fibrinopeptide-a and Cerebral-Hemorrhage

To test the hypothesis that an impaired coagulation system facilitates rapid expansion of hypertensive intracerebral hemorrhage (HICH), coagulation markers were assayed in plasma and their relations to both the hemorrhage size and its progressive expansion were analyzed. Ninety patients with HICH were studied. On admission, plasma samples were taken for the coagulation assay. Hematoma volume was calculated from a computed tomography (CT) scan and its enlargement was estimated by comparison to the volume of the hematoma calculated from a second CT scan taken later within 24 hr. Nine out of 90 patients showed enlargement in their hematoma size (enlarged hematoma group). Four of the enlarged hematoma group fell into acute fatal deterioration and died. Plasma levels of both fibrino peptide A (17.2+/-7.8 vs. 4.0+/-0.6 ng/ml, P < 0.05) and thrombin-antithrombin complex (21.9+/-3.1 vs. 7.4+/-2.8 ng/ml, not significant) were higher in the unchanged group than those in the enlarged hematoma group. In the hematoma-enlarged group fibrino-peptide A level did not exceed 10 ng/ml. In the hematoma unchanged group thrombin-AT-III complex values were positively correlated to hematoma volume. Thus, the coagulation system seemed to be highly activated depending on the hemorrhage volume within three hr after ictus in hypertensive intracerebral hemorrhage patients. When thrombin generation was not sufficient after bleeding, the hematoma seemed to be progressively enlarged. In conclusion, plasma levels of the coagulation markers on admission could be useful predictors of the possible enlargement of hematoma which leads to a poor outcome.

Topics: Aged; Aged, 80 and over; Antithrombin III; Blood Coagulation Disorders; Cerebral Hemorrhage; Disease Progression; Female; Fibrinogen; Fibrinopeptide A; Hematoma; Humans; Incidence; Intracranial Hypertension; Male; Middle Aged; Peptide Hydrolases; Platelet Count; Prothrombin Time

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

The well-known coagulation inhibitors antithrombin and protein C, and the more recently described inhibitors, heparin cofactor II and extrinsic pathway inhibitor, were measured in plasma during a 7-day observation period, from patients with pneumonia (n = 13), and in stroke patients with infarction (n = 9) and haemorrhage (n = 9). In patients with pneumonia, elevated fibrinopeptide A levels and subnormal antithrombin and protein C levels suggested some degree of consumption of the inhibitors. Later, an increase was observed for all the inhibitors, but was most conspicuous for heparin cofactor II which reached high normal values. C-reactive protein, initially markedly elevated, decreased rapidly. This finding suggests that heparin cofactor II might act as a delayed acute phase reactant. In stroke patients only small, not statistically significant, changes occurred during the observation period, except for heparin cofactor II which increased in patients with haemorrhagic stroke.

Topics: Acute-Phase Proteins; Adult; Aged; Anticoagulants; Antithrombins; C-Reactive Protein; Cerebral Hemorrhage; Cerebral Infarction; Cerebrovascular Disorders; Female; Fibrinopeptide A; Glycoproteins; Heparin Cofactor II; Humans; Male; Middle Aged; Pneumonia

Topics: Acute Disease; Aged; Blood Coagulation; Brain Injuries; Cerebral Hemorrhage; Disseminated Intravascular Coagulation; Female; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Fibrinopeptide A; Fibrinopeptide B; Humans; Hypertension; Male; Middle Aged; Peptide Fragments