thromboplastin and Cerebral-Hemorrhage

Progressive hemorrhagic injury (PHI) can be divided into coagulopathy-related PHI and normal coagu- lation PHI. Coagulation disorders after traumatic brain injuries can be included in trauma-induced coagulopathy (TIC). Some studies showed that TIC is associated with PHI and increases the rates of disability and mortality. In this review, we discussed some mechanisms in TIC, which is of great importance in the development of PHI, including tissue factor (TF) hypothesis, protein C pathway and thrombocytopenia. The main mechanism in the relation of TIC to PHI is hypocoagulability. We also reviewed some coagulopathy parameters and proposed some possible risk factors, predictors and therapies.

Topics: Blood Coagulation Disorders; Brain Injuries, Traumatic; Cerebral Hemorrhage; Fibrin Fibrinogen Degradation Products; Humans; Incidence; Protein C; Risk Factors; Thromboplastin

Topics: Animals; Antithrombin III; Blood Coagulation; Brain; Cerebral Hemorrhage; Disease Models, Animal; Epoprostenol; Hemostasis; Humans; Microcirculation; Nitric Oxide; Plasminogen Activator Inhibitor 1; Protease Nexins; Stroke; Thrombomodulin; Thromboplastin; Thrombosis; Tissue Plasminogen Activator

Recombinant activated factor VIIa (rFVIIa) has many clinical applications for patients with congenital bleeding disorders and in a variety of clinical settings. Additional studies in the future are ongoing and should provide the clinical anesthesiologist an additional option during certain bleeding states. Specific recommendations as to timing of administration and frequent monitoring of ionized calcium status are suggested at this time. Optimization of fibrinogen levels, platelet levels, pH, and body temperature will enhance efficacy of rFVIIa.

Topics: Cerebral Hemorrhage; Factor VIIa; Hemophilia A; Hemophilia B; Humans; Postpartum Hemorrhage; Recombinant Proteins; Thromboplastin; Warfare; Wounds and Injuries

Recombinant activated coagulation factor VII (rFVIIa) was developed for the treatment of patients with hemophilia who have developed inhibitors against the factor they are missing. Hemophilia is a serious bleeding disorder and patients with hemophilia develop repeated spontaneous CNS, joint and muscle bleeding. Any trauma, even mild events, may cause life-threatening bleeding, and without treatment, these patients have a life expectancy of about 16 years. Thus, hemophilia can be regarded as a model of severe bleeding, and an agent capable of inducing hemostasis in severe hemophilia independent of the hemophilia proteins (FVIII or FIX) may also be effective in patients without hemophilia who experience serious bleeds. The availability of rFVIIa stimulated research on the role of FVII and tissue factor (TF) in the hemostatic process. As a result, a picture partly different from the one suggested by previous models has emerged. These previous models basically neglected the role of cells and cell membranes. The importance of platelets and platelet membrane phospholipids in hemostasis has been demonstrated, and the new concept of the hemostatic process, focusing on cell surfaces, has been outlined.

Topics: Cerebral Hemorrhage; Clinical Trials as Topic; Dose-Response Relationship, Drug; Factor VII Deficiency; Factor VIIa; Hemophilia A; Hemophilia B; Hemostatics; Infusions, Intravenous; Recombinant Proteins; Thromboplastin

Factor VII appears to be the key regulatory protein in the initiation of both the intrinsic and extrinsic systems of coagulation. The single chain, or zymogen form, of factor VII possesses enzymatic activity which makes it an ideal candidate for the initiation of coagulation following vascular injury. A number of interactions between the intrinsic and extrinsic systems of coagulation have been identified. It appears that factor VII is capable of directly activating factor IX and vice versa. The study of factor VII variants with associated thromboembolic complications may provide a number of answers regarding the initiation and regulation of the blood coagulation process.

Topics: Blood Coagulation; Blood Coagulation Tests; Cerebral Hemorrhage; Enzyme Activation; Factor IX; Factor VII; Factor VII Deficiency; Hemarthrosis; Hemophilia A; Humans; Lipoproteins; Liver Diseases; Neutralization Tests; Partial Thromboplastin Time; Radioimmunoassay; Thromboplastin; Thrombosis; Vitamin K Deficiency

Topics: Anticoagulants; Blood Coagulation Tests; Cerebral Hemorrhage; Cerebrovascular Disorders; Coumarins; Heparin; Humans; Middle Aged; Myocardial Infarction; Phenindione; Postoperative Care; Prothrombin Time; Rheumatic Heart Disease; Thromboembolism; Thrombophlebitis; Thromboplastin

Topics: Blood Coagulation Factors; Blood Coagulation Tests; Blood Transfusion; Cerebral Hemorrhage; Epistaxis; Factor VIII; Gastrointestinal Hemorrhage; Hemarthrosis; Hematuria; Hemophilia A; Hemorrhage; Humans; Oral Hemorrhage; Thromboplastin; Wounds and Injuries

