Overview ARDS is an acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability, increased lung weight, and a loss of aerated tissue. Clinical hallmarks of ARDS are hypoxemia and bilateral radiographic opacities, while the pathological hallmark is diffuse alveolar damage.

Clinical Presentation

• 6 to 72 hours of an inciting event and worsen rapidly
• Tachypnoea
• Tachycardia
• Diaphoresis
• Accesory muscle use
• Dyspnea
• Cyanosis (hypoxemia)
• Diffuse crackles
• +/- Cough and chest pain

Clinical Course

• The first several days of ARDS are characterized by hypoxemia requiring a moderate to high concentration of inspired oxygen
• Most patients who survive this initial course begin to exhibit better oxygenation and decreasing alveolar infiltrates over the next several days.
• Some patients, however, have persistent, severe hypoxemia and remain ventilator-dependent. Pulmonary proliferative changes and fibrosis may progressively replace the pathological findings of diffuse alveolar damage as early as ten days after the onset of the respiratory failure.

Diagnostic Criteria – Berlin Definition

• Acute onset of symptoms of a known clinical insult (<1 week)
• Bilateral opacities consistent with pulmonary edema on Chest X-ray or CT. Other causes ruled out:
  • Pulmonary nodules
  • Lung collapse
  • Pleural effusion
• Cardiac failure and fluid overload ruled out
• Decreased (moderate to severe) oxygenation must be present
  • Mild
  • Moderate
  • Severe

Aetiology

• Indirect lung injury: sepsis, shock, trauma, pancreatitis, drug OD, intracranial haemorrhage, blood-transfusion related lung injury
• Direct lung injury: aspiration, inhalational injury, embolism

Pathophysiology

• Insult → release of inflammatory mediators promoting neutrophil accumulation in microcirculation oflung
• Neutrophils damage vascular endothelium + alveolar epithelium
• Leads to pulmonary oedema, hyaline membrane formation & difficult gas exchange

• Mechanical ventilation using high PEEP & low tidal volumes to prevent ventilator-associated injury
• O2 therapy: aim PaO2>60mmHg or SpO2>90% with permissive hypercapnia
• Treat underlying disorder/precipitant
• Conservative fluid Mx strategy: aim to minimize or eliminate positive fluid balance that can → pulmonary oedema
• Supportive care
  • Haemodynamic support to maintain MAP>60mmHg
  • Enteral nutritional support
  • DVT & stress ulcer prevention

Complications of ARDS

• Barotrauma
• Nosocomial infection
• Deep Vein Thrombosis
• Delirium
• Gastrointestinal ulcer
• Poor nutrition