Decreased perihematomal edema in thrombolysis-related intracerebral hemorrhage compared with spontaneous intracerebral hemorrhage.

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.

[1]  M. Cowan,et al.  American Heart Association. , 2018, P & T : a peer-reviewed journal for formulary management.

[2]  Frans Van de Werf,et al.  An international randomized trial comparing four thrombolytic strategies for acute myocardial infarction. , 1993, The New England journal of medicine.

[3]  T Brott,et al.  Intracerebral hemorrhage more than twice as common as subarachnoid hemorrhage. , 1993, Journal of neurosurgery.

[4]  J. Grotta,et al.  Early presentation of hemispheric intracerebral hemorrhage , 1994, Neurology.

[5]  A P Dhawan,et al.  3-D image analysis of intra-cerebral brain hemorrhage from digitized CT films. , 1995, Computer methods and programs in biomedicine.

[6]  L Pilote,et al.  Regional variation across the United States in the management of acute myocardial infarction. GUSTO-1 Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. , 1995, The New England journal of medicine.

[7]  J T Hoff,et al.  Intracerebral infusion of thrombin as a cause of brain edema. , 1995, Journal of neurosurgery.

[8]  R. Myers,et al.  Lobar intracerebral hemorrhage model in pigs: rapid edema development in perihematomal white matter. , 1996, Stroke.

[9]  R. Keep,et al.  Edema from intracerebral hemorrhage: the role of thrombin. , 1996, Journal of neurosurgery.

[10]  N. Kawai,et al.  Mechanisms of edema formation after intracerebral hemorrhage: effects of thrombin on cerebral blood flow, blood-brain barrier permeability, and cell survival in a rat model. , 1996, Journal of neurosurgery.

[11]  J. Broderick,et al.  Early hemorrhage growth in patients with intracerebral hemorrhage. , 1997, Stroke.

[12]  N. Kawai,et al.  Mechanisms of edema formation after intracerebral hemorrhage: effects of thrombin on cerebral blood flow, blood-brain barrier permeability, and cell survival in a rat model. , 1996, Journal of neurosurgery.

[13]  I. Drury,et al.  Seizures induced by intracerebral injection of thrombin: a model of intracerebral hemorrhage. , 1997, Journal of neurosurgery.

[14]  J. Broderick,et al.  Role of blood clot formation on early edema development after experimental intracerebral hemorrhage. , 1998, Stroke.

[15]  R. Califf,et al.  Thrombolysis-related intracranial hemorrhage: a radiographic analysis of 244 cases from the GUSTO-1 trial with clinical correlation. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. , 1998, Stroke.

[16]  J. Broderick,et al.  Ultra-early clot aspiration after lysis with tissue plasminogen activator in a porcine model of intracerebral hemorrhage: edema reduction and blood-brain barrier protection. , 1999, Journal of neurosurgery.