The Bleeding Dog

The current understanding of hemostasis is focused on the cell-based model, which gives a more physiologic representation of blood clotting compared to the traditional cascade model. It consists of initiation, amplification and propagation phases. Initiation occurs when injury allows cells bearing tissue factor (Factor III) to react with Factor VII, ultimately resulting in the generation of a small amount of thrombin (Factor II). This reaction is amplified when the initial thrombin activates platelets and cleaves von Willebrand factor (vWf) from Factor VIII, allowing the former to promote platelet aggregation and adhesion to exposed subendothelial collagen. Coagulation is then propagated on the activated platelet surface, which ultimately results in generation of a large amount of thrombin, which converts fibrinogen (Factor I) to fibrin and stabilizes the aggregated platelet plug. While the cell-based model gives a better understanding of the integration of the various steps of hemostasis, the traditional model remains the most useful for daily clinical work. The traditional model divides hemostasis into primary and secondary hemostasis. Primary hemostasis refers to the interactions between the blood vessel wall, platelets and vWf. Primary hemostatic defects may be inherited or acquired. Classically primary hemostatic defects cause petechiae, ecchymoses, and mucosal bleeding at multiple sites, and excessive and prolonged bleeding after injury, although this characterization is influenced by thrombocytopenia, which the most common defect. Secondary hemostasis consists of the coagulation factor cascades that ultimately result in stabilizing a platelet plug with fibrin. The coagulation factors are: I (fibrinogen), II (prothrombin), III (tissue factor or platelet phospholipid), IV (calcium), V, (there is no factor VI), VII, VIII, IX, X, XI, XII (Hageman Factor), and XIII. The factors are named more in order of discovery and naming than functional order. Bleeding due to coagulopathies may be localized or widespread. Hemarthrosis, pericardial bleeding, hemothorax, hemoabdomen and subcutaneous hematomas may occur, which are not typical of primary hemostatic defects. Excessive bleeding may also be delayed after injury, and rebleeding may occur, especially with defects in the intrinsic system. In the traditional view of hemostasis this occurs because bleeding is initially controlled by primary hemostasis, but the platelet plug is not converted into a firm clot. In the cell-based model, this occurs because the initiation phase initially controls bleeding, but the thrombin burst of the propagation phase does not occur. Depending on severity, vitamin-K antagonist poisoning may be characterized by either immediate or delayed bleeding after injury.