Morphologic development of human shock lung.
In the initial phase of shock, edema spreads throughout the alveolar interstitium even before injury occurs in the alveolar epithelium and endothelium. The endothelium and the epithelium are damaged only subsequently, causing reduction in the average barrier thickness of the epithelium and the endothelium. A point of irreversibility is reached by the end of the first week. While early cell regeneration may be observed within the alveolar endothelium and epithelium, proliferation of fibroblasts and fibrosis of the alveolar wall occur in addition to edema which spreads within the interstitium. This widening of the gas exchange barrier may be considered as the anatomic substrate of respiratory insufficiency induced by shock. This enlargement continues up to the moment when thickening of the alveoli impedes satisfactory functioning of the lung, and, as consequence, threatens the life of the patient.
D002455:Cell Division; D004727:Endothelium / Q000648:ultrastructure; D004848:Epithelium / Q000648:ultrastructure; D005342:Fibrinolysis; D005347:Fibroblasts / Q000648:ultrastructure; D006801:Humans; D008066:Lipolysis; D008854:Microscopy, Electron; D011650:Pulmonary Alveoli / Q000648:ultrastructure; D011658:Pulmonary Fibrosis / Q000150:complications; D012038:Regeneration; D012128:Respiratory Distress Syndrome / Q000150:complications / Q000473:pathology*; D013997:Time Factors