TY - JOUR
T1 - Immediate anticoagulation of embolic stroke
T2 - Brain hemorrhage and management options
AU - Hart, Robert G.
AU - Lock-Wood, Kathleen I.
AU - Hakim, Antoine M.
AU - Koller, Richard
AU - Davenport, John G.
AU - Coull, Bruce M.
AU - Brey, Robin
AU - Furlan, Anthony J.
AU - O'neill, Bernard J.
AU - Pettigrew, L. Creed
AU - Nath, Avindra
AU - Yatsu, Frank M.
AU - Sherman, David G.
AU - Easton, J. Donald
AU - Miller, Vincent T.
PY - 1984
Y1 - 1984
N2 - The clinical implications of hemorrhagic transformation of embolic brain infarction were explored by studying 30 patients with cardiogenic brain embolism and either hemorrhagic infarct (HI) or intracerebral hematoma (ICH) on CT. At the time of identification of hemorrhage, 19 patients were receiving anticoagulants and 11 were not. Eight anticoagulated patients and three nonanticoagulated patients developed late HI without attendant worsening after an initial CT was non hemorrhagic. Hemorrhagic transformation without worsening most often occurred after 12 hours but before 48 hours following stroke onset and was associated with large infarcts (82%) but not with age, blood pressure or embolic source. Seven anticoagulated patients, six with large infarcts, and one nonanticoagulated patient with a small infarct abruptly worsened from eight hours to 11 days after stroke, with CT revealing ICH or severe HI. Excessive anticoagulation or acute hypertension potentially contributed to hemorrhagic transformation in four of five patients who were receiving heparin. Brain hemorrhage in embolic strokes most often occurs with large infarcts. Early CT may not allow the identification of large embolic infarcts that are destined to later undergo spontaneous hemorrhagic transformation. For large embolic infarcts, a delay of several days before anticoagulation and special efforts to avoid excessive anticoagulation and hypertension may be prudent. The initial administration of large, bolus doses of heparin should perhaps be avoided.
AB - The clinical implications of hemorrhagic transformation of embolic brain infarction were explored by studying 30 patients with cardiogenic brain embolism and either hemorrhagic infarct (HI) or intracerebral hematoma (ICH) on CT. At the time of identification of hemorrhage, 19 patients were receiving anticoagulants and 11 were not. Eight anticoagulated patients and three nonanticoagulated patients developed late HI without attendant worsening after an initial CT was non hemorrhagic. Hemorrhagic transformation without worsening most often occurred after 12 hours but before 48 hours following stroke onset and was associated with large infarcts (82%) but not with age, blood pressure or embolic source. Seven anticoagulated patients, six with large infarcts, and one nonanticoagulated patient with a small infarct abruptly worsened from eight hours to 11 days after stroke, with CT revealing ICH or severe HI. Excessive anticoagulation or acute hypertension potentially contributed to hemorrhagic transformation in four of five patients who were receiving heparin. Brain hemorrhage in embolic strokes most often occurs with large infarcts. Early CT may not allow the identification of large embolic infarcts that are destined to later undergo spontaneous hemorrhagic transformation. For large embolic infarcts, a delay of several days before anticoagulation and special efforts to avoid excessive anticoagulation and hypertension may be prudent. The initial administration of large, bolus doses of heparin should perhaps be avoided.
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U2 - 10.1161/01.STR.15.5.779
DO - 10.1161/01.STR.15.5.779
M3 - Article
C2 - 6474527
AN - SCOPUS:0021141996
SN - 0039-2499
VL - 15
SP - 779
EP - 789
JO - Stroke
JF - Stroke
IS - 5
ER -