Role of local hyperfibrinolysis in the etiology of chronic subdural hematoma

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Abstract
Material aspirated from chronic subdural hematomas was studied. Patients were given 51Cr-labeled red cells prior to aspiration, and it was possible to demonstrate that the mean daily hemorrhage into the hematoma space amounted to 10.2% of its volume. Immunoelectrophoresis of the aspirated hematoma fluid by monospecific anti-human fibrinogen revealed the presence of fibrin and fibrinogen degradation products that, measured by hemagglutination-inhibition immunoassay techniques, varied between 5.0 and 10,500 .mu.g/ml with an average of 2604 .mu.g/ml in 18 cases. The tissue activator was demonstrated by Todd''s histilogical localization in the outer membrane of the chronic subdural hematoma in 11 cases, but not in the inner membrane. If a clot in the subdural space causes the formation of neomembrane, and excessive fibrinolysis occurs, the subdural clot would not only liquefy, but also enlarge by continuous hemorrhage from the neomembrane. Local hyperfibrinolysis and continuous bleeding are important in the etiology of the chronic subdural hematoma.