Articles: subarachnoid-hemorrhage.
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Letter Clinical Trial
Antifibrinolytic therapy in subarachnoid hemorrhage.
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Journal of neurology · Jan 1985
Long-term prognosis of subarachnoid hemorrhages of unknown etiology.
Forty-nine patients who suffered a spontaneous subarachnoid hemorrhage (SAH), and in whom panangiography did not show the cause of the bleeding, were evaluated after a long follow-up (median 8 years). No relationship was found between outcome and antifibrinolytic treatment or blood pressure level. Angiography was repeated in cases with spasm or after rebleeding: one aneurysm was found (7%). ⋯ The early mortality was 2%. Late functional capacity was normal in 94% of the patients. No particular restrictions should therefore be recommended.
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21 patients (aged 28-81 years) with recent subarachnoid hemorrhage (10 saccular aneurysms, 3 arteriovenous angiomas, 8 normal angiograms) were continuously infused with tranexamic acid at a dosage of 5 g daily for up to 14 days. Therapy was surveyed by daily measurement of the available plasminogen activity (aPl) with the chromogenic substrate S-2251 and by a modified bioassay, whereby the concentration of tranexamic acid was determined thrombelastographically and expressed as antifibrinolytic equivalent. ⋯ Intra- and interindividual changes were relatively small for aPl, when compared with the antifibrinolytic equivalent measured by the bioassay. In 2 elderly patients tranexamic acid infusion had to be terminated because of clinical and laboratory signs of disseminated intravascular coagulation, whereby aPl fell below the therapeutic range, elucidating that this method is a sensitive indicator for a hypercoagulable state and useful for the surveillance of therapy with antifibrinoltic agents.
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Acta neurochirurgica · Jan 1985
The pathogenetic and prognostic significance of blood-brain barrier damage at the acute stage of aneurysmal subarachnoid haemorrhage. Clinical and experimental studies.
In a retrospective study, pathological tissue enhancement was found in nearly two fifths of patients with acute SAH on contrast-enhanced cranial computed tomography. By means of absorption measurements with the region of interest technique over the basal ganglia, it was proved indirectly that pathological tissue enhancement should be brought about not only by hyperaemia, i.e., a blood volume increase, but also by extravasation of the contrast material, i.e., blood-brain barrier (BBB) disruption. A similar conclusion was drawn from the retrospective isotope brain scintigraphy study. ⋯ Measurements on the water, electrolyte, albumin contents of brain tissue, as well as the immunohistochemical localization of albumin, clearly indicated that the brain oedema developing at the acute stage of experimental SAH could be classified as having a primary vasogenic component in addition to the cytotoxic component. This increased capillary permeability was found to be brought about by opening of tight junctions and pinocytosis in the endothelial cells. The pathological capillary permeabilit
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It is well known that abnormalities of coagulation and fibrinolysis frequently take place during the course of cerebrovascular diseases. In this paper, coagulation and fibrinolytic studies were performed during the course of acute stage through chronic stage of subarachnoid hemorrhage. Tested items were partial thromboplastin time, prothrombin time, FDP, alpha 2-plasmin inhibitor, antithrombin III, fibrinogen, besides, fibrinopeptide A (FPA), and fibrinopeptide B beta (FPB beta) which were being worthy of note. ⋯ Increase of fibrinogen delayed from the peaks of FPA and FPB beta showing the peaks at the seventh to the fourteenth day from the onset of subarachnoid hemorrhage. In three cases with symptomatic vasospasm, FPA and FPB beta showed maximal values two to four days prior to the appearance of symptomatic cerebral vasospasm. Other tests were all within normal limits.(ABSTRACT TRUNCATED AT 250 WORDS)