Watanabe H, Ishii S, Matsuda T
No Shinkei Geka. 1978 Jun;6(6):563-9.
Repeated fibrinogen determination were made in 24 patients suffering from subarachnoid hemorrhage(SAH), in order to know the influence of blood content of fibrinogen upon the ischemic complications following vasospasm. In 11 cases (group II) among those 24 patients admitted within two weeks after the last SAH due to ruptured intracrainal aneruysm, a rise in fibrinogen over 600 mg/dl occurred, while in remaining 12 cases (group I) the levels of fibrinogen were kept below 600 mg/dl during the acute stage. In cases of group II, fibrinogen began to increase in accordance with the augmentation of vasospasm and reached to peak within 4 to 9 days after the onset of SAH. Blood viscosity also increased showing positive correlation with the increase in fibrinogen, and rose over 1.5 times normal value when fibrinogen exceeded 600 mg/dl. Reduction of anti-thrombin III was also observed in group II patients previous to the increase in fibrinogen, suggesting the occurrence of hypercoagulability in association with the appearance of vasospasm. In most cases of group II, their neurological signs deteriorated markedly at the time when fibrinogen rose over 600 mg/dl. The mortality in group II whose fibrinogen increased over 600 mg/dl was of 6 of 11, with poor recovery of function among the survivors; of those with levels below 600 mg/dl (group I), only 1 of 12 died and all of remaining 11 made a reasonably good functional recovery. These facts suggest that the increase in fibrinogen would cause the aggression of the ischemic complications following vasospasm through the diminution the cerebral microcirculation induced by the raised blood viscosity, and the critical level of fibrinogen increase as the alarming sign for the ischemic complications was 600 mg/dl. One should attract attention to the changes of fibrinogen level as one of the risk risk factors in acute stage of SAH.
对24例蛛网膜下腔出血（SAH）患者进行了多次纤维蛋白原测定，以了解纤维蛋白原的血液含量对血管痉挛后缺血性并发症的影响。在这24例因颅内动脉瘤破裂导致最后一次SAH后两周内入院的患者中，11例（第二组）纤维蛋白原升高超过600mg/dl，而其余12例（第一组）在急性期纤维蛋白原水平保持在600mg/dl以下。在第二组病例中，纤维蛋白原随着血管痉挛的加剧而开始升高，并在SAH发病后4至9天内达到峰值。血液粘度也增加，与纤维蛋白原的增加呈正相关，当纤维蛋白原超过600mg/dl时，血液粘度升高超过正常值的1.5倍。在第二组患者中，在纤维蛋白原升高之前也观察到抗凝血酶III减少，这表明与血管痉挛的出现相关的高凝状态的发生。在第二组的大多数病例中，当纤维蛋白原升高超过600mg/dl时，他们的神经体征明显恶化。纤维蛋白原升高超过600mg/dl的第二组患者的死亡率为11例中的6例，幸存者的功能恢复较差；在纤维蛋白原水平低于600mg/dl的患者（第一组）中，12例中仅1例死亡，其余11例均有较好的功能恢复。这些事实表明，纤维蛋白原的增加会通过血液粘度升高引起的脑微循环减少，导致血管痉挛后缺血性并发症的加重，纤维蛋白原增加的临界水平600mg/dl是缺血性并发症的警示信号。在SAH急性期，应将纤维蛋白原水平的变化作为危险因素之一予以关注。
