Spontaneous thrombosis of ruptured intracranial aneurysms during treatment with tranexamic acid (AMCA). Report of three cases.
Radiographically verified spontaneous disappearance of medium-sized arterial cerebral aneurysms is seldom reported, and only three times in connection with antifibrinolytic therapy (EACA). In our clinic repeat angiograms have shown non-filling of the aneurysms in three patients during treatment with tranexamic acid (AMCA) two, three, and four weeks respectively after primary bleeds. Initially, all three patients had severe radiological vasospasm associated with neurological deterioration. Follow-up angiograms have demonstrated partial reappearance of the aneurysm after one month in one patient and complete disappearance of the aneurysms in the other two patients after 9 and 22 months respectively. In two cases occlusion of cerebral arteries occurred. With regard to the higher risk of severe vasospasm and occlusion of cerebral arteries in our opinion it should not be a therapeutic goal to try to achieve a thrombosis of a ruptured aneurysm with antifibrinolytic drugs. The reason for spontaneous aneurysm thrombosis during treatment with AMCA may be a local inhibition of plasminogen activators in and around the aneurysm wall. It may also be related to the sympathomimetic property of the drug, with vasospasm and a subsequent flow-reduction inside the aneurysm or a possible interaction with other drugs and substances.
D000328:Adult; D000933:Antifibrinolytic Agents / Q000009:adverse effects / Q000627:therapeutic use; D005260:Female; D006801:Humans; D002532:Intracranial Aneurysm / Q000150:complications* / Q000188:drug therapy; D002542:Intracranial Embolism and Thrombosis / Q000209:etiology*; D008297:Male; D012421:Rupture; D014148:Tranexamic Acid / Q000009:adverse effects / Q000627:therapeutic use
D000933:Antifibrinolytic Agents; D014148:Tranexamic Acid