Articles: subarachnoid-hemorrhage.
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Fifty-two patients were each given a constant infusion of 1.5 g of epsilon-aminocaproic acid (EACA) per hour after subarachnoid hemorrhage (SAH) from an intracranial aneurysm. Each patient's available plasminogen activity (APA), a measure of plasma fibrinolytic activity, was determined by fluorometric assay before and during EACA treatment. Five categories of potential EACA complications were identified: rebleeding, cerebral vasospasm, hydrocephalus, thrombosis, and miscellaneous (bleeding time prolongation, thrombocytopenia). ⋯ It is apparent from these studies that, after the initiation of EACA treatment, a maximal steady state inhibition of fibrinolytic activity is not achieved for 2 days and, after the cessation of EACA therapy, normal fibrinolytic activity is not restored for a period of 3 to 4 days. In addition, patients with thrombotic events may show persistently low serum plasminogen activity after discontinuance of EACA therapy, probably due to continuing thrombosis and consumption of plasminogen. These results indicate that patients with recurrent preoperative aneurysmal hemorrhage while on EACA therapy may have inadequate fibrinolytic inactivation, and this may be an important factor contributing to rebleeding episodes.(ABSTRACT TRUNCATED AT 250 WORDS)
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Acta neurochirurgica · Jan 1984
Prediction of cerebral vasospasm value of fibrinogen degradation products (FDP) in the cerebro-spinal fluid (CSF) for prediction of vasospasm following subarachnoid haemorrhage due to a ruptured aneurysm.
In a new treatment regimen with antifibrinolytic drugs in patients with aneurysmal subarachnoid haemorrhages, we have systematically controlled the level of fibrinogen degradation products (FDP) in the cerebrospinal fluid (CSF). The frequency of severe vasospasm with clinical ischaemia has been compared with the patient's initial level of FDP. Fifty patients have been included in this study. (All in Hunt and Hess's grades I or II on their arrival.) Patients with a secondary deterioration unrelated to vasospasm were excluded. ⋯ Furthermore, two different groups may be discriminated by their initial FDP level: FDP greater than 80 mcg/ml; n = 23, 65% severe vasospasm; FDP less than 80 mcg/ml; n = 27.8% no severe vasospasm (p less than 0.001). These results do not imply a direct role of FDP in pathophysiological mechanisms of vasospasm, but they suggest a relationship between the clot lysis and the appearance of vasospasm with clinical ischaemia. To our knowledge this is the first time that such a predictive role can be attributed to the initial FDP level in the prognosis of vasospasm.
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It is generally considered that the peak incidence of rebleeding after aneurysmal subarachnoid hemorrhage is at the end of the 1st or the beginning of the 2nd week after the initial rupture. However, in a series of 2265 patients admitted within 3 days of their first subarachnoid hemorrhage, the peak of rebleeding occurred on the same day as the initial hemorrhage and there was no later peak. These data suggest that new management strategies for minimizing rebleeding must be considered for patients admitted soon after aneurysm rupture.
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Cerebral vasospasm after SAH from AVMs is rare. Only few reports have been made. ⋯ This high incidence (31%) might be attributable to the timing from the last SAH attack until angiography. The existence of massive subarachnoid blood clots around the arteries of the circle of Willis is the most important factor causing vasospasm after SAH from AVMs.