fibrin and Hematoma--Subdural

From the present review it seems clear that the physiopathogenesis of the chronic subdural hematoma is far from being completely understood. However, an analysis of the known data can be summarized as follows: The development of subdural hematomas most likely occurs following minimal trauma in those patients with predisposing factors. Experimental data substantiates the fact that an accumulation of clotted blood in the subdural or subcutaneous space induced the formation of the fibroplastic neomembrane. The hypothesis that blood must come in contact with cerebrospinal fluid in order for the growth to occur, is still controversial. It has been virtually disproven that osmosis, referring to the electrolyte gradient as measured by freezing point depression, has any significance as a growth inducing factor. The protein oncotic gradient theory, having been the most widely accepted explanation as to the progressive enlargement of the subdural hematoma sac, has little experimental data supporting it. A larger body of clinical evidence exists supporting the concept that plasma and/or erythrocytes continuously penetrate into the subdural cavity, where enhanced fibrinolytic activity is present. However, this chronic rebleeding cannot fully explain the observed growth, because the composition of the hematoma fluid is smoewhat different from serum or plasma, and the protein content is also progressively diluted by fluid arising from an unknown source. There is some clinical and experimental evidence to suggest that a production-reabsorption balance may be a significant growth variable. No work has been done to define the role, if any, of local inflammatory mechanisms in the chronic subdural hematoma. Sound clinical evidence has shown that after the initial formation of the subdural clot, growth follows, than a slow, complete reabsorption usually occurs. Aside from the plausible production-reabsorption balance concept, it is not known why the evolution proceeds in this manner.

Topics: Animals; Blood Proteins; Disease Models, Animal; Fibrin; Fibrinogen; Hematoma, Subdural; In Vitro Techniques; Male; Osmolar Concentration; Osmotic Pressure

Topics: Aged; Brain Neoplasms; Fibrin; Hematoma, Subdural; Humans; Lymphoma, Large B-Cell, Diffuse; Male

Bile acids are known to pass the blood-brain barrier and are present at low concentrations in the brain. In a previous work, it was shown that subdural hematomas are enriched with bile acids and that the levels in such hematomas are higher than in the peripheral circulation. The mechanism behind this enrichment was never elucidated. Bile acids have a high affinity to albumin, and subdural hematomas contain almost as high albumin levels as the peripheral circulation. A subdural hematoma is encapsulated by fibrin which may allow passage of small molecules like bile acids. We hypothesized that bile acids originating from the circulation may be 'trapped' in the albumin in subdural hematomas. In the present work, we measured the conjugated and unconjugated primary bile acids cholic acid and chenodeoxycholic acid in subdural hematomas and in peripheral circulation of 24 patients. In most patients, the levels of both conjugated and free bile acids were higher in the hematomas than in the circulation, but the enrichment of unconjugated bile acids was markedly higher than that of conjugated bile acids. In patients with a known time interval between the primary bleeding and the operation, there was a correlation between this time period and the accumulation of bile acids. This relation was most obvious for unconjugated bile acids. The results are consistent with a continuous flux of bile acids, in particular unconjugated bile acids, across the blood-brain barrier. We discuss the possible physiological importance of bile acid accumulation in subdural hematomas.

Topics: Adult; Aged; Aged, 80 and over; Albumins; Biological Transport; Blood-Brain Barrier; Chenodeoxycholic Acid; Cholic Acid; Female; Fibrin; Hematoma, Subdural; Humans; Male; Mass Spectrometry; Middle Aged; Protein Binding; Subdural Space

After infant deaths due to non-accidental head injury (NAHI) with subdural hematoma (SDH), the magistrates ask experts to date the traumatic event. To do so, the expert only has tools based on adult series of NAHI. We aimed to develop an SDH dating system applicable to infants aged under 3 years.. We studied a retrospective multicenter collection of 235 infants who died between the ages of 0 and 36 months, diagnosed with SDH by forensic pathological examination and with known posttraumatic interval (PTI). Two pathologists assessed blindly and independently 12 histomorphological criteria relating to the clot and 14 relating to the dura mater in 73 victims (31 girls, 42 boys) whose median age was 3.8 months. Histopathological changes were significantly correlated with PTI for the appearance of red blood cells (RBCs) and the presence or absence of siderophages, and regarding the dura mater, the quantity of lymphocytes, macrophages, and siderophages; presence or absence of hematoidin deposits; collagen and fibroblast formation; neomembrane thickness; and presence or absence of neovascularization. Dating systems for SDH in adults are not applicable to infants. Notably, neomembrane of organized connective tissue is formed earlier in infants than in adults.. Our dating system improves the precision and reliability of forensic pathological expert examination of NAHI, particularly for age estimation of SDH in infants. However, the expert can only define a time interval. Histopathology is indispensable to detect repetitive trauma.