Cerebral injury and brain death is associated with apparent hypercoagulation and poor organ outcome. This experimental study challenges the hypotheses that i) brain death causes hypercoagulation and microvascular thrombosis and that ii) neutralizing systemic tissue factor (TF) by in vitro addition of a TF inhibitor (recombinant active site-inhibited factor VIIa (ASIS)) can reverse the hypercoagulable profile.. Using a validated pig model of intracranial hemorrhage and brain death, 20 pigs were randomized to either control or brain death. The primary endpoints were coagulation parameters measured with whole blood thromboelastometry (ROTEM), thrombin generation and a porcine TF-sensitive plasma clotting time assay. In vitro spiking experiments with ASIS were performed in parallel with the latter two assessments. The kidneys were examined histologically for microvascular thromboses.. Brain death induced hypercoagulation, as demonstrated with ROTEM, thrombin generation, and reduced TF-sensitive plasma clotting time. In vitro inhibition of TF with ASIS did not reverse the hypercoagulation. No microvascular thromboses were found in the kidneys.. Brain death causes hypercoagulation; however, inhibition of TF does not reverse the coagulopathy. Thus, TF release does not seem to be the primary cause of this hypercoagulation. Minor changes in the levels of protein C suggest that the protein C pathway may be linked to the observed coagulopathy.

Topics: Animals; Blood Coagulation; Blood Coagulation Tests; Brain Death; Cerebral Hemorrhage; Disease Models, Animal; Random Allocation; Swine; Thrombelastography; Thrombophilia; Thromboplastin

Topics: Antithrombins; Atrial Fibrillation; Benzimidazoles; beta-Alanine; Blood Coagulation; Case-Control Studies; Cerebral Hemorrhage; Dabigatran; Humans; Thromboplastin; Warfarin

To determine the effective index of coagulogram after acute intracerebral hemorrhage (ICH) for predicting the outcome of ICH.. A total of 641 patients with ICH were divided into two groups: the effective treatment group (healing well and improving) and ineffective treatment group (non-improving and dying). The coagulogram results of the two groups were analyzed with SPSS software 13.0, including PT, APTT, TT, and Fbg. The differences in these parameters were found by independent samples T test and Kruskal-Wallis test between the two groups. Then, the different parameters were obtained by logistic regression, which were significantly associated with the prognosis of acute cerebral hemorrhage patients. In addition, the odds ratio for the special indicators was calculated by chi-square test.. Only PT had a significant difference between the groups (p<0.05) among the four parameters. The binary logistic regression analysis indicated that PT (p=0.003) and APTT (p=0.043) were related to the outcome of ICH patients. According to the chi-square test, the OR (odds ratio) of prolonged PT is 2.40 (1.34-4.29 with 95% CI) and that of prolonged APTT is 1.57 (1.01-2.42 with 95% CI).. Prolonged PT and APTT are risk factors affecting the prognosis of ICH patients. Monitoring and controlling PT and APTT are advisable for improving the prognosis of ICH patients.

Topics: Blood Coagulation Factors; Cerebral Hemorrhage; Chi-Square Distribution; Female; Follow-Up Studies; Humans; Magnetic Resonance Imaging; Male; Odds Ratio; Predictive Value of Tests; Prognosis; Prothrombin; Retrospective Studies; Thrombin; Thromboplastin; Tomography, X-Ray Computed; Treatment Outcome

Topics: Animals; Brain; Cerebral Hemorrhage; Factor VIIa; Mice; Mice, Inbred C57BL; Organ Specificity; Thromboplastin

The association between brain damage and respiratory dysfunction has been recognized although mechanistic link between the two is still poorly defined. Intracerebral hemorrhage is accompanied by brain injury, stroke, and parenchymal hematoma formation with surrounding inflammation. Increase intracranial pressure as a result of intracerebral hemorrhage may promote localized activation of cytokines and coagulation system including tissue factor release. However, whether intracerebral hemorrhage triggers inflammation in noncerebral organs has not been elucidated. The aim of the present study was to examine the impact of intracerebral hemorrhage on lung inflammatory response. Intracerebral hemorrhage was induced by stereotaxic intrastriatal administration of bacterial collagenase. Expression of intracellular adhesion molecule-1 (ICAM-1), IKB-alpha, tissue factor, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta) was evaluated by Western blot analysis. Our results revealed that intracerebral hemorrhage upregulated expression of ICAM-1 and tissue factor in both brain and lung, whereas it enhanced TNF-alpha and IL-1beta mainly in brain within 6 and 24 h of the brain injury. Levels of IKB-alpha remained unchanged in brain and lung tissues. Appearance of inflammatory markers in the lung was accompanied by morphological pulmonary damage. These data suggest that intracerebral hemorrhage may trigger acute inflammatory response in both brain and lung.

