Blood coagulation changes in shock.

A secondary coagulopathy develops in a state of hypovolemic shock; in endotoxin shock, the coagulopathy is primary. As the changes in the hemodynamic and metabolic functions advance in hypovolemic shock, a state of hypercoagulability appears which reinforces the irreversible nature of this condition. In endotoxin shock, a primary mixed coagulopathy develops as an event directly related to the presence of bacterial lipopolysaccharides. The first finding is the activation of the fibrinolytic system through the activation of the serum complement system by means of the participation of the properdin, the so-called alternate pathway to the complement system. At the same time and by an identical mechanism, the activation of Factors VII and XI occurs through the activation of the Fletchner Factor, while the Hageman trait is activated by kinogen. Immediately after and following an antigen-antibody type reaction, endotoxin stimulates activation of platelets in the presence of gamma-2-globulin along the classical pathway of activation of the serum complement.