Fibrinolysis

The end result of the clotting pathway is the production of thrombin, which converts soluble fibrinogen to insoluble fibrin. The fibrin aggregates and forms a clot together with platelets, blocking the damaged blood vessel and preventing further bleeding. The fibrinolytic system (Figure 7.3) is directly influenced by the septic process and, in most patients with sepsis, it is suppressed while coagulation proceeds. Two key inhibitors of fibrinolysis that are produced by sepsis are plasminogen activator inhibitor 1 and thrombin activeatable fibrinolysis inhibitor.

Suppressed fibrinolysis via increased plasminogen activator inhibitor 1, thrombin activatable fibrinolysis inhibitor and reduced protein C

Suppressed fibrinolysis via increased plasminogen activator inhibitor 1, thrombin activatable fibrinolysis inhibitor and reduced protein C

Plasminogen

Plasminogen activator inhibitor 1

Tissue plasminogen activator (TPA) synthesised by endothelial cells

Plasmin

FIBRIN (insoluble and forms clot with platelets)

proteolysis

FIBRIN DEGRADATION PRODUCTS

Figure 7.3 Fibrinolysis (clot breakdown). Venous occlusion or thrombin stimulates tissue plasminogen activator release. Sepsis produces PAI -1. Activated protein C inactivates PAI -1. Fibrin degradation products (FDPs) are used clinically to measure the activity of the fibrinolytic system, but d-dimers are more specific - produced by the digestion of cross-linked fibrin

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