(Stroke. 2000;31:596.)
© 2000 American Heart Association, Inc.
Original Contributions |
Decreased Perihematomal Edema in Thrombolysis-Related Intracerebral Hemorrhage Compared With Spontaneous Intracerebral Hemorrhage
From the Department of Neurology, University of Pittsburgh Medical Center (J.M.G.), , Pittsburgh, Pa; Department of Neurology, Mayo Clinic Educational Foundation (T.G.B.), , Jacksonville, Fla; Departments of Neurology and Cardiology, Cleveland Clinic Foundation (C.A.S., E.J.T.), Cleveland, Ohio; and Departments of Neurology and Emergency Medicine, University of Cincinnati Medical Center (T.A.T., E.J., S.S., J.K., R.M., A.P., J.E.D., J.P.B.), Cincinnati, Ohio.
Correspondence and reprint requests to James M. Gebel, MD, University of Pittsburgh Medical Center Stroke Institute, 200 Lothrop Street, C-420 PUH, Pittsburgh, PA 15213. E-mail jgebel{at}stroke.upmc.edu
Background and Purpose—Intracerebral hemorrhage (ICH) is a highly morbid disease process. Perihematomal edema is reported to contribute to clinical deterioration and death. Recent experimental observations indicate that clotting of the intrahematomal blood is the essential prerequisite for hyperacute perihematomal edema formation rather than blood-brain barrier disruption.
Methods—We compared a series of patients with spontaneous ICH (SICH) to a series of patients with thrombolysis-related ICH (TICH). All patients were imaged within 3 hours of clinical onset. We reviewed relevant neuroimaging features, emphasizing and quantifying perihematomal edema. We then analyzed clinical and radiological differences between the 2 ICH types and determined whether these factors were associated with perihematomal edema.
Results—TICHs contained visible perihematomal edema less than half as often as SICHs (31% versus 69%, P<0.001) and had both lower absolute edema volumes (0 cc [25th, 75th percentiles: 0, 6] versus 6 cc [0, 13], P<0.0001) and relative edema volumes (0.16 [0.10, 0.33] versus 0.55 [0.40, 0.83], P<0.0001). Compared with SICHs, TICHs were 3 times larger in volume (median [25th, 75th percentiles] volume 69 cc [30, 106] versus 21 cc [8, 45], P<0.0001), 4 times more frequently lobar in location (62% versus 15%, P<0.001), 80 times more frequently contained blood-fluid level(s) (86% versus 1%, P<0.001), and were more frequently multifocal (22% versus 0%, P<0.001).
Conclusions—The striking qualitative and quantitative lack of perihematomal edema observed in the thrombolysis-related ICHs compared with the SICHs provides the first substantial, although indirect, human evidence that intrahematomal blood clotting is a plausible pathogenetic factor in hyperacute perihematomal edema formation.
Key Words: brain edema • cerebral hemorrhage • hematoma • thrombolysis
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