The carotid artery as alternative access for endoluminal aortic aneurysm repair☆☆☆
Article Outline
Abstract
Endograft treatment of aortic aneurysms has become a common procedure in many centers. However, not all patients are candidates for this new technology, because of their vascular anatomy and device limitations. One common problem is iliofemoral occlusive disease, which when present, even in a moderate degree, may preclude introduction of the large-diameter delivery devices currently in use. We present a case of a high-risk male patient with a thoracic aortic aneurysm and severe occlusive disease of the iliac arteries. An alternative approach for device delivery through the carotid artery was used and the procedure was successful with no neurologic complications. We recommend this technique for highly selected patients with an aneurysm who can undergo tube endograft repair without feasible access through the iliac or femoral arteries. (J Vasc Surg 2001;33:650-3.)
The application of endoluminal devices to treat aortic aneurysms has become widespread, on the basis of favorable reports of efficacy and safety.1, 2, 3 However, depending on the experience of the center and the endograft device used, 50% to 75% of patients are not candidates for this approach because of their anatomic considerations and the limitations of currently available devices.4, 5, 6, 7, 8 Anatomic constraints include a short infrarenal neck, aneurysmal or ectatic iliac arteries, extreme tortuosity of the aneurysm or iliac vessels, and iliofemoral occlusive disease.
Almost 25% of patients with aortic aneurysms have significant iliofemoral occlusive disease,9 but a smaller number of patients have bilateral disease severe enough to preclude device delivery through a femoral artery. Also, heavy calcification may preclude introduction of the delivery device in the presence of luminal stenosis or even mild tortuosity and increases the risk of vessel fracture or rupture. In some patients with distal iliac occlusive disease, successful endograft repair can still be accomplished by means of retroperitoneal exposure and iliac reconstruction,10 creation of a sidearm common iliac graft for vascular access, or iliac artery cutdown. Unfortunately, the benefits of a short hospital stay and quick return to function after endograft repair are mitigated under these circumstances.
In this case report, we present a patient with a thoracic aortic aneurysm and a severe medical comorbidity that precluded safe open repair. Infrarenal access for endograft repair was not feasible because of severe calcific occlusive disease involving the distal aorta and iliac arteries. In the setting of compassionate device use, we chose the left common carotid artery as the access site for endograft repair.
Case report
The patient was a 53-year-old man with end-stage renal failure, type 1 diabetes mellitus, congestive heart failure, and severe coronary artery disease who came to a local hospital because of hypoglycemia. He was found to have pleural effusions by means of a chest radiography and a saccular 4.8-cm aneurysm of the descending aorta (Fig 1) with the configuration of a pseudoaneurysm was revealed by means of a chest computed tomographic study.
Fig. 1.
Computed tomographic scan through the midthorax. There is a 4.8-cm saccular aneurysm (arrow ) of the mid-descending aorta.
On admission, the patient was comfortable and afebrile. He was pale and appeared chronically ill. His carotid pulsations were normal without bruit, and he had a patent dialysis fistula in the left arm. Breath sounds were diminished at the bases, and the abdomen was benign. The femoral arteries were calcified and pulseless, but distal perfusion was satisfactory. No tissue loss was present. He was vigorous and led an active lifestyle that was moderately restricted because of cardiopulmonary disease.
A computed tomographic study of the abdomen was performed, and a circumferential calcification of the infrarenal aorta and severe calcific occlusive disease of the common and external iliac arteries was demonstrated. The results of surveillance blood cultures and a tagged leukocyte scan were negative, confirming that the aneurysm was not mycotic. Markedly reduced ventricular function was demonstrated by means of a cardiac scan, and, in addition, moderate to severe pulmonary hypertension was suggested by means of an echocardiogram.
In this patient, the configuration and location of the aneurysm were ideal for tube endograft treatment, but iliofemoral access was not possible without extensive aortofemoral reconstruction. We considered the left common carotid artery as an alternative access site because of its large caliber, easy accessibility, and in-line orientation with the thoracic aorta. Minimal carotid bifurcation disease bilaterally with vessel diameters of 9 to 10 mm was shown by means of duplex ultrasound scanning and magnetic resonance imaging.
An extensive discussion was held with the patient. We thought this aneurysm occurred from a localized disruption of the aortic wall, probably from an atheromatous ulcer, and posed a significant risk of death due to rupture in the near future. We concluded that the patient had a prohibitive risk for open repair, but did not have uncompensated medical disease that would severely limit life expectancy. We offered the patient endoluminal repair through the left carotid artery and cited a slightly increased risk of stroke related to this approach. Approval was obtained from the institutional review board for compassionate application of an aortic endograft in this specific circumstance.
Procedure details
The patient was prepared with a radial artery line and pulmonary artery catheter with ventricular pacing leads. He was placed supine on a fluoroscopy operating table in a reversed position, with the head facing away from anesthesia. The left neck and upper chest were prepared and draped.
The left common carotid artery was exposed via a low anterior neck incision. It was soft and free of disease, and a Rumel tourniquet was placed proximally. A 19-gauge needle was used as a means of accessing the vessel, and a .038-in 15J guidewire (Cook, Bloomington, Ill) was advanced with fluoroscopic control into the thoracic aorta. A 6F sheath (Cook) was placed, a 5F pigtail catheter (Angiodynamics, Queensbury, NY) with 1-cm measurement markers was used to perform an aortogram with 40 mL Visipaque contrast (Nycomed, Princeton, NJ; Fig 2), and the distal and proximal graft attachment sites were positioned with a marker board device (Guidant, Menlo Park, Calif).
Fig. 2.
Intraoperative aortogram before endograft deployment.
