Optic nerve injury-associated blunt cerebrovascular injury
نویسندگان
چکیده
RATIONALE Blunt cerebrovascular injury (BCVI) is a rare complication that may occur after craniocervical trauma. The current literature is limited to extracranial carotid artery injuries; however, no reports have been published on blunt intracranial carotid injury (BICI), especially those associated with optic nerve injury. PATIENT CONCERNS Here we report on 3 BICI cases that demonstrated optic nerve injuries after craniofacial injuries. All 3 patients showed post-trauma vision loss on the injured side. DIAGNOSES Optical canal fractures can be found in these patients, and carotid sulcus was compressed by the fragments. Computed tomography angiography (CTA) and digital subtraction angiography (DSA) were performed in all 3 patients. INTERVENTIONS Case 1 was given no further treatment, except for symptomatic support and rehabilitation therapy. Case 2 was treated with antiplatelet therapy for 3 days, and then a stent was inserted in the injured internal carotid. Case 3 received antiplatelet therapy and a internal carotid compression test was performed simultaneously for 2 weeks, then the injured internal carotid was completely blocked. OUTCOMES Case 1 developed cerebral infarction that resulted in unilateral hemiplegia. Due to timely treatment, the remaining 2 patients had a better prognosis. LESSONS CTA should be performed primarily to exclude vascular injury and for CTA-positive patients, a further DSA should be performed to investigate pathological changes and for a definitive diagnosis. At last, the current therapeutic protocols for BCVI are not entirely applicable to intracranial vascular injury, and appropriate protocols for the treatment of BICI should be selected based on the combination of test results and the actual condition of the patient.
منابع مشابه
Optic nerve injury in fracture of the canal.
A case of unilateral blindness following blunt injury to the skull is presented. The patient died 4 days after the initial injury, presenting the rare opportunity of a detailed histopathological study of the acute features of the condition. The findings are discussed in the context of current theories of the pathogenesis of optic nerve injury in fractures of the optic canal.
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