In ARDS, all are seen except :
Acute respiratory distress syndrome
Aetiology and pathogenesis
Acute respiratory distress syndrome (ARDS) is a diffuse neutrophilic alveolitis caused by a range of conditions and characterised by bilateral radiographic inﬁltrates and hypoxaemia. Activated neutrophils are sequestered into the lungs and capillary permeability is increased, with damage to cells within the alveoli. The pathophysiology is part of the inﬂammatory spectrum, and the triggers are similar: infective and non-infective inﬂammatory processes. These processes result in exudation and accumulation of protein-rich cellular ﬂuid within alveoli and the formation of characteristic ‘hyaline membranes’. Local release of cytokines and chemokines by activated macrophages and neutrophils results in progressive recruitment of inﬂammatory cells. Secondary effects include loss of surfactant and impaired surfactant production. The net effect is alveolar collapse and reduced lung compliance, most marked in dependent regions of the lung (mainly dorsal in supine patients). 
The affected airspaces become ﬂuid-ﬁlled and can no longer contribute to ventilation, resulting in hypoxaemia (due to increased pulmonary shunt) and hypercapnia (due to inadequate ventilation in some areas of the lung): that is, ventilation–perfusion mismatch.
Reference: : Davidson P R I N C I P L E S   and Practice O F M E D I C I N E 23rd edition page no  198
Dilated bronchioles
Edema
Fibrosis
Alveolar damage