Topics: Bilirubin; Child, Preschool; Collagen; Dura Mater; Erythrocytes; Female; Fibrin; Fibroblasts; Forensic Pathology; Hematoma, Subdural; Humans; Infant; Infant, Newborn; Intracranial Thrombosis; Lymphocytes; Macrophages; Male; Neovascularization, Pathologic; Postmortem Changes; Reticulin; Retrospective Studies

The age estimation of injuries, e.g., subdural hematomas (SDH), can play an important role in medicolegal cases. Various forensic textbooks provide tables of histomorphological changes in SDH in time. The analysis of these data showed that these tables employed different time intervals, although they were all based on only a single publication with a limited number of cases in some of the time periods. The present study aimed to add cases to the original article and to standardize the dating system of SDH. Results from two well-documented studies and 64 additional cases were analyzed, and the use of a number of immunohistochemical staining methods, which could support the histomorphological analysis of some of the changes, was proposed. The results showed that correct age estimation was achieved in approximately 95 % of the cases. Based on the cumulative data from the two published studies and the analysis of the additional cases, a simplified timing table was developed, and the potential pitfalls were addressed. This study shows that accurate age estimation of SDH is possible, provided that the rules established by this study are observed.

Topics: Adult; Aged; Bilirubin; Cell Proliferation; Dura Mater; Erythrocytes; Female; Fibrin; Fibroblasts; Forensic Pathology; Hematoma, Subdural; Humans; Leukocytes; Lymphocytes; Macrophages; Male; Middle Aged; Phagocytosis; Postmortem Changes; Time Factors; Young Adult

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 fibrin/fibrinogen 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 immuno-blotting, 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 1 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.

Topics: Chronic Disease; Densitometry; Electrophoresis, Polyacrylamide Gel; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinolysin; Hematoma, Subdural; Humans; Molecular Weight

The aim of the study was to improve the detection of small hemorrhages with minimal symptoms and of unruptured aneurysms after a subdural and subarachnoid bleeding by the control of the intravascular hemostatic system.. Prospective, open study.. Neurosurgical intensive care unit of a university hospital.. 44 patients undergoing a cranial trepanation. Patients of group 1 (control n = 11) had an intrasellar hypophysoma, patients of group 2 (n = 12) a chronic subdural hematoma without a previous traumatic incident and patients of group 3 (n = 15) a subarachnoid hemorrhage caused by an intracranial aneurysm.. After cranial trepanation changes of plasmatic hemostasis have been assessed by means of immunologically determined parameters of coagulation. The investigation included blood parameters (hemoglobin, hematocrit, thrombocytes), clotting status (prothrombin time, partial thromboplastin time, thrombin time, fibrinogen, plasminogen, antithrombin III [AT III] activity and proteinase inhibitors), as well as immunological methods such as fibrinopeptide A (FPA), thrombin-antithrombin III (TAT), protein C and factor XIII activity (F XIII activity).. In comparison to group 1 (control) a significant difference (p < 0.001) was seen in groups 2 and 3 for thrombin-antithrombin III (TAT), fibrinopeptide A (FPA), protein C, and the antithrombin III activity. Intra- and postoperatively increased TAT levels in groups 2 (16.9 ng/ml) and 3 (21.1 ng/ml) and decreased protein C levels (group 2: 61% and group 3: 58%) demonstrated an intravascular thrombin generation. On account of the elevated FPA levels in groups 2 (6.5 ng/ml) and 3 (5.7 ng/ml) and decreased AT III activity in groups 2 (58%) and 3 (62%), this thrombin generation was only incompletely compensated. Caused by proteolytic thrombin effects, another sign for a thrombin-induced turnover of clotting factors is the significant reduction (p < 0.001) of F XIII activity in groups 2 (40%) and 3 (44%). In comparison to group 1 this significantly reduced F XIII activity in groups 2 and 3 was correlated (r = 0.99) to changes in FPA and TAT plasma levels, an indication of latent chronic clotting activity. No significant difference was found concerning total amount of infusion, intra- and postoperative blood loss and blood parameters. Eight patients (group 2: 5 patients, group 3: 3 patients) showed a rebleeding episode without operative interventions. In these patients increased clotting activity (TAT, FPA, protein C) caused by proteolytic thrombin effects was combined with a factor XIII activity smaller than 40%.. The results of the recent study indicated that immunologically determined TAT, FPA, protein C, factor XIII and AT III activities might serve to improve management in patients with intracranial bleeding events. In view of these parameters the evaluation of risks for a rebleeding is improved. A decrease of the plasma factor XIII activity under 40% associated with a latent clotting activity induced by a thrombin generation caused a higher risk of rebleeding after an initial intracranial bleeding event. The necessity of substituting factor XIII in such cases should be elucidated to minimize risks of rebleeding.

