#Trauma triad of death Activator
#Trauma triad of death series

All three phases are regulated by the properties of cell surfaces, receptors, and coagulation proteins. This model considers the process as three overlapping phases: initiation, amplification and propagation. Under any normal physiological state, the blood coagulation status is a dynamic process and is the balance of clot formation, anti-coagulation and fibrinolysis.Īnother description of the coagulation process is a cell-based model of hemostasis. The fibrinolytic system is regulated through the generation of plasmin from the activities of tPA, PAI and an antiplasmin inhibitor.

#Trauma triad of death Activator

The activity of tPA can be inhibited by plasminogen activator inhibitors (PAI). Plasmin is generated from inactive protein plasminogen via tissue-type plasminogen activator (tPA).

In addition, fibrin clots, once formed, are subject to fibrinolysis by plasmin. Activated protein C, the product of the thrombomodulin-thrombin complex, inactivates prothrombinase and the intrinsic pathway. Tissue factor pathway inhibitor inhibits factor Xa and eliminates the contribution of the extrinsic pathway to clot formation. Circulating antithrombin III inhibits factor Xa and thrombin, with 2000-fold amplified effects by heparin. The formation of fibrin clots is counterbalanced by its inhibitory and anti-coagulation processes. Clinical standard plasma tests of prothrombin time (PT) and activated partial thromboplastin time (aPTT) reflect the overall enzyme activities involved in the extrinsic and intrinsic pathways, respectively.

This classic cascade model provides a biochemical description of the coagulation process and the basis for clinical assessments of coagulation but it is now considered incomplete because it does not take into consideration the coagulation inhibition in plasma. The factor VIIa/tissue factor complex, once produced, activates additional factor VII, initial thrombin, factor Xa complex, and platelets, resulting in the exponential thrombin burst for rapid clot formation. The extrinsic pathway is triggered by plasma factor VIIa binding with tissue factor (factor III) released from the injury sites. The intrinsic pathway, or contact activation pathway, consists of the activations of factor VIII, IX, X, XI, XII and Xa complex, resulting in thrombin generation from precursor prothrombin (factor II). The two pathways converge to form a common pathway to generate thrombin. Biochemically, blood clotting is initiated via the intrinsic and/or extrinsic pathways. The essence of the process is the production of fibrin clots from fibrinogen (factor I), and thrombin plays a central role catalyzing the reaction.

#Trauma triad of death series

This review summarizes the current knowledge of coagulation complications following trauma.īlood coagulation is an important physiological process, including a series of physical, biochemical and cellular responses after various stimuli. However, to date, our understanding of the underlying mechanisms remains incomplete. The recognition of this early coagulopathy leads to the use of new terminology and proposed hypotheses. The hemostatic manifestation is associated with increased blood transfusion requirements, longer hospital stay, and higher mortality. Over the past decade, clinical observations around the globe have independently shown that coagulopathy may be present as early as hospital admission in some trauma patients. Hypothermia, acidosis, and resuscitative hemodilution have been considered as the significant contributors to coagulation dysfunction after trauma. Uncontrolled hemorrhage from coagulation dysfunction is one of the main potentially preventable causes of the mortality in both civilian and military settings. Traumatic injury remains one of the leading causes of death, accounting for about 40% of prehospital death.