Mortality after aneurysmal subarachnoid hemorrhage (aSAH) is augmented by rebleeding and delayed cerebral ischemia (DCI). A range of assays evaluating the dynamic process of blood coagulation, from activation of clotting factors to fibrinolysis, has emerged and a comprehensive review of hemostasis and fibrinolysis following aSAH may reveal targets of treatment. We conducted a systematic review of existing literature assessing coagulation and fibrinolysis following aSAH, but prior to treatment. PubMed, Embase, and Web of Science were searched on November 18, 2020, without time boundaries. In total, 45 original studies were eventually incorporated into this systematic review, divided into studies presenting data only from conventional or quantitative assays (n = 22) and studies employing dynamic assays (n = 23). Data from conventional or quantitative assays indicated increased platelet activation, whereas dynamic assays detected platelet dysfunction possibly related to an increased risk of rebleeding. Secondary hemostasis was activated in conventional, quantitative, and dynamic assays and this was related to poor neurological outcome and mortality. Studies systematically investigating fibrinolysis were sparse. Measurements from conventional or quantitative assays, as well as dynamic fibrinolysis assays, revealed conflicting results with normal or increased lysis and changes were not associated with outcome. In conclusion, dynamic assays were able to detect reduced platelet function, not revealed by conventional or quantitative assays. Activation of secondary hemostasis was found in both dynamic and nondynamic assays, while changes in fibrinolysis were not convincingly demonstrable in either dynamic or conventional or quantitative assays. Hence, from a mechanistic point of view, desmopressin to prevent rebleeding and heparin to prevent DCI may hold potential as therapeutic options. As changes in fibrinolysis were not convincingly demonstrated and not related to outcome, the use of tranexamic acid prior to aneurysm closure is not supported by this review.

动脉瘤性蛛网膜下腔出血 (aSAH) 后的死亡率因再出血和迟发性脑缺血 (DCI) 而增加。已经出现了一系列评估血液凝固动态过程的检测方法，从凝血因子的激活到纤维蛋白溶解，对 aSAH 后止血和纤维蛋白溶解的全面回顾可能会揭示治疗目标。我们对现有文献进行了系统评价，评估了 aSAH 后但在治疗之前的凝血和纤溶。PubMed、Embase 和 Web of Science 于 2020 年 11 月 18 日进行了检索，没有时间限制。总共有 45 项原始研究最终被纳入本系统评价，分为仅提供来自常规或定量分析的数据的研究（n  = 22）和采用动态分析的研究（n = 23)。来自常规或定量测定的数据表明血小板活化增加，而动态测定检测到可能与再出血风险增加有关的血小板功能障碍。继发性止血在常规、定量和动态测定中被激活，这与较差的神经系统预后和死亡率有关。系统地研究纤维蛋白溶解的研究很少。常规或定量测定以及动态纤维蛋白溶解测定的测量结果显示与正常或增加的裂解相矛盾的结果，并且变化与结果无关。总之，动态分析能够检测到血小板功能降低，而传统或定量分析没有发现。在动态和非动态测定中都发现了二次止血的激活，而纤维蛋白溶解的变化在动态或常规或定量测定中都不能令人信服地证明。因此，从机制的角度来看，去氨加压素预防再出血和肝素预防 DCI 可能具有作为治疗选择的潜力。由于纤溶的变化没有得到令人信服的证明并且与结果无关，因此本综述不支持在动脉瘤闭合前使用氨甲环酸。