Fibrinolysis in Dogs with Intracavitary Effusion: A Review

SIMPLE SUMMARY: In blood vessels there is a balance between clot formation and its dissolution. Fibrinolysis normally allows the breakdown of blood clots during the healing of injured blood vessels. This process is mediated by the activation of a blood enzyme (plasmin) which breaks down a meshed protein (fibrin) which holds blood clots at the site of the vessel injury. In some diseases, the activation of plasmin becomes excessive, leading to bleeding tendencies (hyperfibrinolysis). Under normal conditions, abdominal and thoracic cavities are filled with a small amount of fluid deriving from the blood. The results of recent studies have shown that, in dogs, all types of pathologic intracavitary fluids have an increased fibrinolytic activity. This increased fibrinolytic activity is also present in their blood, in some cases reaching a hyperfibrinolytic state. Hyperfibrinolysis and bleeding tendencies have also been documented in cardiopathic dogs with ascites. The latter result is surprising considering that thrombotic events are commonly documented in humans and cats with some cardiac diseases. ABSTRACT: Physiologic fibrinolysis is a localized process in which stable fibrin strands are broken down by plasmin in response to thrombosis. Plasmin activation can also take place separately from the coagulation process, resulting in pathologic fibrinolysis. When plasmin activation exceeds the neutralizing capacity of plasmin inhibitors, severe bleeding can potentially take place. Although the processes which regulate coagulation and fibrinolysis in the blood are well known, it is less clear as to what extent the same processes take place in the body cavities and whether they influence systemic hemostasis. The results of the studies herein cited demonstrate that coagulation followed by fibrinogenolytic/fibrinolytic activity takes place in all kinds of canine ascitic and pleural fluids. Moreover, systemic clotting abnormalities suggesting primary fibrinolysis/primary hyperfibrinolysis (i.e., elevated plasma fibrin/fibrinogen degradation products [FDPs] and normal D-dimer concentrations with fibrinogen concentrations ≤ 100 mg/dL or above this cut-off, respectively) occur in dogs with intracavitary effusion. Enhanced fibrinolytic activity in dogs with intracavitary effusion can also be detected using rotational thromboelastometry (ROTEM), although the degree of agreement between ROTEM and FDPs, D-dimer and fibrinogen concentrations is poor. Finally, contrary to the thrombotic events commonly documented in some humans and cats with cardiac diseases, bleeding tendencies due to primary fibrinolysis/primary hyperfibrinolysis have been documented in dogs with cardiogenic ascites.