ABSTRACT
Hemorrhagic transformation (HT) of brain infarction is a common complication of acute ischemic stroke. HT has been historically described as red softening into a bland (pale, anemic) infarction, occurring as a natural consequence of ischemic brain injury. Autopsy studies have reported that the incidence of HT is variable up to 71% (Fisher and Adams, 1951; Jorgensen and Torvik, 1969; Lodder et al., 1986). Fisher and Adams’ pivotal paper rst established the propensity for infarcts of embolic origin to undergo HT (Fisher and Adams, 1951). Several subsequent studies have con-rmed that cardioembolism is the cause of stroke most commonly associated with HT, up to 15% of HT cases (Hakim et al., 1983). After embolic arterial occlusion, the nal process underlying HT is spontaneous (or drug induced) vessel reopening with reperfusion of the ischemic tissue (Álvarez-Sabín et al., 2013). Recanalization
9.1 Introduction .................................................................................................. 165 9.2 Classication of HT after t-PA Thrombolysis .............................................. 171 9.3 Predictors of HT ........................................................................................... 171
9.3.1 Clinical Predictors of HT ................................................................. 171 9.3.2 Neuroimaging Predictors of HT ....................................................... 176 9.3.3 HT Risk Scores ................................................................................. 178
9.4 Conclusive Remarks and Future Directions ................................................. 180 Abbreviations ......................................................................................................... 181 Acknowledgments .................................................................................................. 182 References .............................................................................................................. 182
consequent to embolus fragmentation with distal clot migration exposes the ischemic area to reperfusion and bleeding. Another mechanism of reperfusion is that occurring independent of recanalization, that is, through leptomeningeal collaterals while artery occlusion persists (Fisher and Adams, 1951; Álvarez-Sabín et al., 2013). The loss of both microvascular integrity and neurovascular homeostasis can lead to extravasation of blood elements in the brain parenchyma. Intravenous thrombolysis with recombinant tissue plasminogen activator (t-PA) proved effective in salvaging ischemic brain tissue and improving stroke outcomes (The NINDS t-PA Study Group, 1995). However, there are a number of detrimental side effects related to the use of this drug among which HT is the most feared one.
