Subclavian Steal Syndrome Treatment & Management

No medical therapy is known to effectively treat subclavian steal syndrome. However, if the cause of subclavian steal syndrome is atherosclerotic stenosis or occlusion of the proximal subclavian artery, treat patients with lifelong antiplatelet therapy to reduce the risk of associated myocardial infarction, stroke, and other vascular causes of death.

The goal of surgical therapy is to restore antegrade blood flow in the vertebral artery, thereby alleviating symptoms. This goal can be achieved by restoring adequate perfusion pressure to the affected arm so that collateral blood flow from the head and neck are not required during arm exercise.

Endarterectomy

Direct surgical approaches to the proximal subclavian artery are of only historical interest because endarterectomy has largely been replaced by less invasive extrathoracic bypass procedures. With endarterectomy, the artery is opened after obtaining vascular control, and the plaque, diseased intima, and internal elastic lamina of the vessel are removed, thus disobliterating the lumen. Since the occlusive lesions in the proximal left subclavian develop as an extension of plaque from the aortic arch, partial occlusion of the arch must be performed to ensure that the entire lesion is effectively removed. Surgical exposure must be obtained through an anterolateral thoracotomy in the left third intracostal space. On the right side, exposure can be accomplished through a transverse incision in the base of the neck without the need for thoracotomy.

Endovascular Treatment

Endovascular treatment (catheter-based procedures) of the proximal subclavian artery is the most common way that proximal subclavian lesions are treated today. The technical success rate is 86-100%, and the complication rate is low. Moreover, most can be performed as outpatient endovascular procedures. Although balloon angioplasty has been used in the past, primary stenting of the subclavian artery is the procedure of choice. Stenting improves perfusion to the arm and treats subclavian steal syndrome, as depicted in the image below. Since plaque in the proximal subclavian is actually part of the atherosclerotic lesion in the aortic arch, the stent must traverse the entire plaque and protrude slightly into the lumen of the aortic arch.

Extrathoracic carotid-subclavian bypass

Extrathoracic carotid-subclavian bypass using a prosthetic conduit has largely replaced subclavian endarterectomy. Surgical exposure is easily obtained through a transverse incision at the base of the neck extending 5-7 cm laterally from the sternal notch parallel to the clavicle. Conventionally, 6- to 8-mm Dacron or polytetrafluoroethylene (PTFE) prosthetic grafts are used. End-to-side (graft-to-artery) anastomoses are performed without difficulty. The procedures are well tolerated, and patients do not require a prolonged hospital stay or recovery period.

Transposition

The subclavian artery can also be transposed to a new origin on the side of the common carotid artery. This operation is performed through a transverse incision at the base of the neck as well and has the advantage of not requiring prosthetic material. The required dissection is more extensive, and care must be taken to avoid injury to the thoracic duct on the left side. An end-to-side (subclavian-to-carotid) anastomosis is performed. The long-term results of subclavian transposition procedures are similar to those of carotid-subclavian bypass.

Axillary-axillary bypass

Axillary-axillary bypass offers no real advantage over carotid-subclavian bypass. This procedure is not often used because it requires a long segment of prosthetic graft material to be passed underneath the skin overlying the sternum. The position of the graft, with its proximity to the skin, adds the risk of graft infection and skin erosion. Should a sternotomy be required in the future, the graft would have to be exposed and at least temporarily divided. Consider axillary-axillary bypass only if the ipsilateral common carotid is so severely diseased that using it for inflow would be problematic. In addition, the contralateral axillary artery must be relatively free of occlusive disease.

Endovascular details

The arch aortogram can be performed through a right femoral access using a multi-sidehole catheter and a power injector. The patient needs to be placed in a 30° left anterior oblique (LAO) position to obtain a reasonable image of the aortic arch and great vessels. As with any endovascular treatment, a guidewire must first be placed across the lesion. This may be more easily accomplished using the ipsilateral brachial artery in a retrograde direction if the origin of the subclavian artery is not well defined. On the other hand, if a stump of the patent proximal subclavian artery is visible, an antegrade approach through a right femoral artery access can be attempted.

When performing these procedures, both access sites (brachial and femoral) should be made available by proper preparation. If stenting is planned, the patient is given 5000 U of intravenous heparin. In general, balloon-expandable stents perform well in this location. They offer precise placement and have greater radial strength than self-expanding stents. Ensure that the subclavian stent does not compress the lumen of the ipsilateral vertebral artery or internal mammary artery. After stent placement, a selective subclavian arteriogram is taken to confirm the technical success of the procedure.

Post endovascular details

Most of these procedures are performed as outpatients. Patients should be monitored for 3-4 hours in a recovery area to insure that no bleeding or hematoma has occurred in the access site. If a closure device has been used on the access site, patients can be discharged as soon as any sedative medication has worn off. Neurological status should also be monitored and the blood pressure should be recorded in both arms.

Arch aortography must be performed to ensure that the proximal common carotid and distal subclavian arteries are relatively free of disease. During this procedure, also visualize the carotid and vertebral arteries because these vessels often contain other hemodynamically significant lesions that can contribute to the symptoms of subclavian steal.