Topics: Aneurysm, Ruptured; Antithrombin III; Blood Coagulation Factors; Blood Coagulation Tests; Cerebral Hemorrhage; Factor XIII; Fibrin; Fibrinogen; Fibrinopeptide A; Hematoma, Subdural; Hemostasis, Surgical; Humans; Intracranial Aneurysm; Peptide Hydrolases; Plasminogen; Postoperative Complications; Protein C; Recurrence; Reference Values; Trephining

Fibrinogen, fibrin monomer, and D dimer were analyzed in 41 cases of chronic subdural hematoma (SDH) to characterize local rebleeding, coagulation, and fibrinolysis using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting. Chronic SDH's were divided into five groups according to their appearance on computerized tomography: high-density, isodensity, low-density, mixed-density, and layering types. The concentration of fibrinogen, which indicates rebleeding, was higher in the mixed-density (15.7 +/- 3.4 mg/dl (mean +/- standard error of the mean)) and layering (15.7 +/- 2.6 mg/dl) types of hematoma, and lower in the low-density hematomas (1.4 +/- 0.6 mg/dl) compared with the isodense hematomas (6.9 +/- 1.1 mg/dl). Fibrin monomer, which indicates coagulative activity, had a distribution similar to that of fibrinogen: 87 +/- 22, 18 +/- 8, 175 +/- 40, and 177 +/- 23 micrograms/ml in isodense, low and mixed-density, and layering types of hematomas, respectively. The D dimer, which indicates fibrinolytic activity, was higher in the layering hematoma type (2032 +/- 384 micrograms/ml), and lower in low-density hematomas (301 +/- 164 micrograms/ml) compared to isodense (1310 +/- 256 micrograms/ml) and mixed-density (1039 +/- 207 micrograms/ml) types of hematomas. These observations suggest the following characterization of each type of chronic SDH. The layering type is active, with a high tendency to rebleed and for hyperfibrinolytic activity. The mixed-density type has a high tendency to rebleed with lower hyperfibrinolytic activity than the layering type. The low-density hematoma is stable with a low tendency to rebleed and to fibrinolytic activity.

Topics: Adult; Aged; Aged, 80 and over; Blood Coagulation Disorders; Chronic Disease; Electrophoresis, Polyacrylamide Gel; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Hematoma, Subdural; Humans; Immunoblotting; Male; Middle Aged; Recurrence; Sodium Dodecyl Sulfate

To characterize local hyperfibrinolysis in the pathogenesis of chronic subdural hematoma (CSDH), fibrin degradation products (FDPs) were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) to identify each FDP fragment (fragments HMW, YY, DY and DD) by immunoblotting. The electrophoretic patterns of FDP in 40 hematomas from 33 patients could be categorized into 3 patterns; (i) type 1, the sharp DY and DD bands; (ii) type 2, the broad DY and DD bands; and (iii) type 3, the sharp DY and DD with two bands with higher molecular weights than fragment DY and DD. The broadening of DY and DD bands was reproduced by incubating the sample containing sharp DD and DY bands with the hemolyzed peripheral blood cells. These results indicated that the hyperfibrinolysis in CSDH could be characterized by the constant and incomplete proteolysis of fibrinogen and fibrin by plasmin and further degradation of FDPs by non-plasmin proteases released from hemolyzed blood cells.

Topics: Electrophoresis, Polyacrylamide Gel; Endopeptidases; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysin; Hematoma, Subdural; Humans; Immunoblotting; Male

Globular hyaline microthrombi are characterized by their diameter (2-30 micron), globular form, and positive PAS and PTAH reaction. They are a morphologic indicator of disturbed microcirculation and hemostasis, such as that occurring in shock. In two of our cases, we observed large globular hyaline microthrombi, some with central webbed degradation progressing to the formation of closed or open hollow globules. The electron microscopic findings were similar to those observed by other investigators in typical shock bodies. On the basis of the morphologic findings, the authors conclude that degradation phenomena start at the center of globular hyaline microthrombi and can progress to the surface where accelerated fibrinolysis is possible. The cellular elements that other investigators have described as a possible condensation center for fibrin precipitate proved to be structurally intact cells that are apparently located in niches of open hollow globules or in the center of circular hyaline microthrombi. The diagnostic relevance, vitality, and temporal classification are discussed.

