Because DIC involves unregulated thrombin and plasmin generation, the clinical manifestation of DIC in bleeding patients will be determined by the level of coagulation activity relative to the level of fibrinolytic activity. A deficiency of tissue factor pathway inhibitor (TFPI) increases susceptibility to the development of DIC [72], but possible TFPI dysregulation as a mechanism of bleeding-associated coagulopathy has not been investigated. Most often DIC is a hypercoagulable state characterized by diffuse non-specific deposition of microthrombi in smaller vessels causing a thrombotic microangiopathy, which obstructs microvascular flow, disrupts oxygen delivery to tissue, and results in organ system dysfunction or failure. [72] The coagulopathy that occurs from consumption of platelets and coagulation factors in microvascular thrombi exacerbates hemorrhage. Fibrinolysis may compensate for intravascular microthrombosis, and therefore antifibrinolytic therapy for bleeding-associated DIC is not recommended, except in rare cases when fibrinolysis dominates the clinical course (hyperfibrinolysis)