Trauma induced coagulopathy and fibrinogen levels: why do we need to measure them, and what are the supplementation strategies? - Critical Care Science (CCS)

Letter to the Editor

Trauma induced coagulopathy and fibrinogen levels: why do we need to measure them, and what are the supplementation strategies?

Crit Care Sci. 2023;35(3):328-330

DOI: 10.5935/2965-2774.20230132-pt

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INTRODUCTION

Fibrinogen is a large glycoprotein produced in the liver. With a normal plasma concentration of 1.5 – 3.5g/L, fibrinogen is the most abundant blood coagulation factor. The final stage of blood clot formation is the conversion of soluble fibrinogen to insoluble fibrin, leading to a stable clot.() In cases of severe bleeding, fibrinogen reaches critically low plasma concentrations at an earlier stage than other coagulation factors.() Fibrinogen also binds to glycoprotein IIb/IIIa receptors on the platelet membrane, promoting platelet aggregation and clot stabilization.() The importance of fibrinogen in clot firmness can be better illustrated by an analogy to a wall, as proposed by Lang and von Depka.() If we consider the platelets as bricks and fibrinogen as cement, a balanced ratio allows us to build a stable wall or a stable clot. On the other hand, if the number of bricks is reduced (thrombocytopenia) and the amount of cement is increased (hyperfibrinogenemia), the wall will not break, and the clot will be stable due to the higher levels of fibrinogen. However, if there are bricks but no cement (hypofibrinogenemia), the risk of wall collapse is high or, analogously, the risk of bleeding is high as well.

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