Topics: Adult; Cerebral Veins; Fibrin; Hematoma, Subdural; Humans; Hyalin; Intracranial Embolism and Thrombosis; Male; Malignant Hyperthermia; Microscopy, Electron; Middle Aged; Portal Vein; Shock; Thrombosis

Various biochemical processes in hematoma fluid arising from chronic subdural bleeding have not yet been clearly explained. We examined the question whether formation of hematoma fluid after onset of bleeding is preceded by complete clotting with fibrin formation and subsequent lysis of the clot. 22 samples of hematoma fluid taken during operation were used. The protein content was 5.7 +/- 9.8 g/l (mean +/- SD), and coagulable fibrinogen could not be demonstrated whereas 0.99 +/- 0.45 mg/ml fibrin(ogen) break-down products were found immunologically. The high levels of crosslinked D-D fibrin derivatives (0.32 +/- 0.26 mg/ml) were conspicuous: there was a correspondingly high degree of crosslinking (86.2% x/- 12.2%) of the fibrin(ogen) break-down products (calculated from the proportion of dimeric to monomeric gamma-chains). Monoclonal antibodies specific for D-D were employed for the first time to answer the question. The characterization of the crosslinked fibrin derivatives together with their submolecular sub-units and the quantification of the D-D content serve to prove that fibrin is both formed and broken down in chronic subdural hematomas.

Topics: Adult; Aged; Blood Protein Electrophoresis; Chronic Disease; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Hematoma, Subdural; Humans; Middle Aged; Molecular Weight

We report experimental studies showing the relationship of the reflectivity of blood clot to both the red cell mass and the fibrin mesh. The highest amplitude echoes are returned by the fibrin mesh. These studies are compared with clinical examples of the different types of neonatal intracranial haemorrhage, as demonstrated by ultrasound. We conclude that the typical high-amplitude echoes characteristic of intracerebral haemorrhage are primarily due to the amount of fibrin mesh present, and not to the intact red cell mass, as has been previously suggested.

Topics: Blood Coagulation; Cerebral Hemorrhage; Cerebral Ventricles; Chronic Disease; Erythrocyte Volume; Fibrin; Hematoma, Subdural; Humans; Infant, Newborn; Subarachnoid Hemorrhage; Ultrasonography

Topics: Adolescent; Adult; Age Factors; Aged; Animals; Blood Coagulation; Body Temperature; Cerebral Hemorrhage; Cerebrospinal Fluid; Child; Child, Preschool; Dogs; Female; Fibrin; Fibroblasts; Haplorhini; Hematoma, Subdural; Humans; Infant; Intracranial Pressure; Male; Middle Aged; Osmotic Pressure; Sex Factors; Subarachnoid Hemorrhage; Subdural Space

Topics: Animals; Brain; Cerebrospinal Fluid; Chronic Disease; Disease Models, Animal; Dogs; Fibrin; Haplorhini; Hematoma, Subdural; Hemiplegia; Macaca

Topics: Animals; Blood Coagulation; Cerebrospinal Fluid; Chronic Disease; Dogs; Fibrin; Haplorhini; Hematoma, Subdural; In Vitro Techniques

Topics: Anticoagulants; Blood Coagulation Disorders; Blood Coagulation Factors; Cerebral Arterial Diseases; Chromatography; Chromatography, Gel; Diagnosis, Differential; Fibrin; Fibrinogen; Hematoma, Subdural; Humans; Infant; Iodine Radioisotopes; Male; Middle Aged; Molecular Weight; Postoperative Complications; Thromboembolism; Thrombosis

Topics: Blood Coagulation Disorders; Blood Coagulation Tests; Cerebral Hemorrhage; Child; Diagnosis; Enzymes; Factor XIII; Fibrin; Genetics, Medical; Hemarthrosis; Hematoma; Hematoma, Subdural; Hemorrhagic Disorders; Humans; Knee Joint

Topics: Central Nervous System Diseases; Cerebral Hemorrhage; Child; Encephalitis; Fibrin; Hematoma; Hematoma, Subdural; Humans; Hydrocephalus; Intracranial Embolism; Intracranial Embolism and Thrombosis; Meningitis; Pathology