To describe a new pathophysiological mechanism for endotension.
Case Reports:
Four patients developed aneurysm sac expansion after repair of abdominal aortic aneurysms, one with a conventional polytetrafluoroethylene (PTFE) graft and the others with a variety of commercially made endografts (2 PTFE, 1 Dacron). Pressures within the sacs were nonpulsatile and approximately half the systemic blood pressure. Attenuation on computed tomography (CT) was significantly less in the sac than in the graft in 3 of the patients. A clear, highly viscous fluid was aspirated from all 4 sacs, supporting the diagnosis of aneurysm sac hygroma. Prominent local hyperfibrinolysis in the sac was combined with signs of local coagulation activation.
Conclusions:
A new mechanism for continued sac expansion based on aneurysm sac hygroma is proposed. Measurement of attenuation may be of diagnostic value. It is further proposed that local hyperfibrinolysis/coagulation may promote rebleeding, liquefaction, and continued expansion analogous to the chronic subdural hematoma.
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