[Studies on the fibrinolytic system in ruptured intracranial aneurysm.--Part 2: Fibrinogen changes in acute stage of SAH as a risk factor of the ischemic complications following vasospasm (author's transl)].

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.