No hyperfibrinolysis following subarachnoid or intracerebral haemorrhage: a prospective cohort study.

: Changes in fibrinolysis following subarachnoid haemorrhage (SAH) and intracerebral haemorrhage (ICH) are sparsely investigated. To investigate fibrinolysis in the acute phase in SAH and ICH patients compared with healthy individuals, fibrinolysis after 24 h in ICH patients and the in-vivo effect of tranexamic acid (TXA) on fibrinolysis in SAH patients. Further, ex-vivo studies were performed by addition of several haemostatic agents to blood samples obtained at admission. Blood was sampled from 46 SAH and 41 ICH patients upon admission. In ICH patients, a second blood sample was obtained 24 h after symptom onset, and in SAH patients after TXA treatment. A sex-matched healthy control group was used for comparison. Fibrinolysis and clot stability were assessed by a dynamic fibrin clot lysis assay, and measurements of plasminogen activator inhibitor I, tissue plasminogen activator and coagulation factor XIII were performed. On admission, no difference in lysis time was found in SAH or ICH patients compared with healthy controls (all P values >0.15). For SAH and ICH patients, median plasminogen activator inhibitor I, tissue plasminogen activator and factor XIII levels were within the reference intervals. In ICH patients, lysis time remained within 24 h after symptom onset (P = 0.63). In SAH patients, the clot lysis curve showed a complete block of fibrinolysis after TXA administration. Ex-vivo addition of solulin and prothrombin complex concentrate reduced fibrinolysis (P < 0.001). SAH and ICH patients showed no hyperfibrinolysis on admission. Fibrinolysis remained normal in ICH patients, and TXA treatment obliterated fibrinolysis in SAH patients.

Thromboelastometry Shows Early Hypercoagulation in Patients with Spontaneous Subarachnoid Hemorrhage.

BACKGROUND: The ability to achieve hemostasis after spontaneous subarachnoid hemorrhage (SAH) plays a pivotal role in outcome. Changes in coagulation in the early hours after SAH have been only sparsely investigated. OBJECTIVE: To investigate changes in coagulation after SAH and illuminate underlying mechanisms. METHODS: We enrolled 46 patients with spontaneous aneurysmal SAH. Blood samples were collected at admission and 24 hours after symptom onset. Thromboelastometry (ROTEM) was performed using the standard assays EXTEM, INTEM, and FIBTEM. Platelet maximum clot elasticity was calculated based on ROTEM results. Thrombin generation, levels of thrombin-antithrombin complex, fibrinogen, and coagulation factor XIII were measured. All data were compared with a gender-matched healthy control group. RESULTS: At admission (median, 3 hours 39 minutes from symptom onset), maximum clot firmness (EXTEM, P < 0.0001; INTEM, P = 0.08; FIBTEM, P < 0.0001) and platelet maximum clot elasticity (P < 0.0001) were higher in patients with SAH than in healthy controls. Thrombin generation showed higher, although nonsignificant, endogenous thrombin potential in patients with SAH than in healthy controls (P = 0.06), and thrombin-antithrombin complex levels were above the reference interval. Median fibrinogen and coagulation factor XIII levels were both within the reference parameters and remained increased 24 hours after symptom onset, whereas endogenous thrombin potential (P = 0.01) and thrombin-antithrombin complex levels decreased (P < 0.0001). CONCLUSIONS: Patients with SAH were in a hypercoagulable state at admission and remained so 24 hours after SAH. Increased clot firmness could be caused by increased platelet function, because platelet maximum clot elasticity was increased despite normal fibrinogen and coagulation factor XIII levels.

Coagulation Profile after Spontaneous Intracerebral Hemorrhage: A Cohort Study.

BACKGROUND: Intracerebral hemorrhage (ICH) causes death or disability and the incidence increases with age. Knowledge of acute hemostatic function in patients with ICH without anticoagulant and antiplatelet therapy is sparse. Increased knowledge of the coagulation profile in the acute phase of ICH could improve acute treatment and recovery. We investigated coagulation at admission and changes in coagulation during the first 24hours after symptom onset. METHODS: Enrolled were 41 ICH patients without anticoagulant or antiplatelet therapy admitted to Aarhus University Hospital, Denmark. Blood samples were collected at admission, 6, and 24hours after symptom onset. Thromboelastometry (ROTEM), thrombin generation, and thrombin-antithrombin (TAT) complex were analyzed. Clinical outcome was evaluated using the National Institute of Health Stroke Scale, the Modified Rankin Score, and mortality. RESULTS: At admission, compared with healthy individuals, ICH patients had increased maximum clot firmness (EXTEM P < .0001; INTEM P < .0001; FIBTEM P < .0001), increased platelet maximum clot elasticity (P < .0001) in ROTEM, higher peak thrombin (P < .0001) and endogenous thrombin potential (P = .01) in thrombin generation, and elevated TAT complex levels. During 24hours after significantly, while thrombin generation showed decreased peak thrombin (P < .0001) and endogenous thrombin potential (P < .0001). Coagulation test results did not differ between patients when stratified according to clinical outcome. CONCLUSIONS: ICH patients without anticoagulant or antiplatelet therapy demonstrated activated coagulation at admission and within 24hours after symptom onset.