Electrophoretic demonstration of high molecular weight fibrin degradation products persisting in chronic subdural hematomas
Local hyperfibrinolysis plays an important role in the pathogenesis of chronic subdural hematoma (CSH). The purpose of this study is to elucidate the nature of the local hyperfibrinolysis in CSH, by comparing the pattern of fibridfibrinogen degradation product (FDP) of hematomas with that of purified fibrin clots digested by plasmin in vitro. Forty-seven hematoma samples were subjected to the analysis. FDPs of CSH and the purified fibrin clots digested by plasmin for different incubation times were identified using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting, and then quantified by densitometry. The effect of alpha-2 plasmin inhibitor (A2-PI) on the degradation process was also studied. The FDP pattern of CSH was similar to those of purified fibrin digested by plasmin for 0.75-2 h. The FDP composition of CSH was closest to that of purified fibrin digested for l h . By adding the physiological concentration of A2-PI at the second hour, further degradation of high molecular weight FDPs was inhibited and the early FDP pattern persisted after 24 h. Local hyperfibrinolysis in CSHs is characterized by incomplete fibrinolysis, which occurs only on the solid fibrin clot, and is arrested in the liquid hematoma. As a result, high molecular weight FDPs persist in CSHs for weeks or months in the hematoma. A2-PI seems to play an important role in producing this unique FDP pattern in CSH.