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Published on: September 22, 2012
Hematoma Coagulation is Associated with Perihematoma Edema Volume in Patients with Acute Intracerebral Hemorrhage
Gabriel Galan Castro1, Seth B Boren1, Faruk Md Hossain2
1Institute for Stroke and Cerebrovascular Diseases and Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
Background:
In acute intracerebral hemorrhage (ICH), hematoma mass and perihematomal edema (PHE) contribute to elevated intracranial pressure (ICP). The release of red blood cell lysis products accelerates PHE formation. Animal studies show that the accumulation of blood-clotting factors contributes to PHE growth. Controlling hematoma expansion (HE) remains a medical priority. Promoting hematoma coagulation reduces HE; however, coagulation may increase PHE. Using quantitative magnetic resonance imaging (MRI) for imaging coagulation status, we studied the interaction between coagulation and PHE.
Methods:
Twenty patients with hypertensive ICH who completed three consecutive MRIs at three time points (T1, T2, T3) within the first 72 h after onset were included in this study. Images were obtained on a 3 T MRI system with three-dimensional (3D) FLAIR, T1w, and multi-gradient echo (mGRE) sequences. FLAIR and mGRE images quantified the hematoma volume (HV) and PHE volume, while clotted blood volume (CBVol) was measured via Quantitative Susceptibility Maps (QSM). Within the hematoma, voxels with susceptibility greater than 0.5 ppm were considered clotted blood. CBVol was analyzed in relation to hematoma and PHE volumes. Group-wise comparisons across serial time points were performed using Wilcoxon signed-rank tests.
Results:
Among 12 M/8F patients, the mean age was 63.4 ± 11.5 years. Between the first (T1) and last imaging (T3), the PHE volume (22.6 ± 14.2 to 31.5 ± 20.2 mL; p = 0.005), and CBVol (3.21 ± 3.3 to 5.58 ± 4.8 mL; p = 0.0007) significantly increased. The CBVol demonstrated a significant positive correlation with PHE volume at T2 (r = 0.543, p < 0.05) and T3 (r = 0.80, p < 0.001). After adjusting for HV, the association remained independently significant at T3 [(partial r = 0.554, p = 0.021)]. Similarly, HV showed a strongly significant association with PHE volume at all time points (p < 0.001), and after adjusting for CBVol, the association remained significant across all time points [(partial r = 0.578-0.692, all p < 0.02)].
Conclusions:
Both hematoma clotting and hematoma size influence PHE volume. The findings of this study have implications for clinical management when treating patients with procoagulant therapies.
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