The incision used for either carotid-subclavian bypass or subclavian transposition is made approximately 2 cm cephalad to the clavicle, extending lateral from the sternal notch. The attachments of the clavicular head of the sternocleidomastoid muscle are incised. The scalene fat pad is identified, and care is taken to preserve the phrenic nerve that traverses the anterior aspect of the scalenus anticus muscle. The muscle is divided, exposing the subclavian artery. The common carotid artery is easily exposed through the medial aspect of the same incision.

On the left side, the thoracic duct must be avoided. This structure is visualized near its junction with the proximal internal jugular vein. Following systemic heparinization, a bypass is performed using an 8-mm PTFE or Dacron prosthetic graft. End-to-side anastomoses are performed to the common carotid and subclavian arteries. Subclavian transposition requires more proximal dissection of the subclavian artery to ensure that enough length of artery is available to perform the anastomosis without undue tension. A partial occluding clamp on the common carotid is not necessary.

Complete carotid occlusion with a proximal and distal clamp affords a better view of the intima, and the short period of ischemia is generally well tolerated. Shunting of the common carotid artery during occlusion is usually unnecessary. However, if the contralateral common or internal carotid arteries are occluded, it may be reasonable to use an intraluminal shunt during the carotid anastomosis. Following completion of the anastomoses, protamine is administered to reverse the heparin.

Patients require observation for 24 hours in a monitored unit. Head elevation helps reduce swelling in the surgical incision. Brachial blood pressures are taken in both arms and are expected to be remarkably similar following the procedure. Patients are sent home with instructions to take 325 mg of aspirin daily as an antiplatelet agent.

Patients are seen at 3- to 6-month intervals for the first year and yearly thereafter. Always check blood pressures in both arms. A decline in pressure on the operated side may be the first sign that recurrent stenosis may be developing. Follow-up duplex scans of the reconstruction should be obtained at 6-month and 1-year intervals. Patients who have had subclavian stents should be treated with both aspirin and clopidogrel for a period of 6-12 months. Thereafter, a single antiplatelet agent is appropriate.

Complications related to surgical treatment may be classified as local or cerebral. Local complications are related to injury to adjacent structures that may be encountered during the course of the operation (eg, thoracic duct injury, phrenic nerve injury) and are quite uncommon. Cerebral complications are related to brain ischemic symptoms and can be caused either by thrombosis of the repair or by embolism up the carotid and/or vertebral arteries during the course of the procedure. Cerebral ischemia during common carotid occlusion is most unusual; therefore, a shunt is not used for the procedure.

Complications related to endovascular treatment can occur at the access site (femoral or brachial artery) or at the target vessel (subclavian or vertebral artery). Access site bleeding or hematoma is very uncommon but can occur. Target vessel thrombosis, dissection, or distal embolization have also been reported. These complications occur less than 4% of the time.

Patients with asymptomatic flow reversal in a vertebral artery have a benign natural history, and no specific treatment is required. With proximal subclavian artery occlusive disease, patients may first seek medical treatment for symptoms of exercise-induced arm pain rather than for neurologic symptoms associated with arm exercise Furthermore, if a patient has undergone coronary revascularization using a left internal mammary artery (LIMA) graft, new onset angina may herald proximal left subclavian stenosis. With subclavian steal syndrome, if neurologic symptoms do occur, they tend to be transient (ie, transient ischemic attack) and seldom lead to stroke.

The outcome for patients who have antegrade vertebral blood flow reestablished by either surgical revascularization or endovascular stenting of the diseased subclavian artery is highly favorable. The stroke risk from the procedure is low, and the long-term durability is excellent.

The operative mortality rate from transthoracic subclavian artery revascularization is substantially higher than for extrathoracic repair, mainly because of the morbidity associated with thoracotomy. Recognizing this problem, surgeons have virtually abandoned this approach in favor of extrathoracic revascularization, either carotid-subclavian bypass or subclavian transposition. The operative mortality rate for either of these extrathoracic procedures approaches zero. Moreover, the morbidity rate is very low.

The results of percutaneous subclavian angioplasty and/or stent placement are also excellent. Most authors document initial success rates of 91-100%, and the complication rate is reasonably low (3-17%). After successful stenting of the subclavian artery, the restenosis rate is 0-16% after 12-48 months follow-up. The technical success rate of subclavian angioplasty varies from 86-100%. The restenosis rate following subclavian angioplasty is 5-22% with follow-up from 28-60 months.

With recent improvements in angioplasty and stent placement techniques, surgery will probably have a smaller role for the treatment of subclavian steal syndrome in the future. Because the results of treatment for subclavian stenosis with angioplasty or stent placement are so good, surgery will likely be reserved for those patients who have had prior unsuccessful attempts at endovascular treatment. These unsuccessful cases usually involve a chronic subclavian occlusion of considerable length. In these cases, traversing the lesion with a guidewire is difficult, thus inducing a higher failure rate.