3 clinical and pathological phases of ARDS
- lasts 3-5 days
- severe defect in oxygenations
- ¯ lung compliance
- bilateral pulmonary infiltrates
- endothelial and epithelial cell injury ̃
permeability of endothelial and epithelial
accumulation of protein-rich oedema fluid in interstitium and air spaces.
Contains RBCs, WBCs and hyaline membranes.
- abnormal surfactant/inactivation of surfactant
- neutrophil sequestration and migration in lung are histological hallmarks of
ARDS. Result from both chemotactic stimuli released within lung and activation
of neutrophils by circulating mediators
- followed either by recovery or progression to sub-acute phase
- starts 5-7 days after onset
- increased alveolar dead space
- persistently decreased lung compliance
- persistent oxygenation defect
- CXR: persistent, largely unchanging bilateral infiltrates
- Histology: interstitial fibrosis with proliferation of alveolar type II
cells. Obstruction and destruction of portions of microcirculation of lung.
- Followed by recovery or progression to chronic phase
- After 14 days there is a gradual transition to chronic phase
- Persistent low compliance
- Markedly increased VD/VT (>0.6)
- Extensive pulmonary fibrosis with obliteration of normal alveolar
architecture and progressive development of emphysematous regions of lung
including development of discrete bullae.
Pulmonary vascular changes
- early in ARDS pulmonary vasoconstriction, thromboembolism and interstitial
oedema, all of which are potentially reversible, can increase pulmonary vascular
resistance resulting in increased pulmonary artery pressure
- after several weeks, more permanent structural changes, such as fibrous
obliteration of the microcirculation and increased arterial muscularization,
contribute to pulmonary hypertension.