Topics: Animals; Brain; Cerebral Hemorrhage; Female; I-kappa B Proteins; Inflammation; Intercellular Adhesion Molecule-1; Interleukin-1; Lung; NF-KappaB Inhibitor alpha; Rats; Rats, Sprague-Dawley; Thromboplastin; Time Factors; Tumor Necrosis Factor-alpha

The mechanism by which intracerebral hemorrhage leads to the formation of brain edema is unknown. This study assesses the components of blood to determine if any are toxic to surrounding brain. Various solutions were infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later; brain edema and ion contents were measured. Whole blood caused an increase in brain water content and ion changes consistent with brain edema. Concentrated blood cells, serum from clotted blood, and plasma from unclotted blood all failed to provoke edema formation when infused directly into the brain. On the other hand, activation of the coagulation cascade by adding prothrombinase to plasma did produce brain edema. The edema response to whole blood could be prevented by adding a specific thrombin inhibitor, hirudin, to the injected blood. This study indicates that thrombin plays an important role in edema formation from an intracerebral blood clot.

Topics: Animals; Basal Ganglia; Blood Cells; Blood Coagulation; Blood Physiological Phenomena; Brain Edema; Cerebral Hemorrhage; Hematoma; Injections; Male; Plasma; Rats; Rats, Sprague-Dawley; Stereotaxic Techniques; Thrombin; Thromboplastin

A syndrome of intracranial hemorrhage with gross prolongation of the prothrombin and partial thromboplastin times, with normal thrombin time, fibrinogen concentrations, and coagulation factor assays is described in four children with homozygous beta-thalassemia. Mixing experiments and plasma thromboplastin inhibition tests revealed a persistent abnormality which was consistent with the presence of a circulatory prothrombinase inhibitor. The origin of this previously unreported inhibitor in thalassemia remains speculative.

Topics: Cerebral Hemorrhage; Child; Female; Humans; Immunoglobulin M; Male; Partial Thromboplastin Time; Prothrombin Time; Thalassemia; Thromboplastin

Topics: Animals; Butylated Hydroxytoluene; Cerebral Hemorrhage; Cricetinae; Dogs; Guinea Pigs; Hemorrhage; Liver; Mice; Phenols; Prothrombin Time; Quail; Rabbits; Rats; Thromboplastin

The hemostasis function was studied in 33 patients with epileptical seizures of a different etiology. The studies were conducted at the moment of the epileptical seizure or epileptical status and in the interattack period during hyperventilation. The concentration of products of blood fibrinogen degradation, the degree of platelet agregation, their number and prothrombine index were estimated. The data obtained were compared with those of normals. The results of the studies indicate the existence of the syndrome of intravascular coagulation during an epileptical seizure and epileptical status.

Topics: Blood Cell Count; Blood Platelets; Cerebral Hemorrhage; Disseminated Intravascular Coagulation; Epilepsy; Fibrin Fibrinogen Degradation Products; Humans; Intracranial Embolism and Thrombosis; Male; Platelet Aggregation; Status Epilepticus; Thromboplastin

Topics: Alanine Transaminase; Anemia; Aspartate Aminotransferases; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Platelets; Blood Transfusion; Cerebral Hemorrhage; Ecchymosis; Female; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Male; Prognosis; Prothrombin; Prothrombin Time; Seizures; Spinal Puncture; Subarachnoid Hemorrhage; Thrombin; Thromboplastin; Vitamin K

Topics: Blood Coagulation; Cerebral Hemorrhage; Factor VII; Factor VII Deficiency; Female; Heterozygote; Homozygote; Humans; Infant; Pedigree; Thromboplastin

Topics: Adenine Nucleotides; Amines; Aspirin; Blood Platelet Disorders; Blood Platelets; Carbon Isotopes; Cell Membrane; Cerebral Hemorrhage; Collagen; Contusions; Ecchymosis; Female; Humans; Infant, Newborn; Infant, Newborn, Diseases; Intestinal Secretions; Platelet Adhesiveness; Serotonin; Thromboplastin; Vitamin K Deficiency Bleeding

Topics: Autopsy; Blood Cell Count; Blood Coagulation Factors; Blood Coagulation Tests; Blood Platelets; Blood Vessels; Cerebral Hemorrhage; Disseminated Intravascular Coagulation; Erythroblastosis, Fetal; Female; Fibrin; Fibrinogen; Hemoglobins; Hemorrhage; Humans; Infant, Newborn; Liver; Lung; Pregnancy; Retrospective Studies; Subarachnoid Hemorrhage; Thrombin; Thromboplastin

Topics: Blood Coagulation Tests; Blood Transfusion; Cerebral Hemorrhage; Factor X; Female; Hematoma; Humans; Hypoprothrombinemias; Infant; Infant, Newborn; Male; Melena; Pedigree; Pregnancy; Thrombelastography; Thromboplastin