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Abstract
Objectives: Toxic components released from the intracerebral blood clot, such as thrombin and hemoglobin, potentially trigger brain edema formation and therefore favor an early evacuation of the clot. Despite a significant reduction in hematoma size in our porcine model of hematoma induction by injecting autologous blood ICP-controlled into the right frontal white matter with subsequent fibrinolysis using recombinant tissue-plasminogen activator (rt-PA) and aspiration of the liquefied clot (n=9), local rt-PA promoted delayed perihematomatous edema formation and invoked a substantial inflammatory reaction compared with controls (n=11).
Methods: We therefore modified our formerly developed porcine model of intracerebral hemorrhage in removing the hematoma by open craniotomy and suction of the clot in seven animals. The residual hematoma size and extent of perifocal edema were evaluated over 10 days on planimetry of the MRI data, and correlated to the histopathological changes of edema and inflammation found at autopsy.
Results: The edema volume on day 4 was significantly less in the surgical group compared with the lysis group (p<0.03). On day 10, however, the difference in edema size was not statistically significant compared with the lysis group (p<0.07) and the control group (p<0.09). The inflammatory response was minor compared with the lysis and control group.
Discussion: In conclusion, despite a significant reduction in hematoma size by surgical removal of the clot, only the inflammatory response, but not the extent of delayed edema can be positively influenced.