Focal Neurologic Symptoms and Diminished Flow to an Upper Extremity Arteriovenous Fistula

Following Placement of a Thoracic Aortic Endograft: Successful Treatment with Carotid Subclavian Bypass

Introduction

Most traumatic thoracic aortic disruptions occur in the proximal descending thoracic aorta. A significant number of patients with thoracic aortic pathology are found to have disease adjacent to the origin of the great vessels. Endovascular treatment of these injuries often requires either partial or complete intentional coverage of the origin of the left subclavian artery (LSA) in order to obtain an adequate length of the proximal landing zone. The majority of these patients will not require subsequent revascularization of the LSA. There are, however, specific clinical situations where revascularization of the left subclavian and vertebral arteries may be required either prior to or following placement of the thoracic endograft. Herein, we describe an unusual clinical case in which a dialysis-dependent man was treated with an endograft for a thoracic injury. The patient developed symptoms suggestive of vertebrobasilar insufficiency and diminished flow to a left upper extremity arteriovenous (AV) fistula. Subsequent revascularization of the LSA was required to restore adequate flow and function to the AV fistula. To our knowledge, this complication of LSA occlusion following endograft placement has not been described in literature.

Case Report

A 32-year-old was involved in a motor vehicle accident in which he was the restrained driver of a car that hit a barricade in a frontal collision. The patient was taken to another institution in town where he was found to have sustained a concussion and multiple rib fractures. Computed tomography (CT) revealed a thoracic aortic injury with a pseudoaneurysm along the lesser curvature of the proximal descending aorta. He underwent endovascular repair of the thoracic aortic injury with placement of a Gore Thoracic Aortic Endograft (TAG) 26 x 10 endoprosthesis (W.L. Gore & Associates, Inc, Flagstaff, Arizona). During follow-up imaging studies at the other institution, there was a question of an endoleak, and the patient was subsequently transferred to our institution for further management. The patient’s past medical history is complex and significant for congenital glomerulonephritis. The patient has had renal failure for almost 20 years. He has had a total of 4 failed kidney transplants; the most recent of these was placed in 2005 and failed in 2006.

Following this, the patient returned to hemodialysis via a left forearm AV fistula that had been patent and functional for about 19 years. His other medical history included hyperparathyroidism (status-post parathyroidectomy), atrial fibrillation, hypertension, and anemia of chronic kidney disease. At our institution, a CT angiogram of the arch vessels confirmed a thoracic endograft with an endoleak filling the aortic pseudoaneurysm cavity at the level of the aortic isthmus along the lesser curvature. In addition, there was subtotal (~ 90%) occlusion of the origin of the LSA and a patent, dominant left vertebral artery with a hypoplastic right vertebral artery. At this time, the patient was noted to have diminished flow rates in the left forearm AV fistula on attempted hemodialysis, with decreased finger pressures when compared with the contralateral side. In addition, the dialysis unit reported trouble with cannulation of the fistula and frequent infiltration. A subsequent fistulogram demonstrated a patent, mature, left-forearm radiocephalic AV fistula with a few areas of mild stenosis and a patent central venous system on the ipsilateral side. At the same time, the patient described perioral numbness, blurry vision, tinnitus, and decreased hearing in the left ear. These symptoms were suggestive of vertebrobasilar insufficiency.¹ The patient subsequently underwent a left carotid-to-subclavian artery bypass with a 7 mm Dacron graft and ligation of the LSA proximal to the origin of the large left vertebral artery. The postoperative course was uncomplicated, and the patient was discharged home in good condition. Following revascularization of the LSA, the patient was noted to have resolution of the facial numbness, hearing changes, and blurry vision. In addition, the left forearm AV fistula now had a robust thrill. The dialysis flow rates and AV fistula function returned to pre-injury baseline. A CT angiogram performed 3 days postoperatively showed a patent left carotid-subclavian bypass with normal flow to the left vertebral artery and distal left subclavian and axillary arteries. In addition, the endoleak was noted to have resolved. CT angiography performed at 6-month follow up showed a well-placed endograft with no evidence of endoleak. The patient continues to do well. The AV fistula is functioning well, and he has had no recurrence of his neurologic symptoms.