We were concerned about proximal attachment site migration once it was released from the device because we were deploying the endograft “backward” relative to the blood flow stream. We hypothesized that the proximal graft could be subject to drift because of “windsock” forces once it separated from the device before balloon insufflation. To minimize this risk, we temporarily lowered the systemic blood pressure and used adenosine to introduce temporary asystole so we could deploy the proximal attachment site and move the balloon with a minimum of “windsock” stress on the graft. A test dose of 24 mg of adenosine was given by means of rapid bolus, and 7 seconds of asystole was observed, with a rapid return to baseline hemodynamics. Once the mean arterial pressure was lowered to 50 mm Hg, the distal attachment site was deployed, the balloon was inflated, and 48 mg of adenosine was given. When asystole commenced, the balloon was rapidly deflated and moved proximally after the release of the proximal attachment site and was used to set the proximal hooks. Normal cardiac function quickly resumed, and no drift was observed. The graft was dilated proximally to distally with a 22-mm Tyshak balloon (B. Braun Medical, Bethlehem, Pa) at 1.5 atm. Successful exclusion of the aneurysm was demonstrated by means of a follow-up anteroposterior and lateral angiogram (Fig 3).
Fig. 3.
Postdeployment aortogram demonstrating exclusion of the aneurysm.
The patient woke neurologically intact and was discharged on the second postoperative day. Correct graft placement without attachment site leakage and partial aneurysm thrombosis was shown by means of a computed tomographic scan of the chest on postoperative day 1.
Discussion
Endoluminal repair of aortic aneurysms is particularly appealing for functional patients who have a severe medical comorbidity, particularly coronary artery disease. This group of patients is also more likely to have diabetes mellitus, renal insufficiency, and peripheral vascular disease, and consequently, these cases present greater difficulties with endograft access through the femoral or iliac arteries.
Because of severe aortoiliac disease, our patient did not have a suitable device access site for conventional deployment techniques through the lower extremities. We chose the carotid artery as an alternative because of its large caliber, easy access, and “in-line” orientation with the descending aorta. We also considered the right axillary artery, but it was revealed by means of duplex ultrasound scan to have a luminal diameter of 6 mm, which was judged to be too small for the deployment device. The subclavian artery was also considered, but because of the increased risk of peripheral nerve injury and local wound complications associated with exposure, we did not use it. Furthermore, we think that the axillary and subclavian approaches carry some risk of vertebral artery embolization, particularly when the deployed device is withdrawn. The left carotid was chosen as a matter of convenience for right-handed surgeons.
Our main concern was the risk of stroke from cerebral hypoperfusion or emboli. Minimal (< 20%-30%) stenosis at the carotid bifurcation, mild thickening of the common carotid bilaterally, and patent vertebral arteries with prograde flow were demonstrated by means of duplex ultrasound scanning. We also measured the luminal diameter to be 8 to 9 mm and found that suitable for insertion of a 24F catheter. The patency and size of the extracranial carotid vessels were confirmed by means of magnetic resonance angiography.
We considered the risk of cerebral ischemia caused by common carotid clamping to be low. Generally, common carotid artery clamping is well tolerated because of collateral flow through the external carotid system. Berguer et al11 documented this in their series of 182 great vessel reconstructions via the cervical approach. Three perioperative strokes (1.6%) were attributable to intraoperative ischemia or embolization, and the remaining five strokes were associated with early graft occlusion. No shunts or electroencephalographic monitoring was used in these patients. We acknowledge that there may be a role for cerebral monitoring in cases like ours, but given the approach and the size of the deployment device, in-line shunting through the carotid artery was not possible. Consequently, we did not use electroencephalographic monitoring, and we minimized the period of induced hypotension to 5 minutes, because that time represented the greatest risk of cerebral hypoperfusion injury. We were also reassured that collateral perfusion was adequate after observing brisk backbleeding from the distal common carotid artery at the start of the procedure. During the remainder of the procedure, the mean arterial pressure was maintained at 80 to 90 mm Hg.
Systemic anticoagulation with heparin was induced before needle access, and the distal common carotid artery was clamped during device insertion and deployment to minimize the risk of embolization. The repaired artery was vigorously flushed and backbled before completing the closure while still anticoagulated.
The Ancure endograft was deployed in a reversed fashion from its original design relative to flowing blood. Ordinarily, the proximal attachment site is deployed first, and subsequent filling of the graft facilitates body and limb expansion before distal deployment. In our case, the distal attachment site was deployed first, so “windsock” forces actually favor graft collapse as they exert pressure on the outside of the fabric tube. We were concerned that with release of the proximal attachment site there could be graft migration from these forces before we could move the integrated balloon up and “seat” the proximal attachment site hooks. To minimize “windsock” force, we lowered the mean arterial pressure to 50 mm Hg and gave a bolus of adenosine that induced profound bradycardia and further hypotension that completely reversed after 10 seconds. This time interval was sufficient to deploy and seat the proximal stent, and no graft migration was observed.
In summary, we describe a novel approach for endograft treatment of aortic aneurysms through the carotid artery. Although it carries some increased risk of cerebrovascular complications, the carotid approach offers a technically straightforward access site for tube endograft deployment in patients who would not otherwise be candidates for open repair or endograft placement through the femoral or pelvic approach.
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☆ Competition of interest: nil.
☆☆ Reprint requests: James M. Estes, MD, Department of Surgery, New England Medical Center/Tufts University School of Medicine, 750 Washington St, Boston, MA 02111 (e-mail: jestes@lifespan.org ).
PII: S0741-5214(01)52502-1
doi:10.1067/mva.2001.111739
© 2001 Society for Vascular Surgery and The American Association for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
