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ARDS is characterised by damage to the arteriolar-capillary endothelium and alveolar epithelium, including type I and type II pneumocytes. Damage to the latter results in surfactant deficiency and atelectasis. Even though surfactant abnormalities in ARDS are not the primary pathogenic factor, surfactant deficiency , either in presence or absence of type II pneumocyte alterations, may result from primary or secondary inhibition or inactivation of pulmonary surfactant in the alveolar space. Surfactant deficiency will further induce alveolar collapse and pulmonary oedema, leading to the characteristic pathophysiology of ARDS.
