fibrin and Crush-Syndrome

The authors' and literature data on the liver changes at different types of shock are summarized with consideration of the role of etiology and pathogenetic factors. Three groups of similar liver alterations reflecting the severity of impairment of the reticulo-endothelial system (RES), microcirculation and parenchyma are distinguished. No clear-cut dependence between the liver morphological changes and the severity of shock is noted. At the same time the characteristic structural alterations for some forms of shock differing at their early stages by a predominance of neuro-reflectoral, hypovolemic or toxic component are revealed. A rapidly developing hydropic degeneration, the absence of the compensatory changes, signs of the RES deficiency with the progressing necrobiotic and necrotic processes in the liver are characteristic for a neuro-reflectoral shock. Endotoxic shock is associated with widespread intravascular thrombi, liver cell necrosis, combination of the destruction of reticuloendotheliocytes with the signs of their preceding activation, foci of a smooth cytoplasmic network hyperplasia of centrolobular hepatocytes; hypovolemic shock is characterized by activation of compensatory processes.

Topics: Animals; Crush Syndrome; Disseminated Intravascular Coagulation; Energy Metabolism; Fibrin; Kupffer Cells; Liver; Microcirculation; Microscopy, Electron; Mitochondria, Liver; Pain; Phagocytosis; Platelet Aggregation; Rabbits; Rats; Shock; Shock, Hemorrhagic; Shock, Septic

Topics: Adult; Antibodies, Monoclonal; Crush Syndrome; Fibrin; Humans; Indium Radioisotopes; Male; Radionuclide Imaging; Shock, Traumatic