Thromboembolism

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Abstract
Thromboembolism may be considered as one of the manifestations of the response of blood to injury. Other manifestations of this include hemostasis, increased vessel permeability, and vasculitis; disturbances of the microcirculation may lead to tissue injury and organ dysfunction. The factors that can initiate these changes by stimulation of platelets are exposure of subendothelial tissue (collagen, basement membrane) and intravascular stimuli such as antigen-antibody complexes, viruses, bacteria, and endotoxin. These stimuli have a number of effects on blood; the interaction of the platelets with the above stimuli leads to the release of platelet constituents including ADP; the ADP causes the platelets to adhere to each other; the aggregated platelets cause acceleration of clotting; this and changes in blood flow promote the formation of fibrin around the platelet aggregates. Some of the stimuli such as collagen and antigen-antibody complexes also activate blood coagulation through factor XII; some of the materials released from these platelets affect the vessel wall. The initial platelet mass is transformed to a fibrin mass. There are compounds that inhibit the platelet release reaction, platelet aggregation, and blood coagulation and activate the fibrinolytic mechanism. It appears that by the selective use of these compounds we can improve our management of all aspects of thromboembolic disease related to vascular and intravascular stimuli.