✓ The authors describe studies performed on material aspirated from chronic subdural hematomas. 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 µg/ml with an average of 2604 µg/ml in 18 cases. The tissue activator was demonstrated by Todd's histological localization in the outer membrane of the chronic subdural hematoma in 11 cases, but not in the inner membrane. These results indicate that 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. Therefore, local hyperfibrinolysis and continuous bleeding are important in the etiology of the chronic subdural hematoma.

US is reliable for the detection of injuries and the identification of solid-organ injuries despite its poor sensitivity for intestinal injuries.

The structure of macrocapillaries (also called 'sinusoids") in the outer membrane of chronic subdural hematomas was investigated by electron microscopy, with particular attention paid to vascular permeability. One characteristic of macrocapillaries is the frequent formation of gap junctions between adjacent endothelial cells. In endothelial gap junctions 0.6 to 8 microns in diameter, numerous blood components, including red blood cells and plasma, can be seen squeezing or spilling into the interstitial space of the outer membrane. Irregularly deformed erythrocytes are located around the macrocapillaries, and amorphous material is seen among scattered thin collagen fibers. It is suggested that endothelial gap junctions of macrocapillaries play an important role in the leakage of blood, causing enlargement of chronic subdural hematomas.

Active plasmin, available plasmin, and total plasminogen were measured by Enzo-diffusion fibirn plate techniques in 11 cases and level of tissue activator and tissue fibrinolytic activities in another 11 cases with chronic subdural hematoma. The values were too small to be measured in some instances. Anti-plasmin in the hematoma was less than in the blood plasma. The outer membrane contained about three times more tissue activator than the dura mater, although the inner membrane contained none. Increased tissue activator, which exudes from the extremely vascular outer membrane, transforms plasminogen into plasmin in subdural hematoma, so that plasmin breaks down fibrin and fibrinogen and induces continuous hemorrhage.