Thromboelastometry Shows Early Hypercoagulation in Patients with Spontaneous Subarachnoid Hemorrhage
Thromboelastometry Shows Early Hypercoagulation in Patients with Spontaneous Subarachnoid Hemorrhage
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DOI：
10.1016/j.wneu.2019.06.019
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发表时间：
2019-10-01
影响因子：
2
通讯作者：
Hvas, Anne-Mette
中科院分区：
文献类型：
--
作者：
Lauridsen, Signe Voigt;Hvas, Christine Lodberg;Hvas, Anne-Mette
BACKGROUND: The ability to achieve hemostasis after spontaneous subarachnoid hemorrhage (SAH) plays a pivotal role in outcome. Changes in coagulation in the early hours after SAH have been only sparsely investigated.OBJECTIVE: To investigate changes in coagulation after SAH and illuminate underlying mechanisms.METHODS: We enrolled 46 patients with spontaneous aneurysmal SAH. Blood samples were collected at admission and 24 hours after symptom onset. Thromboelastometry (ROTEM) was performed using the standard assays EXTEM, INTEM, and FIBTEM. Platelet maximum clot elasticity was calculated based on ROTEM results. Thrombin generation, levels of thrombin-antithrombin complex, fibrinogen, and coagulation factor XIII were measured. All data were compared with a gender-matched healthy control group.RESULTS: At admission (median, 3 hours 39 minutes from symptom onset), maximum clot firmness (EXTEM, P < 0.0001; INTEM, P = 0.08; FIBTEM, P < 0.0001) and platelet maximum clot elasticity (P < 0.0001) were higher in patients with SAH than in healthy controls. Thrombin generation showed higher, although nonsignificant, endogenous thrombin potential in patients with SAH than in healthy controls (P = 0.06), and thrombin-antithrombin complex levels were above the reference interval. Median fibrinogen and coagulation factor XIII levels were both within the reference parameters and remained increased 24 hours after symptom onset, whereas endogenous thrombin potential (P = 0.01) and thrombin-antithrombin complex levels decreased (P < 0.0001).CONCLUSIONS: Patients with SAH were in a hypercoagulable state at admission and remained so 24 hours after SAH. Increased clot firmness could be caused by increased platelet function, because platelet maximum clot elasticity was increased despite normal fibrinogen and coagulation factor XIII levels.
