Department of Intensive Care, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark; Department of Anaesthesiology, Aarhus University Hospital, Aarhus, Denmark.
Department of Intensive Care, Aarhus University Hospital, Aarhus, Denmark.
World Neurosurg. 2019 Oct;130:e140-e149. doi: 10.1016/j.wneu.2019.06.019. Epub 2019 Jun 14.
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.
To investigate changes in coagulation after SAH and illuminate underlying mechanisms.
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.
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).
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.
自发性蛛网膜下腔出血（SAH）后止血能力对预后起着关键作用。SAH 后数小时内凝血变化仅得到了稀疏的研究。
研究 SAH 后凝血的变化并阐明潜在机制。
我们纳入了 46 例自发性动脉瘤性 SAH 患者。在发病后入院时和 24 小时采集血样。采用 EXTEM、INTEM 和 FIBTEM 标准检测血栓弹性描记法（ROTEM）。根据 ROTEM 结果计算血小板最大凝块弹性。测量凝血酶生成、凝血酶-抗凝血酶复合物、纤维蛋白原和凝血因子 XIII 水平。将所有数据与性别匹配的健康对照组进行比较。
在入院时（中位发病后 3 小时 39 分钟），SAH 患者的最大凝块硬度（EXTEM，P < 0.0001；INTEM，P = 0.08；FIBTEM，P < 0.0001）和血小板最大凝块弹性（P < 0.0001）均高于健康对照组。SAH 患者的凝血酶生成显示出较高的内源性凝血酶潜能，尽管无统计学意义（P = 0.06），且凝血酶-抗凝血酶复合物水平高于参考区间。纤维蛋白原和凝血因子 XIII 的中位水平均在参考参数范围内，并且在症状发作后 24 小时仍升高，而内源性凝血酶潜能（P = 0.01）和凝血酶-抗凝血酶复合物水平降低（P < 0.0001）。
SAH 患者在入院时处于高凝状态，并且在 SAH 后 24 小时仍保持这种状态。增加的凝块硬度可能是由于血小板功能增强引起的，因为尽管纤维蛋白原和凝血因子 XIII 水平正常，但血小板最大凝块弹性增加。
