Pathological fibrinolysis secondary to pseudoaneurysms.
Pathological fibrinolysis due to pseudoaneurysms was observed in a patient 4 years after aortobifemoral bypass graft. The patient presented with a pulsatile abdominal mass and ischemic changes in the legs. Excessive bleeding from venipuncture sites prompted coagulation screening, which disclosed rapid clot lysis, fibrin split products, and low fibrinogen suggestive of pathological fibrinolysis. Therapy with epsilon amino caproic acid (EACA, Amicar) controlled the coagulopathy, permitting angiography and operation. Resection of the pseudoaneurysms resulted in resolution of the abnormal fibrinolysis. Normally, there is a balance between coagulation and fibrinolysis protecting against excessive bleeding or clotting. Clot itself is a powerful stimulus for the activation of the fibrinolytic system, although many other factors have been shown to initiate and sustain the process. Fibrinolysis is pathological when the process becomes excessive or inappropriate. Plasminogen is activated to plasmin which digests fibrin. Both plasmin and fibrin split products inhibit polymerization of fibrin monomers (which is the final step in the coagulation cascade in the formation of a stable clot), resulting in an unstable clot which is rapidly lysed. To our knowledge such a coagulopathy has not been reported to be a complication of pseudoaneurysms.
D015119:Aminocaproic Acid; D000783:Aneurysm / Q000150:complications* / Q000601:surgery; D001012:Aorta, Abdominal / Q000601:surgery; D001014:Aortic Aneurysm / Q000150:complications* / Q000601:surgery; D001778:Blood Coagulation Disorders / Q000188:drug therapy / Q000209:etiology*; D001780:Blood Coagulation Tests; D005263:Femoral Artery / Q000601:surgery; D005338:Fibrin Fibrinogen Degradation Products; D005342:Fibrinolysis; D006801:Humans; D008297:Male; D008875:Middle Aged
D005338:Fibrin Fibrinogen Degradation Products; D015119:Aminocaproic Acid