الفهرس 
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Abstract
Introduction: Stroke is the second most common cause of death worldwide, ranking after heart disease and before cancer. Apart from being the most important cause of severe acquired disability, it is the second commonest cause of dementia and a major cause of depression. About 80% of strokes are ischemic events, due to the occlusion of the lenticulostriate branch of the MCA by a thrombus (or embolus), and 20% are hemorrhagic, due to rupture of an artery. Spontaneous HT of infarction is a frequent ‘‘natural’’ evolution, particularly in acute embolic stroke. HT frequently occurs as a result of the use of thrombolytic therapy in the acute phase of stroke limiting the therapeutic window for reperfusion to 3 h after stroke onset. SICH was defined as a CT- or MRI-documented hemorrhage within 36 hours of treatment, which was temporally related to deterioration in the patient’s clinical condition defined as an increase in the NIHSS score of 4 points or more or led to death. Clinical deterioration could result from causes other than HT such as, ischemic cerebral oedema and mass effect and a large bleeding into the ‘‘silent’’ areas of the brain may be asymptomatic. Bleeding within the infarcted area is a spontaneous event, with a peak occurrence during the first week after stroke. However, its frequency seems to be higher in patients treated with anticoagulant therapy, especially in the context of large-sized ischemic lesions of embolic origin. HT of acute ischemic stroke is an undesirable complication that occurs in 2.2%–44.0% of clinical cases. Postmortem series show petechial hemorrhage associated with cerebral infarction in 50–70% of these patients, and up to 95% of HT are cardioembolic in origin. Treatment with alteplase, inflammation, VEGF, and NOS, free radical production and activation of MMPs may contribute to the development of HT through disruption of BBB
Aim of work: The present study was designed to review the incidence of hemorrhagic transformation of brain infarction and to discuss the factors that may favor the incidence of this transformation and to evaluate the correlation between hemorrhagic transformation and the clinical outcome.
Conclusions: Antithrombotic drugs are not recommended for use in the first 24 h after thrombolytic treatment. Management of patients with HT depends on the amount of bleeding which might require neurosurgical evacuation in deteriorating patients. The decision as to whether or when to restart antithrombotic therapy after HT depends on the risk of subsequent arterial or venous thromboembolism, the risk of recurrent ICH, and the clinical state of the patient