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Intracranial rebleeding

Intracranial rebleeding in moyamoya disease. Journal of Clinical Neuroscience 4 169-172... [Pg.85]

In subarachnoid hemorrhage due to a ruptured intracranial aneurysm or arteriovenous malformation, surgical intervention to clip or ablate the vascular abnormality substantially reduces mortality from rebleeding. The benefits of surgery are less well documented in cases of primary intracerebral hemorrhage. In patients with intracerebral hematomas, insertion of an intraventricular drain with monitoring of intracranial pressure is... [Pg.171]

New England Journal of Medicine 336 28-40 Schwartz TH, Solomon RA (1996). Perimesencephalic nonaneurysmal subarachnoid hemorrhage review of the literature. Neurosurgery 39 433-440 Sluzewski M, van Rooij WJ, Beute GN et al. (2005). Late rebleeding of ruptured intracranial aneurysms treated with detachable coils. American Journal of Neuroradiology 26 2542-2549 Smith ER, Carter BS, Ogilvy CS (2002). [Pg.360]

Subarachnoid hemorrhage (SAH) is most commonly caused by rupture of an intracranial aneurysm. It can produce vasospasm that may cause ischemia and infarction. Currently, vasospasm has surpassed rebleeding as the most important complication after rupture of an aneurysm. Vasospasm due to SAH is thought to occur in the majority of cases of SAH (angiographic vasospasm is detectable in perhaps as many as 60-70% of patients after subarachnoid hemorrhage), but is symptomatic only in about a third of this population [81]. Symptomatic vasospasm carries a 15% to 20% risk of stroke or death. Vasospasm peaks around 1 week after SAH, but it can be seen as early as 3 days or as late as 3 weeks after the initial event [82], The underlying mechanisms are not understood, but vasospasm is clearly related to the amount of blood and its location in the subarachnoid space. Clinical symptoms generally develop slowly over a period of several hours to 1 or 2 days however, clinical evolution can be rapid in the onset with a stroke-like presentation [81, 82]. [Pg.38]

These drugs find clinical utility in settings such as prevention of rebleeding in intracranial hemorrhages, as adjunctive therapy in hemophilia, and of course, in treatment of bleeding associated with fibrinolytic therapy. In most bleeding conditions, however, -aminocaproic acid therapy has not been shown to be of definitive benefit. In recent trials, tranexamic acid was found to reduce red cell transfusion better than -aminocaproic acid or placebo in patients undergoing liver transplantation (136). [Pg.1250]

Molyneux A J. Kerr R S, Yu L M et al. (2005) International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2,143 patients with ruptured intracranial aneurysms a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet 3-9 366 809-917 Richter G, Engelhorn T, Struffert T et al. (2007) Flat panel detector angiographic CT for stent-assisted coil embolization of broad-based cerebral aneurysms. Am J Neurora-diol 28 1902-1908... [Pg.577]


See other pages where Intracranial rebleeding is mentioned: [Pg.771]    [Pg.782]    [Pg.359]    [Pg.419]    [Pg.192]    [Pg.206]    [Pg.206]    [Pg.212]    [Pg.267]    [Pg.272]    [Pg.281]    [Pg.571]    [Pg.559]    [Pg.571]   
See also in sourсe #XX -- [ Pg.180 , Pg.184 ]




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