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Acute intracranial hemorrhage

Vinuela F, Duckwiler G, Mawad M (1997) Guglielmi detachable coil embolization of acute intracranial aneurysm perioperative anatomical and clinical outcome in 403 patients. J Neurosurg 86 475-482 Vora YY, Suarez-Almazor M, Steinke DE, Martin ML, Findlay JM (1999) Role of transcranial Doppler monitoring in the diagnosis of cerebral vasospasm after subarachnoid hemorrhage. Neurosurgery 44 1237-1247 discussion 1247-1248... [Pg.282]

The clinical role of permeability imaging has yet to be assessed by a large clinical trial, but these techniques continue to hold promise for the future, as intracranial hemorrhage is the most significant potential complication of what is currently the only FDA-approved treatment for acute stroke. [Pg.26]

OR 1.81, 95% Cl 1.46-2.24), most of which were related to symptomatic intracranial hemorrhage (OR 3.37, 95% Cl 2.68. 22). In addition, a pooled analysis of six major randomized placebo-controlled IV rt-PA stroke trials (Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke (ATLANTIS) I and II, European Cooperative Acute Stroke Study (ECASS) I and II, and NINDS I and II), including 2775 patients who were treated with IV rt-PA or placebo within 360 minutes of stroke onset, confirmed the beneht up to 3 hours and suggested a potential beneht beyond 3 hours for some patients. The pattern of a decreasing chance of a favorable 3-month outcome as the time interval from stroke onset to start of treatment increased was consistent with the findings of the original NINDS study. ... [Pg.64]

Stenting of an acutely occluded intracranial vessel may provide fast recanalization by entrapping the thrombus between the stent and the vessel wall. A recent study in which 19 patients with acute occlusions at the ICA terminus n = 8), M1/M2 (n = 7), or basilar artery (n = 4) were treated with balloon-expandable stents showed a TIMI 2 and 3 recanalization rate of 79% and no symptomatic intracranial hemorrhages (Fig. 4.5). ... [Pg.87]

Wylie EJ, Hein ME, Adams JE. Intracranial hemorrhage following surgical revascularization for treatment of acute strokes. J Neurosurg 1964 21 212-215. [Pg.133]

ICH, intracranial hemorrhage TIMI, Thrombolysis in Myocardial Blood Flow (TIMI-3 blood flow indicates complete perfusion of the infracted artery). (Reprinted from Spinier SA, de Den us S. Acute Coronary Syndromes. In DiPiro JT, Talbert RL, Yee CC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 303, with permission.)... [Pg.97]

Acute complications of stroke include cerebral edema, increased intracranial pressure, seizures, and hemorrhagic conversion. In the acute setting, several supportive interventions and treatments to prevent acute complications should be initiated. [Pg.166]

Suggested Alternatives for Differential Diagnosis Meningitis, basilar artery blood clots (thrombosis), cardioembolic stroke, cavernous sinus syndromes, cerebral venous blood clots (thrombosis), confusional states and acute memory disorders, epileptic and epileptiform encephalopathies, febrile seizures, haemophilus meningitis, intracranial hemorrhage, leptomeningeal carcinomatosis, subdural pus (empyema), or bruise (hematoma). [Pg.537]

There are currently no standard pharmacologic strategies for treating intracerebral hemorrhage. Medical guidelines for managing blood pressure, increased intracranial pressure, and other medical complications in acutely ill patients in neurointensive care units should be followed. [Pg.174]

Zazulia AR, Diringer MN, Videen TO et al (2001) Hypoperfusion without ischemia surrounding acute intracerebral hemorrhage. J Cereb Blood Flow Metab 21 801-810 Zhu XL, Chan MS, Poon WS (1997) Spontaneous intracranial hemorrhage which patients need diagnostic cerebral angiography A prospective study of 206 cases and review of the literature. Stroke 28 1406-1409... [Pg.170]

Widespread hemorrhagic brain infarcts and intracranial hemorrhages tend to cause an acute or subacute global encephalopathy rather than stroke-like episodes. The diagnosis is confirmed by a low platelet count, low plasma fibrinogen, and raised fibrin degradation products and D-dimer. [Pg.77]


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See also in sourсe #XX -- [ Pg.163 ]




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