.

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.

Summary – Management strategy of ARDS

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