Role of fibrinogen-, factor VIII- and XIII-mediated clot propagation in gelatin haemodilution

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Abstract

Background:

Gelatin solution impairs coagulation. The mechanism of coagulopathy is incompletely defined. The purpose of this study was to evaluate the capacity of single coagulation factors to reverse gelatin-promoted whole-blood coagulation disorders in vitro.

Methods:

Venous blood was withdrawn from 12 volunteers in a crossover study. Four percent succinylated gelatin was added to citrated whole-blood samples to make a 40 vol% end-concentration of gelatin. The baseline and 40 vol% samples, and samples with addition of fresh-frozen plasma (FFP), fibrinogen, coagulation factors XIII (FXIII) or VIII, together with the von Willebrand factor (FVIII+vWF), were analysed by thromboelastometry (ROTEM®). Coagulation was initiated by tissue thromboplastin (ExTEM®) with and without cytochalasin to determine the functional component of fibrinogen (FibTEM®).

Results:

Initiation of coagulation and fibrin formation were delayed at 40 vol% gelatin dilution. At this stage, the median (25th-75th percentiles) maximum clot firmness (MCF) was 76.3 (65.9-80.0) and 32.5 (27.4-45.0)% of the pre-dilution value in ExTEM® and FibTEM® thromboelastometry, respectively. Coagulation time was corrected by addition of fibrinogen and FFP in ExTEM® and FibTEM® analysis, whereas FVIII or FXIII had minimal effects. MCF was partly restored only by FFP in ExTEM®. In FibTEM® analysis, MCF improved more by fibrinogen than by FVIII+VWF, FXIII or FFP.

Conclusions:

Gelatin-induced whole-blood coagulation disorder in vitro is mainly dependent on the initial fibrinogen-fibrin interaction. The proposed mechanism might suggest not to reverse gelatin coagulopathy solely by fibrinogen administration. The administration of FFP, a mixture of different coagulation factors, reversed the gelatin-induced in vitro coagulopathy the best.

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