✓ 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.
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.
From May 1998 to April 2000, we performed partial left ventriculectomy (PLV) in 3 pediatric patients with dilated cardiomyopathy (DCM). At the time of the surgery, their age ranged from eight months to three years. The first patient eventually had to receive a heart transplant, but all patients treated with PLV are alive to this day. Patient #1 was diagnosed with DCM at the age of five months, PLV was done on a semi-urgent basis at the age of eight months, when medium dose IV catecholamine therapy and mechanical ventilation were required. Fraction shortening (FS) as shown by echocardiography increased postoperatively from 8% to 15% along with marked clinical improvement. Her heart failure deteriorated three months after the surgery, and received a heart transplant in the United States when she was one year and two months old. Patient #2 developed severe heart failure two months after correction of a ventricular septal defect. Aggressive medical therapy failed to improve his condition, therefore PLV was done on an elective basis at the age of three years and five months. [The patient was initially hospitalized and underwent low dose catecholamine.] Postoperative course was well. The ventriculography one year after surgery showed an improvement of the left ventricular FS from 12% to 27% after PLV. He was still doing well at his most recent check up. Patient #3 was diagnosed with DCM as a neonate. PLV was done on an elective basis at the age of two years and five months. Her postoperative course was generally well. FS on echocardiography increased postoperatively from 10% to 25% along with marked clinical improvement. The timing of performing PLV is the most essential factor for postoperative course in our experiences. We consider that the best timing is when aggressive catecholamine infusion or mechanical ventilation is required. The mid-term outcome of PLV of pediatric patients is considered to be acceptable. We believe that PLV should be considered as a viable option for severe DCM patients.
SummaryFibrin and fibrinogen degradation products (FDP) were examined in 30 cases of chronic subdural hematoma. Fibrinogen was not found in the contents of subdural hematoma in 29 cases, and only a small amount of fibrinogen was detected in the remaining case. The liquefied hematoma content was not coagulated by the addition of thrombin. Early FDP were present in one third of the cases in which paracoagulation tests were positive. Immunoelectrophoresis of hematoma demonstrated precipitation with anti-human fibrinogen serum, anti-FDP-D serum and anti-FDP-E serum. The amount of FDP in hematoma was 10.0 to 10500 μg/ml by hemagglutination-inhibition immunoassay, whereas FDP values were in the normal range in other body fluids, such as serum, cerebrospinal fluid and urine. These results indicate an increased local fibrinolytic activity in chronic subdural hematoma. It is also presumed that local hyperfibrinolysis plays an important role in the etiology of chronic subdural hematoma.
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