Cerebral Hemorrhage Following Thrombolysis in Stroke

Hemorrhagic transformation (HT) of ischemic brain tissue occurs in treated and non-treated stroke patients with excess after thrombolytic therapy. It has different radiological appearances, and may be detected on CT when the patient deteriorates clinically. HT is thus the main safety concern after thrombolytic therapy. The exact assessment of this risk requires a clear definition of HT in general and especially the definition of hemorrhages that may cause clinical deterioration. This concept should include a description of the assessment of HT, a hypothesis of the cause of HT, and considerations regarding the effects of blood on cerebral function under the conditions of ischemic edema. Observations on the radiological appearances of HT support the view that only dense hemorrhages (hematomas) causing mass effect are clinically relevant. In patients with extended ischemic infarcts causing compression of surrounding brain tissue and sometimes shift of midline structures, the effect of blood within the ischemic tissue is hard to assess. Because HT has a higher incidence in large ischemic lesions, the combination is often observed. It has been shown that HT is associated with tissue reperfusion. Tissue reperfusion is, however, the precondition to keep cerebral infarcts small. If HT is a marker for arterial recanalization and reperfusion of ischemic brain tissue, it may be associated with clinical improvement. The association of HT with reperfusion may explain the observation that treatment with thrombolytics is beneficial despite the excess of HT. The term symptomatic hemorrhage is, therefore, at least questionable and misleading, if not very carefully defined