Acute Respiratory Distress Syndrome

Rahul Illaparambath

EPIDEMIOLOGY

• ARDS occurs in 1-4% of PICU admissions

• 10% of PICU patients who receive mechanical ventilation meet diagnostic criteria for ARDS

• Mortality varies between 20 – 75%

• Multicentered, prospective cohort study - Flori et al. -overall hospital mortality was 22% among children

with a PaO2:FIO2 ratio <300

-ARDS (PaO2: FIO2 <200) had a mortality of 26%

-MC diagnosis associated with ALI and ARDS among

the entire study cohort pneumonia (35%)

American-European Consensus Criteria ALI and ARDS

• Acute onset

• Bilateral pulmonary infiltrates on chest radiography

• Pulmonary artery occlusion pressure >18 mm Hg or no clinical evidence of left atrial hypertension

• PaO2:FIO2 ratio <300 = ALI

• PaO2:FIO2 ratio <200 = ARDS

• Bernard GR, Artigas A, Brigham KL, et al. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 1994;149:818–24.

The Berlin Definition of ARDS

• Respiratory symptoms must have begun within one week of a known clinical insult, or the patient must have new or worsening symptoms during the past week

• Bilateral opacities consistent with pulmonary edema must be present on a chest radiograph or computed tomographic (CT) scan

• The patient’s respiratory failure must not be fully explained by cardiac failure or fluid overload

• A moderate to severe impairment of oxygenation must be present(PaO2/FiO2)

-Mild ARDS – The PaO2/FiO2 is >200 mmHg, but ≤300 mmHg,

-Moderate ARDS – The PaO2/FiO2 is >100 mmHg, but ≤200 mmHg

-Severe ARDS – The PaO2/FiO2 is ≤100

all accompanied by ventilator setting that include PEEP ≥5 cm H2O.

ETIOLOGYDIRECT INJURY INDIRECT INJURY

Common-Pneumonia , -Aspiration of gastric content

Common-Sepsis-Severe trauma

Less common-Pulmonary concussion-Fat embolism-Near drowning-Inhalational injury,

Less common-Cardiopulmonary bypass-Drug overdose-Acute pancreatitis-Blood transfusion

Mechanisms preventing alveolar edema

• Retained intravascular protein• The interstitial lymphatics• Tight junctions btw alveolar epithelial cells

Injury

• Injury causes release of pro-inflammatory cytokines

• Damage to the capillary endothelium and alveolar epithelium

• Functional surfactant is lost• Ability to upregulate alveolar fluid clearance

may also be lost

Consequences

• Impaired gas exchange - ventilation-perfusion mismatching -while increased physiologic dead space impairs carbon dioxide elimination • Decreased lung compliance -stiffness of poorly or non-aerated lung • Pulmonary hypertension -hypoxic vasoconstriction, -vascular compression by positive airway pressure, -parenchymal destruction, airway collapse,

Phases of ARDS Exudative phase ↓pulmonary compliance, arterial hypoxemia, tachypnea,

hypocarbia. ,x ray (pulmonary edema)

Fibroproliferative phase ↑ alveolar dead space / refractory pulmonary hypertension due

to chronic inflammation and scarring of the alveolar-capillary unit.

Recovery phase restoration of alveolar epithelial barrier/ gradual improvement

in pulmonary compliance resolution of arterial hypoxemia/ return to premorbid pulmonary function in many patients .

Clinical features • Fluid accumulation • Lung compliance declines and tachypnea ensues • Regional atelectasis and small-airways closure • Hypoxia / breathing labored• Hypocarbia followed by hypercarbia• Rales over areas of atelectasis or alveolar congestion

and decreased air entry over areas that are largely consolidated. Occasionally rhonchi

Investigations

Chest Xray • Small volume lungs• Diffuse infiltrates• Airbronchograms , atelectasis• Fibrosis with reticular opacitiesCT scan• Heterogenous opacification in dependent

regions

Early ARDS picture

Full blown ARDS picture

CT scan picture

Differentials….

• Cardiogenic pulmonary edema • An acute exacerbation of IPF - previous chest radiographs - subpleural reticulocytic

changes -surgical lung biopsy• Diffuse alveolar hemorrhage• Idiopathic acute eosinophilic pneumonia(IAEP)• Malignancy • Acute interstitial pneumonia (Hamman-Rich syndrome)

Management

• MECHANICAL VENTILATION• FLUID MANAGEMENT• SEDATION AND ANALGESIA• POSITIONING• HFOV• DRUGS

Ventilation-Goals

• Maintain adequate gas exchange• Minimal VILI -Keep FiO2 less than 60% -Avoid volutrauma and barotrauma -Avoid repetitive disconnection

• Controlled oxygen exposure -Direct cellular injury -Absorption atelectasis -Accept saturation of 86-90%• Low tidal volume ventilation -To limit harmful airway pressures -TV of 6 ml/kg

• PEEP -augment anatomical dead space by distending large airways -cardiovascular compromise in high PEEP• Optimal PEEP -Improves oxygenation -Displacement of fluid from alveoli -Recruitment and opening up of collapsed alveoli -Improved FRC• Permissive hypercapnia -Accept high CO2 till pH 7.2

• Most children have concomitant shock• Aggressive fluid resuscitation till stable• Excess lung water will decrease saturation• Adequate sedation and analgesia• Antibiotic therapy for primary cause• Early enteral nutrition

Prone positioning

• Prone position improves V/Q mismatch• Recruitment of dependent portions• Decreases chest wall compliance (transmitting

airway pressure to the alveoli more efficiently and stabilizing alveolar volume over a larger portion of previously nonaerated lung units)

• If no deterioration with prone position, continue for 18-20 hours

Adjuvant Therapies in ARDS

• HFOV• NITRIC OXIDE – pulmonary vasodilatation• STEROIDS• SURFACTANT• ECMO• Inhaled &systemic beta agonists

Predictors of outcome

• Disease-related -Oxygenation-PaO2/FiO2( mild, moderate, and severe

ARDS had mortality rates of 27, 32, and 45 percent, respectively)

-Pulmonary vascular dysfunction(elevated transpulmonary gradient (ie, ≥12 mmHg)

-Underlying cause of the ARDS• Patient related

• Treatment related -Fluid balance-positive fluid balance may be

associated with higher mortality (1) -Treatment with glucocorticoids -Packed red blood cell transfusion-increased

likelihood of death (odds ratio 1.10 per unit transfused, 95% CI 1.04-1.17) (2)

1.Rosenberg AL, Dechert RE, Park PK, et al. Review of a large clinical series: association of cumulative fluid balance on outcome in acute lung injury: a retrospective review of the ARDSnet tidal volume study cohort. J Intensive Care Med 2009; 24:35.

2.Gong MN, Thompson BT, Williams P, et al. Clinical predictors of and mortality in acute respiratory distress syndrome: potential role of red cell transfusion. Crit Care Med 2005; 33:1191.