Mechanism of action

Fibrin sealants are employed for tissue healing and topical hemostasis, so their action mimics the blood coagulation cascade (Figure 9.1) to obtain a final semirigid, insoluble, fibrin clot by mixing the two components. Thrombin catalyzes the step that transforms fibrinogen into fibrin monomers and, with calcium ions as acofactor, activates factor XIII. Fibrin then starts to polymerize by means of electrostatic interactions and hydrogen bonds. In the presence of calcium, active factor XIIIa converts non-covalent bonds to covalent bonds, which render the cross-linked structure of a fibrin clot.

The fibrin clot is degraded by physiological fibrinolysis. The antifibrinolytic agent, aprotinin, supplied in the kit slows the breakdown of the clot by plasmin, the fibrinolytic agent of our organism.

To prevent virus transmission, fibrin sealants are subjected to a variety of chemical treatments to ensure a safe product, free from virus. At present, fibrinogen can be obtained from individual units of blood plasma that are previously tested for the associated risk of hepatitis and human immune deficiency virus (HIV). In addition, for viral inactivation, commercial solutions are purified

Figure 9.1. Mechanism of clotting factor interactions

using a two-step vapor-heating method at 60 and 80 °C, or other methods such as pasteurization (10 h in an aqueous solution at 60 °C), detergent treatments, nanofiltration, chromatography, ultraviolet C light, etc. A combination of these treatments is preferable because none of them is 100% effective. The methods employed by the manufacturers offer a sufficient margin of safety against HIV and hepatitis B and C viruses. In 2000, Gosalbez et al. reported a parvovirus B19 transmission attributed to the use of fibrin sealant [3], but there are no cases of serious viral transmission reported in the literature.

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