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Cerebral Embolism Formation Hemorrhagic Conversion In this example there is a gross parenchymatous hematoma with intraventricular extension, midline

shift, and herniation. Ischemic infarction can be divided into "bland" infarction associated with secondary bleeding -- referred to as hemorrhagic conversion or transformation (HT) -- in ischemically infarcted areas [Mohr JP and Sacco RL, 1992; Teal PA and Pessin MS, 1992; Pessin MS, In: Hacke et al (eds), 1991]. Bland infarction is characterized by bland widespread leukocyte infiltration and macrophage invasion, with only scattered red cells being found. Hemorrhagic conversion may take the form of infarction (HI) or, less commonly, parenchymatous infarction (PH). The occurrence of hemorrhagic conversion is "predominantly a natural tissue consequence of embolism" [Teal PA and Pessin MS, 1992]. An autopsy, HI may vary from patchy petechial bleeding to more confluent hemorrhages, representing multifocal extravasation of blood from capillaries or venules [Teal PA and Pessin MS, 1992]. HI and PH have different incidences, pathogenesis, and clinical outcome, but distinguishing HI and PH on CT may be difficult [Teal PA and Pessin MS, 1992]. Although HI and PH have often been grouped together, there are certain features

on CT that help characterize these two types of hemorrhagic transformation. On CT, HI appears as a discontinuous heterogeneous mixture of high and low densities occurring within the vascular territory of the infarct. In contrast, PH appears as a discrete, homogeneous collection of blood that often exerts mass effect and may extend beyond the original infarct boundaries or even into the ventricles. HI occurs regularly in the natural evolution of acute embolic stroke [Pessin MS, In: Hacke et al (eds), 1991]. In autopsy studies, the occurrence of HI has ranged from 51% to 71% of recent embolic strokes [Teal PA and Pessin MS, 1992]. However, CT studies have shown a lower incidence, with studies of con-coagulated patients who have predominantly embolic infarcts indicating an overall incidence of 26% to 43%. According to another estimate, approximately 20% of patients with cardioembolic stroke have hemorrhagic transformation in the infarcted zone, usually occurring within 48 hours [Leonard AD, Newburg S. J Neurosci Nurs. 1992;24:69]. Transformation of a bland embolic infarct to HT is rare in the first 6 hours. Most HIs are asymptomatic, and it is not uncommon to detect HI on CT patients who are stable or improving. The pathogenesis of HT appears to relate to reperfusion of bleeding from recanalized but ischemically injured vessels by the natural, dynamic dissolution of thrombi [Teal PA and Pessin MS, 1992] -- i.e., an embolus that represents all or part of a thrombus has a spontaneous tendency to lyse and disperse. Reperfusion into the ischemically injured vessels can therefore result in varying degrees of blood extravasation through the damaged blood-brain barrier. As noted by Mohr and Sacco (1992), HI has been often explained as a result of reperfusion of the vascular bed of the infarct, such as would occur after fragmentation and distal migration of an embolus or after early reopening of a large vessel occlusion in the setting of a large infarction; the full pressure of arterial blood into hypoxic capillaries results in a diapedesis or red cells through their hypoxic walls. The concept of restored lumen patency is consistent with greater frequency of hemorrhagic infarction in patients with cardioembolic infarcts. The occurrence of PH in areas of ischemic infarction is less common that that of HI [Teal PA and Pessin MS, 1992]. PH appears to be associated with anticoagulation therapy, with a low incidence of spontaneous PH in areas of ischemic infarction (on the

order of 2% to 9%) in patients no receiving anticoagulation therapy. In contrast to HI, clinical deterioration is often associated with PH. It has been proposed that the pathogenesis of PH may involve "ischemic necrosis resulting in the rupture of small penetrating vessels analogous to hypertensive hemorrhage, leading to massive bleeding rather that the multifocal diapedesis of blood through capillary walls, as seen in HI" [Teal PA and Pessin MS, 1992]. The observation that some hemorrhagic infarctions develop distal to the site of a persisting occlusion suggests that reperfusion is not always a necessary condition. Investigators from Japan examined the brains of 14 patients who died from herniation of the brain after cardioembolic stroke with persistent occlusion of the internal carotidmiddle arterial axis [Ogata J, et al. Stroke. 1989;20:876-83]. The finding of hemorrhagic infarct in 7 of the patients contradicts the concept that reopening a previously occluded vessel is the only pathophysiologic mechanism for the development of hemorrhagic infarct. Analysis of blood pressure after stroke has revealed on or more surges of arterial hypertension or rapid rise of blood pressure in patients with hemorrhagic stroke without a reopening of the occluded artery; it has been speculated that these blood pressure rises might explain hemorrhagic infarction in many cases. A relationship between hyperglycemia and hemorrhagic transformation has also been suggested by he observation that occluding the middle cerebral artery of markedly hyperglycemia cats was associated with 5-fold more frequent and 25-fold more extensive hemorrhage into infarcts than in normoglycemic animals [de Courten-Myers GM, et al. 1992]. Compared with permanent occlusion, temporary restoration of blood flow after 4 hours caused the most extensive hemorrhage into infarcts. It was concluded that hyperglycemia and restoration of blood flow to ischemic territories were strong risk factors for hemorrhagic infarct conversion. The evidence suggests that the marked tissue energy depletion accompanied by acidosis damages brain vessels, causing leakage of edema fluid and red blood cells [de Courten-Myers GM, et al, 1992]. Diffuse HI associated with marked hyperglycemia has been reported in two patients [Broderick JP, et al, 1995]. In summary, HI occurs regularly in the natural evolution of acute embolic stroke and is usually asymptomatic [Pessin MS, In: Hacke et al (eds), 1991]. PHs occur less frequently, but are often symptomatic due to extension and mass effect beyond the original infarct territory. Interest in these issues has been further generated by trials of thrombolytic therapy for acute ischemic stroke.




From: Acute Ischemic Stroke: New Concepts of Care

1998-1999 Genentech Inc. All rights reserved. Click here for information about this CD. onversion.htm

April 27, 2010

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In addition to thrombotic occlusion at the site of cerebral artery atherosclerosis, ischemic infarction can be produced by emboli arising from proximally situated atheromatus lesions to vessels located more distal in the arterial tree [Mohr JP, Sacco RL. In: Barnett HJM, et al (eds). Stroke. Pathophysiology, Diagnosis, and Management. New York: Churchill Livingstone, 1992:271].

A small clot may break off from a larger thrombus and be carried to other places in the bloodstream. When the embolus reaches an artery too narrow to pass through and becomes lodged, blood flow distal to the fragment ceases, resulting in infarction of distal brain tissue due to lack of nutrients and oxygen. As a cause of stroke, embolism accounts for approximately 32% of cases.




From: Acute Ischemic Stroke: New Concepts of Care 1998-1999 Genentech Inc. All rights reserved. Click here for information about this CD.