• H Fodstad.
• Acta Neurochir (Wien). 1982 Jan 1; 63 (1-4): 233-44.

AbstractTwo randomised controlled clinical trials in patients with recently ruptured intracranial aneurysms were undertaken using tranexamic acid (AMCA) to prevent early recurrent bleeding. In our accumulated series of 105 patients 53 were given AMCA and 52 were controls. 13% of the AMCA-treated patients and 31% of the controls rebled. In patients treated with AMCA the recurrent bleeding took place later than the rebleeding in the control patients. Vasospasm and delayed cerebral ischaemic deficits were seen more frequently in patients treated with AMCA. Total mortality from rebleeding and cerebral ischaemia was 25% in AMCA-treated patients and 19% in the controls during the six weeks' observation time. Coagulation factors remained unaffected by the drug. Local fibrinolysis in the cerebrospinal fluid decreased after one week in patients treated with AMCA. After two weeks the fibrinolytic activity was similar in AMCA-treated patients and in the controls. After experimental subarachnoid haemorrhage in 90 rabbits, AMCA was found to suppress plasminogen activator activity, mainly in the leptomeninges. This occurred however only during the first few postbleeding days. Antifibrinolytic agents only appear to reduce the risk of recurrent bleeding during the first ten day period after the primary aneurysm rupture. However they also seem to produce delayed cerebral ischaemia in patients with subarachnoid haemorrhage. Synthetic antifibrinolytics evidently shift the incidence of rebleeding curve to the right but these drugs are probably of diminished value in the subsequent weeks of risk.

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