Spontaneous recanalization after acute common carotid artery occlusion: a case report.

Abstract

Introduction and importance: Albeit rare, spontaneous recanalization after common carotid artery (CCA) occlusion is an important medical phenomenon, as it can lead to increased blood flow to the brain tissue, thereby improving cerebral perfusion. However, it also increases the risk of reperfusion injury and distal cerebral embolism.

Case presentation: The patient was a 54-year-old man who presented with sudden right-sided limb weakness and speech impairment. Emergency computed tomography angiography (CTA) showed complete occlusion of the left CCA and internal carotid artery. CTA on day 1 indicated moderate-to-severe stenosis of the left CCA. Extensive low-density areas and hemorrhagic transformations were observed in the territory supplied by the left middle cerebral artery. Follow-up cranial CT on day 15 showed obvious hemorrhagic transformation following infarction. High-resolution magnetic resonance imaging of the carotid arteries on day 25 revealed no significant stenosis. The patient was given medications to improve circulation and antiplatelet aggregation, as well as lipid-lowering therapy. Follow-up cranial CT on day 37 showed significant absorption of the cerebral hemorrhage.

Clinical discussion: This case report presents a rare spontaneous recanalization of acute CCA occlusion without thrombolysis or thrombectomy. Neurological deficits resolved completely following the delayed recanalization, challenging conventional understanding of intervention timelines. The case highlights potential thrombolytic-independent recanalization mechanisms.

Conclusion: These findings raise questions about the optimal management approach in select common carotid artery occlusion cases and emphasize the importance of individualized treatment decisions based on real-time vascular imaging assessment. Early and rapid spontaneous recanalization can lead to a reperfusion injury; close monitoring and follow-up assessments are essential.