ARDS is a clinical syndrome of acute respiratory failure characterized by hypoxemia and bilateral pulmonary infiltrates that cannot be fully accounted for by heart failure or fluid overload.

Epidemiology

Etiology

• Systemic causes
  • Sepsis (most common cause), e.g., secondary to trauma, infection or peritonitis
  • Trauma
  • Shock
  • Massive transfusion
  • Acute pancreatitis
• Primary damage to the lungs
  • Pneumonia
  • Aspiration
  • Inhaled toxins
  • Drowning incidents

Pathophysiology

• Tissue damage (pulmonary or extrapulmonary) → release of inflammatory mediators (e.g., interleukin-1) → inflammatory reaction → migration of neutrophils into alveoli → excessive release of neutrophilic mediators (e.g., cytokines, proteases, reactive oxygen species) → injury to alveolar capillaries and endothelial cells (diffuse alveolar damage, DAD) leading to:
  • Exudative phase: excess fluid in interstitium and on alveolar surface → pulmonary edema with normal pulmonary capillary wedge pressure (noncardiogenic pulmonary edema) → decreased lung compliance and respiratory distress
  • Hyaline membrane formation: exudation of neutrophils and protein-rich fluid into the alveolar space → formation of alveolar hyaline membranes → impaired gas exchange → hypoxemia
    • Hypoxemia → compensation through hyperventilation → respiratory alkalosis
    • Hypoxemia → chronic hypoxic pulmonary vasoconstriction → pulmonary hypertension and right-to-left pulmonary shunt (increased shunt fraction)
    • Damage to type I and type II pneumocytes → decrease in surfactant → alveolar collapse → intrapulmonary shunting
  • Organizing phase (late stage): proliferation of type II pneumocytes and infiltration of fibroblasts → progressive interstitial fibrosis

Clinical features

• Acute dyspnea
• Tachypnea and tachycardia
• Cyanosis
• Diffuse crackles

Diagnostics

Berlin criteria for ARDS

• Acute onset: respiratory failure within one week of a known predisposing factor (e.g., sepsis, pneumonia) or worsening respiratory symptoms
• Bilateral opacities (on chest x-ray or CT)
  • Similar appearance to pulmonary edema
  • Not sufficiently explained by pleural effusions, lobar or lung collapse, or nodules
• Hypoxemia: PaO2/FiO2 ≤ 300 mm Hg (measured with a minimum of 5 cm H₂O PEEP)
  • Mild ARDS: PaO2/FiO2 = 201–300 mm Hg
  • Moderate ARDS: PaO2/FiO2 = 101–200 mm Hg
  • Severe ARDS: PaO2/FiO2 ≤ 100 mm Hg
• Respiratory failure cannot be fully accounted for by heart failure or fluid overload.

Treatment