Discussion

Endovascular management of aortic pathology has revolutionized the treatment of numerous disease processes, including degenerative aortic aneurysmal disease, aortic dissection, and traumatic aortic injury. Each of these disease processes presents unique anatomic challenges. Therefore, evaluation of the feasibility of treatment with a thoracic endograft should be conducted on a case-by-case basis. The mechanism of blunt thoracic aortic injury typically involves a combination of sudden deceleration and traction at the level of the aortic isthmus (where the aorta is relatively immobile) and continued movement of the more distal, relatively mobile aortic arch.^2,3 These patients often have multiple associated injuries, which can complicate the management of these patients and increase their morbidity and mortality.⁴ The majority of thoracic aortic injuries related to this mechanism occur at the level of the aortic isthmus in the proximal descending aorta near the origin of the left subclavian artery. Endovascular repair in these situations often requires intentional, partial, or complete coverage of the LSA in order to obtain an adequate length of proximal landing zone.⁵ Several groups have suggested that coverage of the LSA can be performed with impunity and is well tolerated^.6–9 These groups advocate that revascularization of the left subclavian and vertebral arteries should be reserved for patients who develop symptoms following endograft deployment. Although rare, severe left upper extremity ischemia with claudication and/or rest pain can develop and requires revascularization of the LSA. There are also recent data to suggest that nonrevascularization of the LSA following graft coverage can increase a patient’s risk for developing spinal cord ischemia.¹⁰ There are some circumstances in which subclavian to carotid transposition or carotid-subclavian bypass needs to be performed prior to or immediately following placement of the thoracic endograft. Such a situation may arise, for instance, in patients with a dominant left vertebral artery with a hypoplastic or absent contralateral vertebral artery, such as the case in our patient. Four-vessel cerebral angiography should be considered preoperatively in patients who are candidates for revascularization, as the discovery of concomitant vascular disease or congenital variants in related vessels can alter operative decision making. Impetus for revascularization can be found in other instances as well, such as in a patient with a patent, left-internal mammary coronary bypass, in order to prevent myocardial ischemia. In the hemodynamically unstable patient, however, placement of the endograft should precede revascularization of the subclavian artery irrespective of such circumstances. In the majority of instances, revascularization of the LSA can be reserved for patients that develop symptoms following placement of the endograft. This includes patients that develop symptoms suggestive of significant vertebrobasilar insufficiency, such as blurred vision/diplopia, vertigo, perioral numbness, and drop attacks. Other clinical symptoms of vertebrobasilar insufficiency can include complete numbness and weakness involving structures on both sides of the body, gait ataxia, oculomotor palsies, oropharyngeal dysfunction, and decreased hearing.¹ These symptoms are reflective of ischemia to the cerebellum, corticospinal and corticobulbar tracts, the reticular activating system, and oculomotor areas in the brainstem; all of which are supplied primarily by blood that flows through the vertebral arteries. In some instances, a type II endoleak may occur related to the subclavian artery, with continued filling of the pseudoaneurysm cavity. This possibility is eliminated by transposition of the LSA to the carotid artery. In our patient, the carotid-subclavian bypass was performed because it was deemed more feasible, due to the location of the vertebral artery. The subclavian artery proximal to the vertebral artery was then ligated. On the follow-up CT angiography, the endoleak (presumably a type II) was noted to have resolved.

This report illustrates an unusual circumstance in which our patient developed impaired flow into the left upper extremity AV fistula caused by subtotal occlusion of the LSA. In this dialysis-dependent man with 4 prior failed kidney transplants, a patent, functional hemodialysis access was of critical importance. The carotid-subclavian bypass restored normal flow to the fistula and allowed him to continue with routine hemodialysis treatments.

Conclusion

Endovascular treatment of traumatic thoracic aortic injuries has been shown to be an acceptable modality in the short term, and may be a viable alternative to conventional open repair, which is associated with significant morbidity and mortality. Partial or complete coverage of the LSA is required in a significant number of patients who undergo such treatment because of the anatomy of the location of the injury and the requirements of available endovascular devices. Revascularization of the left subclavian and vertebral arteries is required only in a minority of patients and can usually be performed after endograft deployment, depending on the subsequent development of symptoms. However, in some situations, it may be best to revascularize the LSA, either prior to or immediately flowing endograft deployment. This case illustrates a circumstance in which revascularization of the LSA was required to salvage function of a left upper extremity AV fistula in a hemodialysis-dependent patient, as well as to alleviate symptoms of vertebrobasilar insufficiency.