Bilateral Cervical Internal Carotid Artery Pseudoaneurysms

AFFILIATION:
Radiology Department, Department of Radiology, MetroHealth Medical Center, Case Western Reserve University, Cleveland, OH

CITATION:
Bilaterial cervical internal carotid artery pseudoaneurysms. Consultant. 2023;63(4):e2. doi:10.25270/con.2022.06.00011

Received December 29, 2021. Accepted March 2, 2022. Published online July 14, 2022.

DISCLOSURES:
The authors report no relevant financial relationships.

DISCLAIMER:
The authors report that informed patient consent was obtained for publication of the images used herein.

CORRESPONDENCE:
Lucas M. Walden, MD, MetroHealth Medical Center/Case Western Reserve University, 2500 MetroHealth Dr, Cleveland, OH 44109 (jprescott@metrohealth.org)

ABSTRACT:

A 67-year-old man who developed new onset neurological symptoms was found to have bilateral internal carotid artery (ICA) pseudoaneurysms on computed tomography angiography. Pseudoaneurysms of the ICA are a rare diagnosis and can lead to significant morbidity and mortality including infarcts and, in some cases, hemorrhagic transformation of infarcts. The primary risk factors for the formation of ICA pseudoaneurysms are trauma and surgery. Other causes include infiltrating metastatic disease, infection, fibromuscular dysplasia, Ehlers-Danlos syndrome, Marfan syndrome, irradiation, and Behçet disease. Endovascular repair with stenting is a highly effective treatment option and preferred in patients with large symptomatic pseudoaneurysms. Depending on the etiology, open repair may be necessary. Individuals with smaller asymptomatic lesions are managed non-operatively with antithrombotic therapy and are followed with serial imaging for significant changes in aneurysm size, which would necessitate procedural intervention.

Key words: internal carotid artery pseudoaneurysm, pseudoaneurysm, endovascular repair

Introduction

Internal carotid artery (ICA) pseudoaneurysms are a rare entity that have the potential for life-threatening complications. In most institutions, the two most encountered etiologies are trauma and surgery. It is important to understand the variety of clinical and imaging parameters that are used to guide therapy. Ultimately, endovascular stenting is the preferred procedural management for large pseudoaneurysms and is performed with high procedural success rates (> 90%).

Case Presentation

A 67-year-old man presented to the emergency department with new-onset left hand weakness that began 2 hours prior.

History. While driving, the patient developed sudden-onset weakness and numbness in his left hand that led him to lose control of his car and collide with a pole at 15 to 20 mph. The patient did not sustain trauma related to the accident. In the emergency department, he stated that the weakness in his left hand had improved but the numbness persisted. He reported that he was now also experiencing dizziness. His medical history was significant for hypertension, hypercholesterolemia, and Raynaud’s syndrome; he also had bilateral retinal detachment that was repaired 1 year ago, and he underwent phacoemulsification 3 years ago for treatment of bilateral cataracts. His current medications are atorvastatin 20mg daily, amlodipine 10mg daily, hydrochlorothiazide 25mg daily.

Physical examination. The patient was alert and oriented. His blood pressure was 138/88 mm Hg, and his other vital signs were stable. Neurologic examination showed paresthesia involving the entire left hand extending to the wrist. There were no other focal neurological deficits or external signs of trauma.

Diagnostic studies. Cranial computed tomography (CT) demonstrated small chronic infarcts within the right frontal lobe (Figure 1) and right temporo-occipital lobes (Figure 2). There was no evidence of intracranial hemorrhage or obvious large vascular territory acute infarct. Computed tomography angiography (CTA) of the head and neck revealed bilateral tortuous cervical internal carotid arteries (ICAs) with large pseudoaneurysms containing eccentric mural thrombus/atherosclerotic plaque (Figures 3-6).

Figure 1. Non–contrast-enhanced CT of the head showing a small, hypodense lesion in the right frontal lobe suggestive of a chronic infarct. CT, computed tomography.

 
Figure 2. Non–contrast-enhanced CT of the head demonstrating right temporo-occipital lobe encephalomalacia suggestive of a chronic infarct. CT, computed tomography.

