Subcutaneous Hematoma Elevates Plasma Levels of FDP and D-Dimer; an Analysis by Animal Model Experiments

Trauma-associated coagulopathy has been considered to develop as a result of increased fibrinolysis due to massive bleeding, tissue damage and hypoperfusion. However, it has not been investigated whether hematoma may cause trauma-associated coagulopathy. Using experimental animal model, we analyzed the effects of hematoma formation on coagulation and fibrinolysis parameters.

Male Wistar rats were used for the studies.

We made an animal model of subcutaneous hematoma without tissue injuries. This model can be categorised as a kind of trauma models. We created experimentally subcutaneous hematomas in test animals using blood collected from other animals. We performed blood sampling to measure blood cell counts and coagulation parameters from test animals at 1, 6, 24, 48 and 96 hours after hematoma generation. Blood samples were collected and immediately sent for measurement of CBC, Prothrombin, FDP, D-dimer, Fibrinogen, Antithrombin, AST and ALT. Furthermore, after 1, 24 and 48 hours, we performed dynamic evaluation of coagulation/fibrinolysis function using thromboelastometry method.

After the hematoma were created, FDP and D-dimer increased over time, and reached a plateau after 48 hours. During the period, there was no decrease in Fibrinogen and Antithrombin, and no thrombocytopenia occurred. Moreover, no obvious changes in coagulation/fibrinolysis function were observed employing thromboelastometry.

Elevated FDP and D-dimer after hematoma creation are assumed to be synthesized in the hematoma, not in the streaming blood. Thromboelastometry also shows that elevated levels of FDP and D-dimer are not caused by intravascular coagulation and subsequent fibrinolysis.

The study showed that subcutaneous hematomas caused increases in FDP and D-dimer levels, without activating the blood coagulation/fibrinolysis system.