Hemostatic activation in spontaneous intracerebral hemorrhage.
OBJECTIVE
There is no in-depth information available on the changes in hemostatic systems in patients in the acute phase of spontaneous intracerebral hemorrhage (ICH). This study was conducted to assess the relationships between the changes in hemostatic systems and clinical parameters in patients in acute-phase ICH.


METHODS
The records of 358 patients admitted within 6 hours of onset of ICH were reviewed to examine the relationships between changes in hemostatic systems and computed tomographic findings and clinical parameters.


RESULTS
-The white blood cell counts and the levels of thrombin-antithrombin complex, plasmin-antiplasmin complex, and D-dimer in patients with intraventricular extension (IVE) or subarachnoid hemorrhage (SAH) were significantly (P<0.05) higher than those in patients without IVE or SAH. Most of the hemostatic system parameters in patients without IVE or SAH showed no significant differences compared with normal subjects. Multiple linear regression analysis revealed that the levels of thrombin-antithrombin complex significantly increased with an increase in the amount of SAH (P<0.001) and IVE (P<0.001). The levels of thrombin-antithrombin complex were not significantly associated with the volume of intraparenchymal hematoma. The level of the complex, however, was significantly (P<0.001) and independently associated with the presence of IVE or SAH (multiple logistic regression analysis).


CONCLUSIONS
The systemic activation of hemostatic systems in ICH patients seems to take place only when blood reaches the subarachnoid space. The intraparenchymal hematoma itself seems unlikely to activate hemostatic systems in peripheral blood, although the hematoma is expected to cause local activation of hemostatic systems.
Departments of Neurosurgery and Integrated Neuroscience, Brain Research Institute, University of Niigata, Niigata, Japan. yfujii@bri.niigata-u.ac.jp
Y
Y
Fujii
S
S
Takeuchi
A
A
Harada
H
H
Abe
O
O
Sasaki
R
R
Tanaka
D000933:Antifibrinolytic Agents / Q000097:blood; D000990:Antithrombin III; D002543:Cerebral Hemorrhage / Q000097:blood* / Q000175:diagnosis / Q000453:epidemiology; D002552:Cerebral Ventricles / Q000098:blood supply / Q000473:pathology; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005341:Fibrinolysin; D006487:Hemostasis; D006801:Humans; D007564:Japan / Q000453:epidemiology; D007958:Leukocyte Count; D008297:Male; D010447:Peptide Hydrolases / Q000097:blood; D012044:Regression Analysis; D012422:Rupture, Spontaneous; D013345:Subarachnoid Hemorrhage / Q000097:blood / Q000175:diagnosis; D013346:Subarachnoid Space / Q000473:pathology; D014057:Tomography, X-Ray Computed; D000979:alpha-2-Antiplasmin
D000933:Antifibrinolytic Agents; D005338:Fibrin Fibrinogen Degradation Products; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C037742:plasmin-plasmin inhibitor complex; D000990:Antithrombin III; D010447:Peptide Hydrolases; D005341:Fibrinolysin