Transfusion-Induced Vasospasm After Coil Embolization of Unruptured Aneurysms

Introduction Cerebral vasospasm is a well‐recognized complication of aneurysmal subarachnoid hemorrhage and has been described with blood transfusion 1‐3 . In contrast, vasospasm after embolization of unruptured aneurysms, to our knowledge. has not been reported 4,5 . Materials/Methods Case report and literature review. Results A 49‐year‐old African American woman with a history of hypertension, iron‐deficiency anemia, and smoking presented with a week of headaches and binocular diplopia. Examination revealed an incomplete right oculomotor nerve palsy with pupillary involvement. Computed tomographic angiography (CTA) demonstrated a 5×5‐mm unruptured saccular aneurysm of the right posterior communicating artery. She underwent urgent coil embolization without procedural complications. On the first postoperative day, her headache had resolved, and her neurologic examination was unchanged. Transcranial Doppler ultrasonography (TCD) at 8 AM showed no evidence of vasospasm. Laboratory studies revealed a hemoglobin level of 6.5 g/dL, and she received one unit of packed red blood cells. Approximately one hour into transfusion, at 10 AM, she developed right gaze deviation and left hemiplegia. Non‐contrast CT excluded intracranial hemorrhage. CTA revealed severe vasospasm of the right middle cerebral artery (MCA), and CT perfusion showed a mismatch in the corresponding territory, consistent with ischemia. She was treated with intravenous fluids and underwent digital subtraction angiography (DSA), which confirmed delayed MCA filling. Intra‐arterial verapamil (27 mg) and nitroglycerin (40 μg) produced modest angiographic improvement. She was able to lift her arm antigravity immediately post procedure. Figure 1 depicts CTA and DSA before (panels A and C) and after (panels B and D) neurologic deficit during blood transfusion. Vasospasm is clearly evidenced. Lumbar puncture performed the following day revealed no xanthochromia. Her left hemiparesis resolved within 48 hours and her right oculomotor nerve palsy improved. Serial TCD studies showed no further vasospasm, and hemoglobin levels remained stable. She was discharged home after seven days. Conclusion This case illustrates transfusion‐associated vasospasm after coil embolization of an unruptured intracranial aneurysm. Although delayed cerebral ischemia due to vasospasm is a well‐known sequela of subarachnoid hemorrhage, its occurrence in unruptured aneurysms has not been reported. Transfusion has been implicated in vasospasm pathophysiology, possibly through reduced bioavailability of nitric oxide within stored erythrocytes 1 . Recognition of this association is important, as prompt diagnosis and treatment may mitigate ischemic injury. We conclude that transfusion‐induced vasospasm should be considered in the differential diagnosis of acute neurologic decline after coil embolization of unruptured aneurysms.