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Successful hemostasis of patients with hemorrhagic shock in the Emergency Department
SEOKRAN YEOM. MD, PhD
Department of Emergency medicine, Pusan National University Hospital
Massive transfusion to patients with hemorrhagic shock in and of itself can cause hypothermia, hemodilution, and platelet dysfunction, and because pRBCs lack plasma and clotting factors, various clotting factor deficiencies and hemodilution associated with fluid loading can also develop, and the risk of acute lung injury, infection, and immunosuppression increases. In contrast, factors that increase transfusion volume when managing hemorrhagic shock patients are bleeding itself and coagulopathy associated with bleeding.
Over the past 40 years, the proposed model of coagulation has evolved from one that incorporates intrinsic and extrinsic pathways to a model of cell-based coagulation that emphasizes the role of cells, and especially platelets. This model involves three phases: initiation, amplification, and propagation. Coagulation is initiated by vascular damage, which exposes the circulating blood to the tissue factor present in the subendothelial layer of the blood vessels. Both factor VIIa and factorbind tothe tissue factor, resulting in the conversion of prothrombin to thrombin, because of the activation of factorTo ensure adequate fibrin deposition, further generation of thrombin is required beyond what occurs during the initiation phase. Thus, duringthe amplification phase, platelets are activated by the initial burst of thrombin, which causes activation of multiple clotting factors, leading to further production of thrombin. During the propagation phase, factorand factorVIIIa bind to the platelet surface, promoting rapid generation of factorresulting in the conversion of prothrombin to thrombin, fibrinogen to fibrin, activation of factor VIII, and stabilization of the platelet plug.
When rFVIIa is administered, hemostasis is enhanced by two pathways that are tissue factor-dependent and In the former, factorX is activated when rFVIIa adheres to the site of vascular injury, and in the latter, factoris activated when rFVIIa adheres to the surface of platelets. By these two pathways, a “thrombin” is brought about and interaction between the platelet surfaces increases.
Treatment with rFVIIa may be especially effective in blunt trauma patient because blunt injury more often leads to diffuse bleeding, in which surgical haemostais might be more difficult to achieve17). In a European guideline of Management of bleeding following major trauma, they suggested the use of rFVIIa be considered if major bleeding in blunt trauma persists despite of standard attempts to control bleeding and best-practice use of blood component. Once major bleeding from damaged vessels has been stopped, rFVIIa may be helpful to induce coagulation in areas of diffuse small vessel coagulopathic bleeding.
Recombinant FVIIa was originally licensed for the treatment of hemophilic patients with antibodies to factoror IX. In recent studies, rFVIIa is being used on an off-label basis to control blood loss in a variety of other clinical situations : postpartum hemorrhage, Intracranial hemorrhage, GI bleeding, Postoperative or postprocedual bleeding. Although off-label use of rFVIIa is expensive, the cost-effectiveness of rFVIIa in saving the lives of patients is considerable, and rFVIIa is available for uncontrolled massive hemorrhage.