title: Local hypercoagulative activity precedes hyperfibrinolytic activity in the subdural space during development of chronic subdural haematoma from subdural effusion.
abstract: The involvement of coagulation and fibrinolysis in the development of chronic subdural haematoma (CSH) from subdural effusion was investigated. Subdural fluid and venous blood samples were obtained from 34 patients with CSH and 9 patients with subdural effusion, and analyzed using enzyme-linked immunosorbent assays for thrombin-antithrombin III complex (TAT), prothrombin fragment F1 + 2 (F1 + 2), tissue factor, tissue factor pathway inhibitor (TFPI) and D-dimer. CSH was classified into the layering type, believed to be active, and other types according to x-ray computed tomography. All markers in the blood of both patient groups were similar to the values of normal subjects. Levels of TAT and F1 + 2 were much higher in the subdural fluid than in the blood of patients with CSH (P < 0.001, P < 0.001) and with subdural effusion (P < 0.05, P < 0.05). The level of D-dimer in the subdural fluid was significantly higher than in the blood (P < 0.001) in patients with CSH, but not in patients with subdural effusion. All markers in the subdural fluid of layering type CSH, except TFPI, were significantly higher than in the other types (P < 0.05). Local hypercoagulative activity in the subdural space is present in subdural effusion and precedes hyperfibrinolytic activity in CSH. Thrombin generation as indicated by TAT and F1 + 2 might be involved in the development of CSH. Propagation of CSH may be modulated by the coagulation system including the extrinsic pathway and fibrinolysis.
authors.affiliation: Department of Neurosurgery, Iwate Medical University School of Medicine, Morioka, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Suzuki
authors.forename: A
authors.initials: A
authors.lastname: Kudo
authors.forename: A
authors.initials: A
authors.lastname: Kitakami
authors.forename: M
authors.initials: M
authors.lastname: Doi
authors.forename: N
authors.initials: N
authors.lastname: Kubo
authors.forename: K
authors.initials: K
authors.lastname: Kuroda
authors.forename: A
authors.initials: A
authors.lastname: Ogawa
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000990:Antithrombin III / Q000378:metabolism; D001779:Blood Coagulation Factors / Q000378:metabolism; D001780:Blood Coagulation Tests; D002908:Chronic Disease; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005342:Fibrinolysis / Q000502:physiology*; D006408:Hematoma, Subdural / Q000097:blood*; D006801:Humans; D008074:Lipoproteins / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000378:metabolism; D010447:Peptide Hydrolases / Q000378:metabolism; D011516:Prothrombin / Q000378:metabolism; D013353:Subdural Effusion / Q000097:blood*; D019851:Thrombophilia / Q000097:blood*; D013925:Thromboplastin / Q000378:metabolism
chemical_list: D001779:Blood Coagulation Factors; D005338:Fibrin Fibrinogen Degradation Products; D008074:Lipoproteins; D010446:Peptide Fragments; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C051928:lipoprotein-associated coagulation inhibitor; C045879:prothrombin fragment 1.2; D000990:Antithrombin III; D011516:Prothrombin; D013925:Thromboplastin; D010447:Peptide Hydrolases