Articles: subarachnoid-hemorrhage.
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Cerebral vasospasm is a major cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage. With improvement in surgical techniques and perioperative care, the results in neurologically intact patients are generally satisfactory. However, cerebral vasospasm remains a major problem in the successful management of neurologically deteriorating patients. Until the pathophysiology of cerebral vasospasm is clarified, a reliable treatment regimen will remain elusive and the overall outlook for patients with aneurysmal subarachnoid hemorrhage will remain limited.
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Review
Antifibrinolytic therapy in subarachnoid hemorrhage caused by ruptured intracranial aneurysm.
There are 25 published studies on the treatment with antifibrinolytic agents of subarachnoid hemorrhage (SAH) caused by ruptured intracranial aneurysm. Twelve of these studies were uncontrolled and, except for one, all reported reduced incidence of rebleeding. ⋯ Three studies showed no effect, and three reported a higher incidence of rebleeding in treated patients. Discrepancies may be due to the multiple clinical variables of SAH and to flaws in methodology; nevertheless, the data fail to demonstrate that antifibrinolytic therapy alters the natural history of the disease.
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Randomized Controlled Trial Clinical Trial
Antifibrinolysis with tranexamic acid in aneurysmal subarachnoid hemorrhage: a consecutive controlled clinical trial.
A randomized controlled clinical trial was carried out to study the effect of tranexamic acid (AMCA, Cyklokapron; AB Kabi, Stockholm, Sweden) in the prevention of early rebleeding after the rupture of an intracranial aneurysm. The incidence of vasospasm, hydrocephalus, cerebral ischemic and thromboembolic complications, morbidity, and mortality was also evaluated. The series comprises 59 patients, 30 treated with tranexamic acid and 29 controls. ⋯ Five patients in each group died from rebleeding. Five additional treated patients and 2 controls died from cerebral ischemic dysfunction. The results suggest that tranexamic acid may protect patients with ruptured aneurysms from rebleeding for 1 or 2 weeks, but that it also may produce cerebral ischemic complications.
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Journal of neurosurgery · Feb 1981
Clinical TrialEarly management of aneurysmal subarachnoid hemorrhage. A report of the Cooperative Aneurysm Study.
The overall results are presented of early medical management and delayed operation among 249 patients studied during the period 1974 to 1977, treated within 3 days of subarachnoid hemorrhage (SAH) and evaluated 90 days after aneurysm rupture. The results included 36.2% mortality, 17.9% survival with serious neurological sequelae, and 46% with a favorable outcome. ⋯ These figures represent the results despite effective reduction in early rebleeding by antifibrinolytic therapy and successful surgery in those patients reaching operation. Further therapeutic advances are needed for patients hospitalized within a few days after SAH.
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Acta neurochirurgica · Jan 1981
Randomized Controlled Trial Clinical TrialCoagulation and fibrinolysis in blood and cerebrospinal fluid after aneurysmal subarachnoid haemorrhage: effect of tranexamic acid (AMCA).
Serial assays of blood coagulation factors as well as of fibrin/fibrinogen degradation products (FDP) and plasminogen activatory activity (PA) on fibrin plates in blood and cerebrospinal fluid (CSF) were performed in 41 consecutive patients with recently ruptured cerebral aneurysms, 21 of whom were randomly treated with tranexamic acid (AMCA). Coagulation factors were unaffected by the drug and plasminogen and FDP decreased in blood after two weeks' treatment. ⋯ An increase in CSF-FDP occurred after rebleeding and in patients with cerebral ischaemic symptoms. The results indicate that AMCA inhibits local fibrinolysis in CSF in patients with aneurysm rupture.