4.5 Article

Process of cerebral edema in the infarct core after reperfusion: A case report

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MEDICINE
卷 101, 期 26, 页码 -

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MD.0000000000029810

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cerebral edema; cerebral infarction; hypoattenuation; reperfusion

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This study investigates the mechanism of cerebral edema in patients with cerebral infarction after reperfusion, providing a new perspective for understanding the impact of reperfusion on cerebral infarction. After reperfusion occurs in the infarct, the process of cerebral edema accelerates significantly, potentially causing more severe brain damage.
Rationale: It is generally believed that cerebral infarction shows hypoattenuation on computed tomography (CT) scans 12 to 24 hours after onset. Cerebral edema affects the occurrence of hypoattenuation, originating from the inner edge of the infarct and extending to the core. When reperfusion occurs in the infarct, the process of cerebral edema changes significantly, affecting the imaging of cerebral infarction on CT scans. This article focused on the mechanism of cerebral edema to provide a new perspective for understanding the impact of reperfusion on cerebral infarction. Patient concerns: We describe the case of a 77-year-old man who presented with an acute onset of right limb weakness with speech difficulties 10 hours before the visit. He had been diagnosed with atrial fibrillation 4 months ago. During the acute phase of infarction, the central area of the hypoattenuated infarct appears as isodensity on CT scans in this case. Diagnoses: The patient was diagnosed with acute cerebral infarction, cardiogenic cerebral embolism, and spontaneous recanalization of left middle cerebral artery occlusion. Interventions: Metoprolol was given to control the ventricular rate. The patient received blood pressure control, symptomatic management, and rehabilitation treatments. Outcomes: Finally, the patient became alert. Lessons: Cerebral edema originating directly in the infarct core after reperfusion could lead to a significantly accelerated edema process and imaging evolution, causing more severe cerebral damage. In such a case, the patient should not receive antiplatelet and anticoagulant therapy in order to prevent bleeding conversion.

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