Nakao Takami, Kitazawa Yasuhide, Masuda Shiori, Hashimoto Naoki
Critical Care Medical Center, Kindai University Nara Hospital, Ikoma-city, Nara, Japan.
Department of Emergency Medicine, Izumi City General Medical Center, Izumi-city, Osaka, Japan.
J Blood Med. 2024 Dec 30;15:557-564. doi: 10.2147/JBM.S479126. eCollection 2024.
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.
创伤相关凝血病被认为是由于大量出血、组织损伤和灌注不足导致纤维蛋白溶解增加所致。然而，血肿是否会导致创伤相关凝血病尚未得到研究。我们使用实验动物模型分析了血肿形成对凝血和纤维蛋白溶解参数的影响。
雄性Wistar大鼠用于本研究。
我们制作了无组织损伤的皮下血肿动物模型。该模型可归类为一种创伤模型。我们使用从其他动物采集的血液在实验动物身上制造皮下血肿。在血肿形成后1、6、24、48和96小时对实验动物进行采血，以测量血细胞计数和凝血参数。采集血样并立即送去检测全血细胞计数、凝血酶原、纤维蛋白降解产物（FDP）、D - 二聚体、纤维蛋白原、抗凝血酶、天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）。此外，在1、24和48小时后，我们使用血栓弹力图法对凝血/纤维蛋白溶解功能进行动态评估。
血肿形成后，FDP和D - 二聚体随时间增加，并在48小时后达到平台期。在此期间，纤维蛋白原和抗凝血酶没有降低，也没有发生血小板减少。此外，采用血栓弹力图法未观察到凝血/纤维蛋白溶解功能有明显变化。
血肿形成后FDP和D - 二聚体升高被认为是在血肿中合成的，而非在流动血液中。血栓弹力图也表明FDP和D - 二聚体水平升高不是由血管内凝血及随后的纤维蛋白溶解引起的。
该研究表明皮下血肿导致FDP和D - 二聚体水平升高，而未激活血液凝固/纤维蛋白溶解系统。
