Abstract
Hypocirculation causes hypercoagulability with an increase of Factors V and VIII, and a diminished platelet count. In shock hypercoagulability is followed by hypocoagulability due to loss of Factors I, II, V, VIII and XIII together with thrombocytopaenia and qualitative alterations in platelet properties. This reversal is caused by disseminated intravascular coagulation consuming clotting factors and platelets—consumptive coagulopathy.
Fibrin deposits occur in the peripheral vasculature of the viscera and are associated with a rising oxygen debt, and, in clinical situations, with haemorrhagic diathesis, visceral necrosis and irreversible shock. Localization of the microthrombi is under the influence of catecholamines, ACTH and aldosterone.
Administration of heparin in clinical shock may prevent the development of consumptive coagulopathy, but is without effect if disseminated intravascular coagulation is already present.
Anti-fibrinolytic therapy is contraindicated whereas streptokinase-induced fibrinolysis has experimental and clinical justifications.
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Selected References
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