Pathology is wet lung is ?

Ref:Textbook of pathology (Harsh mohan) 6th edition,page no. Adult ARDS/Wet Lung. Adult ARDS is known by various synonyms such as shock-lung syndrome, diffuse alveolar damage (DAD), acute alveolar injury, traumatic wet lungs and post-traumatic respiratory insufficiency. The condition was first recognised in adults during World War II in survivors of non-thoracic injuries with shock. Adult ARDS also presents clinically by sudden and severe respiratory distress, tachypnoea, tachycardia, cyanosis and severe hypoxaemia. The mechanism of acute injury by etiologic agents listed above depends upon the imbalance between proinflammatory and anti-inflammatory cytokines: i) Activated pulmonay macrophages release proinflammatory cytokines such as IL8, IL1, and tumour necrosis factor (TNF), while macrophage inhibitory factor (MIF) helps to sustain inflammation in the alveoli. Number of neutrophils in the alveoli is increased in acute injury. Neutrophils on activation release products which cause active tissue injury e.g. proteases, platelet activating factor, oxidants and leukotrienes. ii) Besides the role of cytokines in acute injury, a few fibrogenic cytokines such as transforming growth factor-a (TGF-a) and platelet-derived growth factor (PDGF) play a role in repair process by stimulation of proliferation of fibroblast and collagen. In either case, injury to the capillary endothelium leads to increased vascular permeability while injured pneumocytes, especially type 1, undergo necrosis. The net effect of injury to both capillary endothelium and alveolar epithelium is interstitial and intra-alveolar oedema, congestion, fibrin deposition and formation of hyaline membranes. As a result of coating of the alveoli with hyaline membranes, there is loss of surfactant causing collapse calle 'stiff lung'. There is an attempt at regeneration of alveolar cells by proliferation of type II alveolar cells so as to increase the secretion of surfactant.