Abstract
Symptomatic hemorrhagic transformation (HT) is one of the complications most likely to lead to death in patients with acute ischemic stroke. HT after acute ischemic stroke is diagnosed when certain areas of cerebral infarction appear as cerebral hemorrhage on radiological images. Its mechanisms are usually explained by disruption of the blood-brain barrier and reperfusion injury that causes leakage of peripheral blood cells. In ischemic infarction, HT may be a natural progression of acute ischemic stroke and can be facilitated or enhanced by reperfusion therapy. Therefore, to balance risks and benefits, HT occurrence in acute stroke settings is an important factor to be considered by physicians to determine whether recanalization therapy should be performed. This review aims to illustrate the pathophysiological mechanisms of HT, outline most HT-related factors after reperfusion therapy, and describe prevention strategies for the occurrence and enlargement of HT, such as blood pressure control. Finally, we propose a promising therapeutic approach based on biological research studies that would help clinicians treat such catastrophic complications.
Highlights
Hemorrhagic transformation refers to hemorrhagic infarction that occurs after venous thrombosis or arterial thrombosis and embolism [1, 2]
The frequency of hemorrhagic transformation (HT) is associated with different factors, such as epidemiological factors, characteristics of the infarct, reperfusion techniques in the acute phase, radiological diagnosis (CT or magnetic resonance imaging (MRI) techniques), and use of antithrombotics after the acute phase [20,21,22]
This point can be influenced by the accuracy of imaging modalities used, such as computed tomography (CT) or MRI with or without gradient-echo or susceptibility-weighted sequences [65], which are more sensitive to the detection of blood products [64]
Summary
Hemorrhagic transformation refers to hemorrhagic infarction that occurs after venous thrombosis or arterial thrombosis and embolism [1, 2]. Autopsy studies have reported an HT rate of 18–42% in acute ischemic stroke due to arterial occlusion [1, 3]. Prior to considering the frequency of occurrence of HT, we need to understand the imaging and clinical definitions of HT. Rates of HT in ischemic stroke have been reported, more than half of all cerebral infarctions demonstrate certain stages of HT [5]. On CT scans, the severity of HT is divided into two stages: hemorrhagic infarction (HI) and parenchymal hemorrhage (PH) with or without mass effect. With recent advances in intravenous [9] or endovascular [10] reperfusion therapies for acute ischemic stroke [11], stroke physicians need to deepen their understanding of cerebral hemorrhagic complications. The overall risks of complications have been well-documented in various
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