Babu S C, Bole P, Sharma P, Purdy R, Clauss R H
Surgery. 1980 Feb;87(2):202-4.
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.
在一名接受主动脉双股动脉搭桥移植术后4年的患者中观察到因假性动脉瘤导致的病理性纤维蛋白溶解。该患者表现为腹部搏动性肿块和腿部缺血性改变。静脉穿刺部位的过度出血促使进行凝血筛查，结果显示凝血块快速溶解、纤维蛋白降解产物以及纤维蛋白原水平降低，提示存在病理性纤维蛋白溶解。使用ε-氨基己酸（EACA，氨甲环酸）治疗控制了凝血病，从而能够进行血管造影和手术。切除假性动脉瘤后异常纤维蛋白溶解得到缓解。正常情况下，凝血和纤维蛋白溶解之间保持平衡，以防止过度出血或凝血。凝血块本身是激活纤维蛋白溶解系统的强大刺激因素，尽管已证明许多其他因素也能启动和维持这一过程。当该过程过度或不恰当时，纤维蛋白溶解即为病理性的。纤溶酶原被激活为纤溶酶，后者消化纤维蛋白。纤溶酶和纤维蛋白降解产物均抑制纤维蛋白单体的聚合（这是形成稳定凝血块的凝血级联反应的最后一步），导致形成不稳定的凝血块并迅速溶解。据我们所知，尚未有报道称这种凝血病是假性动脉瘤的并发症。
