Abstract
Blood loss following trauma is controlled by a complex series of interactions involving the vascular surface, blood platelets and ‘activated’ coagulation factors. Activation of the coagulation cascade involves a series of zymogen to enzyme transformations with each enzyme associating with a co-factor on a ‘surface’ such as negatively charged platelet membrane phospholipid to form reaction complexes. In physiological terms it is possible that this system is continuously switched on producing low levels of activated serine proteases which are continuously being neutralised by protease inhibitors and co-factor neutralising reactions which down-regulate blood clotting processes, thus maintaining patency of the vascular tree.
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