Diffuse alveolar damage causes non-cardiogenic oedema, shunt and stiff lungs
Expansion
Pathophysiology
- Diffuse alveolar damage increases alveolar-capillary permeability
- Protein-rich pulmonary oedema floods alveoli, with a normal wedge pressure
- Surfactant is inactivated, causing widespread collapse
- The result is shunt, refractory hypoxaemia and greatly reduced compliance
The Berlin definition requires onset within one week, bilateral opacities not fully explained by effusion or collapse, respiratory failure not explained by cardiac failure or fluid overload, and a PaO2/FiO2 ratio of 300 mmHg or less with at least 5 cmH2O of PEEP. Severity is mild, moderate or severe by that ratio.
The baby lung concept is central to management: aerated lung volume may be only 20 to 30 per cent of normal, so a conventional tidal volume delivered to that small volume causes overdistension. Hence low tidal volume ventilation at about 6 ml per kilogram of predicted body weight, permissive hypercapnia, adequate PEEP, and prone positioning, which improves matching by recruiting dorsal lung.