Clinical Pathology



0-7 days

  • Acute inflammatory reaction in the lung caused by insult to the epithelium
  • Alveoli fill with neutrophils, blood and a protein-rich pulmonary oedema
  • Associated alveolar epithelial and capillary endothelial damage, with loss of alveolar cells and structural integrity
  • Hyaline membranes form composed of cellular debris and plasma proteins (peak 4–5 days)
  • Destruction of the pulmonary vascular bedvDysregulation of coagulation and fibrinolysis leads to microthrombus formation
  • Capillary thrombosis occurs
  • Causes hypoxia due to widespread and profound V/Q mismatching
  • Results from an inflammatory reaction which may be superimposed on direct lung injury
  • Both shunt and dead space increase as alveoli and capillaries respectively are included
  • If severe, right ventricular failure and low cardiac output contribute further to venous admixture and hypoxia
  • Ventilation may increase injury with major causes, including:
    • Volutrauma - overdistension of alveoli:
    • Barotrauma - excessive inflation pressures
    • Atelectrauma - injury due to cyclical opening and closing of alveoli
    • Biotrauma - increased permeability, the release of inflammatory mediators and translocation of pathogens



7-14 days

  • Proliferation of type II pneumocytes and fibroblasts with fibrin deposition
  • Pulmonary vascular resistance increases leading to pulmonary hypertension
  • Thickened alveolar walls lead to reduced diffusion capacity
  • Risk of pneumothorax and pneumonia



>14 days

  • Chronic inflammation, fibrosis and neovascularization occur
  • Global damage to underlying lung tissue
    • Emphysematous lungs (Decreased surface area)
    • Decreased compliance
    • Pulmonary Hypertension
    Pathophysiological mechanisms involved in ARDS