blood brain barrier impairment, a plasmin-dependent effect due to an increased generation of bradykinin.[8]
Bleeding is caused by the generation of fibrinogen degradation products which interfere with regular fibrin polymerization and inhibit platelet aggregation. Moreover, plasmin which is formed in excess in hyperfibrinolysis can proteolytically activate or inactivate many plasmatic or cellular proteins involved in hemostasis. Especially the degradation of fibrinogen, an essential protein for platelet aggregation and clot stability, may be a major cause for clinical bleeding.
Diagnosis
The diagnosis of hyperfibrinolysis is made indirectly with immunochemical methods which detect the elevation of
Viscoelastic methods in whole blood, especially thromboelastometry (TEM) when performed with special reagents detect hyperfibrinolysis very sensitively in a functional approach. The APTEM test, a tissue factor activated, heparin insensitive test performed in the presence of aprotinin (fibrinolysis inhibitor, confirms hyperfibrinolysis by comparing the TEM result of this assay with the EXTEM test (same activator, but without aprotinin). A normalization or improvement of the TEMogram in APTEM versus EXTEM confirms hyperfibrinolysis.[9]
This in vitro approach can predict to a certain level if normal clot formation can be restored by use of an antifibrinolytic drug.
Treatment
Since the use of aprotinin has been abandoned due to major side effects, the treatment or prophylaxis of hyperfibrinolysis is made with synthetic drugs such as
