[Morphology and pathogenetic problems of the crush syndrome]

Abstract

Morphofunctional studies of muscles, heart, liver and kidneys after different periods of compression and decompression, as well as literature data indicate that crush syndrome is one of the most severe forms of traumatic shock. A wide range of pathologic effects of catecholamines and other shock-causing agents in response to the emotional stress and pain occurs already at the compression period and results in hemodynamic disturbances in microcirculation of organs and tissues with the development of dystrophic and necrobiotic processes, depression of the monocytic phagocyte system and immune system. The consequences of shock are mostly manifest after decompression: hypercatecholaminemia, hypovolemia, intoxication with myolysis and pathogenic microflora products result in aggravation of monocytic phagocyte failure, as well as immune system, intravascular coagulation, membrane penetration insufficiency, cell necrosis. Monocytic macrophage depletion favours the progression of hepatic necrobiosis, formation of renal failure and detritus organization in the muscles of the extremities. Hypercatecholaminemia and hypoxia (leading to electrolyte-imbalance contractures of myofibrillar apparatus, metabolism disorder and intracellular conductivity disturbance) from the basis for cardiac insufficiency. Inadequate cardiac function, in its turn, maintains hemodynamic and hypoxic disturbances in tissues. Changes in renal blood flow, hemofiltration and tubular system are shown to reflect different aspects of pathogenesis of the acute renal failure in crush syndrome.