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Prothrombin Complex Concentrate
PCC contains the vitamin K-dependent factors II, VII, IX, and X (4-factor PCC) or II, IX, and X (3-factor PCC). Following the initial approval for hemophilia B, the vial is standardized on factor IX; the content of the other coagulation factors can vary significantly among the different preparations [75]. The concentration of clotting factors is approximately 25-fold that of plasma [15, 29]. Even in severely bleeding trauma patients, thrombin generation might be sufficient to achieve adequate hemostasis [3, 23]. This might be different for trauma patients in shock [76]. Administration of PCC results in a dose-dependent increase in the endogenous thrombin potential for 3 days, indicating a possible risk for thromboembolism [23, 77]. In a systematic review and metaanalysis, PCC administration was not associated with a reduction in mortality in all patient groups taken together (OR 0.83; 95% CI, 0.66–1.06; p = 0.13; I2 = 0%).However, the trauma subgroup showed a significant reduction in mortality when PCC was added to FFP, but not when PCC was administered as a stand-alone therapy (OR 0.64; 95% CI, 0.46–0.88; p = 0.007; I2 = 0%; p for heterogeneity = 0.81) [78]. Yet, due to the very short half-life and almost immediate inhibition in fluid phase by antithrombin, thrombin itself remains elusive, and only indirect measurement of thrombin generation is possible [79]. As the clotting times of VET are not sensitive to reduced anticoagulant levels (e.g., antithrombin), their use as a surrogate remains debatable [80]. For coagulopathic, severe bleeding, an initial bolus of 25 IU/kg BW appears to be effective and for those patients with an increased risk for thromboembolism an initial half-dose bolus of 12.5 IU/kg BW followed by a second dose if microvascular bleeding persists [75]. In an evidence-based algorithm for ROTEM-guided bleeding management, PCC substitution is indicated with an EXTEM CT >80 s and FIBTEM A5 ≥9 mm (trauma) or ≥12 mm (PPH)
凝血酶原复合物浓缩物(PCC)
PCC含有维生素K依赖因子II、VII、IX和X(4因子PCC)或II、IX和X(3因子PCC)。在最初批准用于血友病B之后,凝血因子IX含量是统一标准的,其他凝血因子的含量在不同的制剂中可能有很大不同。PCC中凝血因子的浓度大约是血浆的25倍。即使严重出血的创伤患者中,凝血酶的产生也可能足以止血。而休克创伤患者可能不同。使用PCC会导致内源性凝血酶潜力持续3天呈剂量依赖性增加,表明可能存在血栓栓塞的风险。在一项系统综述和荟萃分析中,PCC给药与所有患者组中的死亡率降低无相关性(OR 0.83;95%CI,0.66-1.06;p=0.13;I2=0%)。然而,当PCC联合FFP时,创伤亚组显示死亡率显著降低,但当PCC作为一种独立治疗时,死亡率无显著降低(OR 0.64;95%可信区间为0.46–0.88;p = 0.007;I2 = 0%;异质性p值= 0.81)。然而,由于半衰期非常短且在液相中几乎立即被抗凝血酶抑制,对凝血酶仍知之甚少,只能间接测量其生成。由于VET测定的凝血时间对降低的抗凝剂水平(如抗凝血酶)不敏感,因此其作为凝血时间的替代物仍有争议。对于凝血病、严重出血,PCC的初始剂量为25 IU/kg BW似乎是有效的,对于血栓栓塞风险增加的患者,初始剂量为12.5 IU/kg BW的半剂量,如果微血管出血持续,则随后给予第二次剂量。在ROTEM引导的出血管理的循证流程中,以EXTEM CT>80 s和FIBTEM A5 ≥9 mm(创伤)或≥12 mm (PPH)为补充PCC的界值。
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