 
Figure 3. Axial CTA of the neck demonstrating bilateral ICA pseudoaneurysms that contain eccentric mural thrombus/atherosclerotic plaque. CTA, computed tomography angiography; ICA, internal carotid artery.

 
Figure 4. Coronal maximum intensity projection CTA of the neck demonstrating extensive bilateral ICA vessel tortuosity and mural thrombus/atherosclerotic plaque containing pseudoaneurysms. CTA, computed tomography angiography; ICA, internal carotid artery.

 
Figure 5. Sagittal CTA of the neck showing left ICA pseudoaneurysm (A) with dense atherosclerotic plaque and right ICA pseudoaneurysm (B) associated with large mural thrombus. CTA, computed tomography angiography; ICA, internal carotid artery.

 
Figure 6. Three-dimensional images reconstructed using Vitrea (Canon Medical Informatics; Minnetonka, MN) and demonstrating significant ICA vessel tortuosity and mucosal irregularities associated with mural thrombus/atherosclerotic plaque containing ICA pseudoaneurysms. Image A demonstrates the left ICA anatomy Image B right demonstrates the right ICA anatomy. ICA, internal carotid artery.

Same-day magnetic resonance imaging (MRI) of the brain confirmed the presence of chronic infarcts within the right frontal and temporo-occipital lobes (Figure 7). This study also revealed several tiny foci of diffusion restriction within the right cerebral hemisphere, likely related to showering emboli (Figure 8).

Treatment and management. The patient was therapeutically anticoagulated (heparin infusion) with plans to transition to dual antiplatelet therapy after 24 hours.

    
Figure 7. Axial T2-weighted images confirming chronic infarcts in the right frontal (A) and temporo-occipital (B) lobes.

   
Figure 8. Diffusion-weighted imaging showing several tiny foci of diffusion restriction within the right frontal (A), parietal (B), and occipital (C) lobes likely related to showering emboli.

Neurointerventional radiology was consulted for possible intra-arterial intervention. The patient was deemed to not be a suitable candidate, however, because deploying a stent across a pseudoaneurysm that demonstrated extensive vessel tortuosity and thrombi would not only be technically challenging but would also carry an unacceptably high risk of iatrogenic stroke. A vascular surgeon was subsequently consulted for possible open pseudoaneurysm repair, but this option was tabled after the patient’s conditioned worsened and he became nonverbal, responding only to pain on physical examination. The patient was transferred to the neurocritical care unit. Cranial CT demonstrated loss of gray-white matter interface involving most of the right cerebral hemisphere (Figure 9). CTA showed occlusion of the right middle cerebral artery (MCA) at the bifurcation and occlusion of the right posterior cerebral artery (PCA) at the temporal occipital and calcarine bifurcation (Figure 10).

 
Figure 9. Axial non–contrast-enhanced CT of the head demonstrating loss of gray-white matter interface and effacement of sulcal spaces involving the right MCA and PCA territories due to acute infarct. A chronic infarct in the right temporo-occipital lobe is again seen. CT, computed tomography; MCA, middle cerebral artery; PCA, posterior cerebral artery.

Figure 10. CTA showing abrupt cutoff of the right MCA at the bifurcation, representing an acute MCA occlusion. CTA, computed tomography angiography; MCA, middle cerebral artery.

The patient was transitioned from a heparin infusion to dual antiplatelet therapy and was given hypertonic saline to decrease intracranial pressure. Shortly thereafter, pupil reactivity was found to be newly decreased. Cranial CT at this time demonstrated hemorrhagic conversion of the MCA territory infarct and new midline shift (Figure 11).

Patient outcome. Neurosurgery was consulted for decompressive craniectomy; however, surgical intervention was not advised because the patient demonstrated clinical signs of devastating brain injury, had received high doses of antithrombotic therapy, and had large unstable thrombi in bilateral ICAs. For these reasons, the health care team felt that surgical management may place the patient at risk for severe hemorrhage and would be unlikely to prevent significant long-term disability. The therapeutic options were discussed with the patient’s family, who declined further intervention. Comfort care only orders were issued for the patient, who died the following day.