Emergent carotid artery stenting for cervical internal carotid artery injury during carotid endarterectomy: A case report

Background: Carotid endarterectomy (CEA) has been the standard preventive procedure for cerebral infarction due to cervical internal carotid artery stenosis, and internal shunt insertion during CEA is widely accepted. However, troubleshooting knowledge is essential because potentially life-threatening complications can occur. Herein, we report a case of cervical internal carotid artery injury caused by the insertion of a shunt device during CEA. Case Description: A 78-year-old man with a history of hypertension, diabetes, and hyperuricemia developed temporary left hemiplegia. A former physician had diagnosed the patient with a transient cerebral ischemic attack. The patient’s medical history was significant for the right internal carotid artery stenosis, which was severe due to a vulnerable plaque. We performed CEA to remove the plaque; however, there was active bleeding in the distal carotid artery of the cervical region after we removed the shunt tube. Hemostasis was achieved through compression using a cotton piece. Intraoperative digital subtraction angiography (DSA) revealed severe stenosis at the internal carotid artery distal to the injury site due to hematoma compression. The patient underwent urgent carotid artery stenting and had two carotid artery stents superimposed on the injury site. On DSA, extravascular pooling of contrast media decreased on postoperative day (POD) 1 and then disappeared on POD 14. The patient was discharged home without sequela on POD 21. Conclusion: In the case of cervical internal carotid artery injury during CEA, hemostasis can be achieved by superimposing a carotid artery stent on the injury site, which is considered an acceptable troubleshooting technique.

Internal Carotid Artery Injury in Transsphenoidal Surgery: Tenets for Its Avoidance and Refit—A Clinical Study

One of the most serious/potentially fatal complications of transsphenoidal surgery (TSS) is internal carotid artery (ICA) injury. Of 6230 patients who underwent TSS, ICA injury occurred in 8 (0.12%). The etiology, possible treatment options, and avoidance of ICA injury were analyzed. ICA injury occurred at two different stages: (1) during the exposure of the sella floor and dural incision over the sella and cavernous sinus and (2) during the resection of the cavernous sinus extension of the tumor. The angiographic collateral blood supply was categorized as good, sufficient, and nonsufficient to help with the decision making for repairing the injury. ICA occlusion with a balloon was performed at the injury site in two cases, microcoils in two patients, microcoils plus a single barrel extra-intracranial high-flow bypass in one case, stent grafting in one case, and no intervention in two cases. The risk of ICA injury diminishes with better preoperative preparation, intraoperative navigation, and ultrasound dopplerography. Reconstructive surgery for closing the defect and restoring the blood flow to the artery should be assessed depending on the site of the injury and the anatomical features of the ICA.

Use of Adenosine to Facilitate Localization and Repair of Internal Carotid Artery Injury during Skull Base Surgery: A Case Report and Literature Review

Background: Internal carotid artery (ICA) injuries represent a rare, potentially fatal complication of endoscopic endonasal skull base surgery (EESBS). The use of adenosine to induce transient hypotension and facilitate management of high-flow, high-pressure arterial lesions has been well-documented in neuro-endovascular literature. A similar setting in which adenosine-induced hypotension may prove beneficial is during the management of major vascular injury encountered during EESBS. Methods: A case of ICA injury and subsequent repair during EESBS is presented. Results: A 74-year-old female underwent endoscopic transsphenoidal resection for a recurrent pituitary adenoma. During suprasellar resection, the right cavernous ICA was inadvertently injured resulting in brisk bleeding. Immediate vascular tamponade was applied, and a crushed muscle graft was obtained. Two intravenous doses of adenosine were administered in quick succession to produce transient hypotension and facilitate repair of the injury with the graft. Neurovascular imaging revealed a small pseudoaneurysm which remained stable throughout the postoperative course. The patient underwent definitive stent embolization of the pseudoaneurysm 1 month following discharge. Conclusion: Prompt repair of ICA injury during EESBS is crucial, but often limited by poor visualization. Adenosine-induced hypotension has demonstrated great efficacy as an adjuvant in neurovascular clipping of intracranial aneurysms and remains a valuable tool for the endoscopic skull-base surgeon as well. In cases with high risk for ICA injury, adenosine should be readily available.