Abstract
Background and purpose
The pathophysiology and clinical significance of perihematomal edema (PHE), a cause of secondary neuronal injury after intracerebral hemorrhage (ICH), is poorly understood. A leading theory proposes that early PHE results from activation of the clotting cascade. We sought to test this theory by examining the relationship between early PHE and warfarin use in ICH patients.
Methods
ICH and PHE volumes were measured in consecutive patients with warfarin-related ICH and compared to those of controls with non-coagulopathic ICH. Subjects were identified from a prospective database of ICH patients. Clinical and radiological predictors of PHE volume and relative PHE (PHE volume/ICH volume) were identified. The relationship between PHE volume and 90-day mortality was determined.
Results
For the 49 consecutive warfarin-related ICH patients and 49 matched controls: median INRs (interquartile ranges) were 3.2 (2.3, 4.1) and 1.1 (1.08, 1.2); median hematoma volumes were 37.8 cm3 (6.7, 102.9) and 18.1 cm3 (9, 51) (P = 0.18); median PHE volumes were 12 cm3 (3.7, 36.7), and 11 cm3 (4.1, 24) (P = 0.87); and median relative PHE was 0.38 (0.28, 0.52) and 2 (1.37, 3.06), respectively. In multivariable analysis, ICH volume and warfarin use independently predicted PHE volume. There was an association between higher PHE volume and decreased 90-day mortality.
Conclusions
Warfarin-related ICH is associated with less early relative edema than non-coagulopathic ICH. This is consistent with the theory that coagulation contributes to early edema. Early edema may be associated with improved functional outcome.
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Acknowledgments
The authors would like to thank David N. Levine, MD for his critical review of this manuscript and Chana Engel, BA for her help in organizing this study. This work was funded by grants from The National Institute of Neurological Disorders and Stroke (K23 NS42695-01 and R01 NS042147-02).
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Levine, J.M., Snider, R., Finkelstein, D. et al. Early edema in warfarin-related intracerebral hemorrhage. Neurocrit Care 7, 58–63 (2007). https://doi.org/10.1007/s12028-007-0039-3
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DOI: https://doi.org/10.1007/s12028-007-0039-3