Quantitative determination of plasma fibrinolytic activity in patients with ruptured intracranial aneurysms who are receiving epsilon-aminocaproic acid: relationship of possible complications of therapy to the degree of fibrinolytic inhibition.
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). The APA of the 37 patients with complications was significantly higher than that of the 15 without complications. Four patients suffered rebleeding episodes and had significantly higher APA levels during EACA therapy when compared to all other patients, i.e., those with and without other complications. Patients with vasospasm, hydrocephalus, and thrombotic complications also had significantly higher APA levels during EACA therapy compared to patients without complications. The latter may be simply a reflection of the activation of fibrinolytic activity that occurs after SAH. 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)
D000293:Adolescent; D000328:Adult; D000368:Aged; D000614:Aminocaproates / Q000009:adverse effects*; D015119:Aminocaproic Acid / Q000008:administration & dosage / Q000009:adverse effects*; D002536:Cerebral Arteries / Q000187:drug effects; D003864:Depression, Chemical; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects*; D006801:Humans; D006849:Hydrocephalus / Q000139:chemically induced; D007263:Infusions, Parenteral; D002532:Intracranial Aneurysm / Q000150:complications*; D002542:Intracranial Embolism and Thrombosis / Q000139:chemically induced; D008297:Male; D008875:Middle Aged; D010960:Plasminogen Activators / Q000494:pharmacology; D012008:Recurrence; D012422:Rupture, Spontaneous; D013345:Subarachnoid Hemorrhage / Q000097:blood* / Q000188:drug therapy / Q000209:etiology; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D000614:Aminocaproates; D014662:Vasoconstrictor Agents; D010960:Plasminogen Activators; D015119:Aminocaproic Acid