Acute Respiratory Distress Syndrome

Section: Critical care Curriculum: Curriculum, page 46

Definition

• ARDS is an inflammatory injury to lung endothelium and epithelium leading to an increase in permeability and accumulation of proteinaceous fluid within alveoli resulting in imparied CO2 excretion
  • It is a life threatening clinical syndrome which can occur secondary to systemic insults such as shock, sepsis, trauma, over transfusion
  • It is characterised by respiratory compromise and bilateral pulmonary infiltrates on CXR
  • The systemic inflammatory response which occurs leads to alveolar damage via a proinflammatory cytokine mediated cascade - IL-1, 6 and TNF alpha which outbalances the antiinflammatory response to overwhelm the local responses and lead to systemic unwellness
  • Alveolar/capillary interface increased permeability via direct damage and inflammatory cascade response leads to loss of surfactant and proteinaceous fluid accumulation within alveoli
  • Thus there is alveolar collapse and hypoxaemia
  • Leading to VQ mismatch and pulmonary HTN - exacerbating shock

General

• Acute, diffuse, inflammatory pulmonary condition
• Life threatening clinical syndrome characterized by severe, progressive impaired gas exchange and bilateral pulmonary infiltrates
• Absence of cardiogenic oedema
• Microsopically typified by capillary endothelial injury and diffuse alveolar damage
• Commences within 7 days of an inciting insult

Aetiology

• Pulmonary (Direct)
  • Pneumonia
  • Aspiration
• Extra-pulmonary (Indirect)
  • Sepsis
  • Pancreatitis
  • Trauma
  • Massive transfusion

Pathology

• Exudative phase
  • Initiation
    • Stimulis
      • Injury to alveolar capillaries and epithelium
  • Inflammatory injury to lung endothelium and epithelium leading to an increase in permeability and accumulation of proteinaceous fluid within alveoli resulting in imparied CO2 excretion
  • The systemic inflammatory response which occurs leads to alveolar damage via a proinflammatory cytokine mediated cascade - IL-1, 6 and TNF alpha which outbalances the antiinflammatory response to overwhelm the local responses and lead to systemic unwellness
  • Alveolar/capillary interface increased permeability via direct damage and inflammatory cascade response leads to loss of surfactant and proteinaceous fluid accumulation within alveoli
  • Thus there is alveolar collapse and hypoxaemia
• Proliferative phase (7-21 days)
  • Inflammatory response begins to subsides and repair begins
  • Resolution of pulmonary edema
  • Delayed resolution due to epithelial and endothelial injury
• Fibrotic phase (>3 weeks)
  • If injury persists or repair is incomplete, chronic inflammation leads to fibrosis

Consequences

• V/Q mismatch - impaired gas exchange
• Decreased lung compliance
• Pulmonary HTN

Histology

• Diffuse Alveolar Damage (DAD):
  • Hallmark of ARDS, seen in both exudative and proliferative phases.
• Hyaline Membranes:
  • Composed of fibrin, plasma proteins, and necrotic epithelial cells, lining alveoli.
• Interstitial and Alveolar Edema.
  • Type II Pneumocyte Hyperplasia (repair phase).
• Fibrosis in advanced stages.

Clinical

• SOB
• Progressive hypoaxaemia
• Increasing O2 requirement
• Bibasal creps, cyanosis

Investigations

• CXR
  • Acute onset bilateral lung infiltrates
• Exclude cardiac cause
  • Non cardiac origin → normal BNP/ECHO
• ABG

Classification

• Berlin Criteria
  1. Resp symptoms within 1 week of insult
  2. Bilateral CXR opacities
  3. Respiratory failure with cardiac cause excluded
  4. PaO2:FiO2 <300mmhg

Severity

• PAO2:FiO2 ratio
  • Mild - 200-300
  • Moderate - 100-200
  • Severe - <100

Management

• Treat underlying cause
• ICU for respiratory support
• Prone
• Steroids

Prognosis

• Can get restrictive lung disease after recovery