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SUBCLAVIAN STEAL SYNDROME

Anthony D. Whittemore M.D.

John A. Mannick M.D.

The subclavian steal syndrome occurs when there is reversal of flow in the ipsilateral vertebral artery distal to a stenosis or occlusion of the proximal subclavian, or, more rarely, the innominate artery. Because of the reduction of pressure in the subclavian artery distal to the obstruction, blood flows antegrade up the contralateral vertebral artery, into the basilar artery, and retrograde down the ipsilateral vertebral artery to supply collateral circulation to the upper extremity (Figs. 50-75 and 50-76) . Thus, blood supply is presumably ""stolen"" from the basilar system and may compromise regional or total cerebral blood flow.

Contorni ⁽³⁾ is credited with reporting the first angiographic visualization of subclavian steal in 1960; however, the potential significance of this problem was not widely appreciated until Reivich and his co-workers reported in 1961 about two patients with clinical signs of cerebral vascular insufficiency associated with reversal of flow through the vertebral artery secondary to subclavian obstruction. ⁽²²⁾ In their report, reversal of flow was demonstrated by angiography and with the electromagnetic flowmeter at the time of surgical correction. In a subsequent editorial discussing this case, Fisher introduced the term subclavian steal syndrome. Since that time, numerous reports have appeared in the literature describing

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Figure 50-75 Diagram of the pattern of flow in the subclavian steal syndrome. Note the retrograde flow in the vertebral artery on the side of the lesion (after Weilbaecher).

patients found to have subclavian steal by angiography. There has been considerable variation, however, in assessment of the clinical significance of the observed phenomenon.

CLINICAL EVALUATION

Classically, the subclavian steal syndrome should be suspected in a patient who manifests symptoms of vertebral basilar arterial insufficiency and is found to have a difference in the brachial systolic blood pressure of at least 30 mm. Hg between the two arms associated with a bruit in the supraclavicular area on the affected side. The cause of the proximal subclavian obstruction is atherosclerosis in most instances and more frequently affects the left side. ⁽⁹⁾ The neurologic symptoms reported in these patients most commonly include vertigo, limb paresis, and paresthesias. Bilateral cortical visual disturbances, ataxia, syncope, and dysarthria occur somewhat less frequently. The symptoms have been encountered initially as transient ischemic attacks of cerebral ischemia in the majority of patients, but a number of instances in which the symptoms progressed to complete stroke have been reported. ⁽⁹⁾ ⁽²²⁾ In patients with innominate artery stenosis, any neurologic manifestations of subclavian steal may be obscured by those associated with concomitant carotid insufficiency.

North and associates reported in 1962 that symptoms of cerebral ischemia were produced by exercise of the affected arm in six of the seven patients encountered with subclavian steal syndrome. ⁽¹⁸⁾ Conflicting experimental evidence has since been reported concerning the effect of proximal subclavian occlusion on cerebral blood flow. Reivich and associates ⁽²²⁾ and Sammartino and Toole ⁽²³⁾ reported that the compensatory increase in forward flow through other major arteries supplying the brain was insufficient to compensate for the flow lost through the steal phenomenon and concluded that a net deficit in cerebral blood flow existed. Handa and associates, however, studied cerebral blood flow in monkeys with an electromagnetic flowmeter and found that reversal of flow in the ipsilateral vertebral artery was accompanied by a compensatory increase of flow in the remaining three arteries supplying the brain, causing a limited 6% decrease in total cerebral blood flow and no evidence of neurologic abnormality. ⁽¹²⁾ Whereas earlier reports suggested that subclavian steal syndrome was associated with disabling neurologic symptoms in most patients in whom it was encountered, ⁽¹³⁾ ⁽¹⁴⁾ ⁽¹⁸⁾ ⁽²²⁾ increasing clinical experience suggested that this syndrome remained asymptomatic in most patients. ⁽⁸⁾ In an early report, Mannick and associates had suggested that the subclavian steal phenomenon was more likely to cause significant neurologic symptoms in patients with disease in other arteries supplying the brain. ⁽¹⁴⁾ The Joint Study of Extracranial Arterial

Figure 50-76 Early (A) and late (B) films of an angiogram of the aortic arch in a patient with the subclavian steal syndrome. In the early film, a stenosis of the origin of the left subclavian artery is seen. In the late film, there is retrograde flow of contrast material down the left vertebral artery, filling the left subclavian artery.

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Occlusion subsequently reported that 80% of 168 patients with subclavian steal syndrome had demonstrable disease involving other extracranial vessels. ⁽⁹⁾ It is of interest that in patients in this study treated medically or receiving no treatment at all, the three (9%) who suffered strokes had associated carotid disease. Patients with subclavian artery disease alone did not have strokes during the follow-up period, whether they were treated medically, surgically, or not at all. It is now apparent that, paradoxically, only a few patients have manifested neurologic symptoms in response to exercise of the involved arm, which would be expected to increase the demand for collateral blood flow.

It appears reasonable to conclude, therefore, that the subclavian steal phenomenon may frequently be clinically asymptomatic but can produce or contribute to symptoms of cerebrovascular insufficiency when it exists in conjunction with other lesions of the extracranial vasculature, particularly carotid bifurcation lesions. Whether the subclavian steal phenomenon produces symptoms in a given individual probably depends on (1) the size of the vertebral artery on the uninvolved side and whether it is free from disease; (2) the variable anatomy of the circle of Willis; (3) the amount of collateral circulation from other sources (particularly the costocervical and thyrocervical trunks) ⁽²⁾ ⁽¹⁷⁾ that develops to supply the affected arm; and (4) the presence of other extracranial vascular lesions.

The diagnosis of subclavian steal is established with retrograde catheter angiography, during which the tip of the catheter is positioned in the aortic root and a delayed filming sequence demonstrates retrograde flow in the ipsilateral vertebral vessel. It has been noted that a forceful injection of contrast material with the catheter tip located close to the origin of the vertebral vessel may in fact produce a spurious demonstration of the subclavian steal syndrome. ⁽²¹⁾ ⁽²⁵⁾

SURGICAL CORRECTION

Indications.

Because the subclavian steal syndrome is rarely symptomatic in the absence of associated extracranial lesions and, contrary to internal carotid artery lesions, rarely causes stroke, the more threatening extracranial lesions should be repaired either initially or concomitantly with reconstruction for subclavian steal. ⁽⁹⁾ In patients for whom the subclavian steal syndrome appears to be responsible for symptoms of vertebrobasilar insufficiency in the absence of other lesions in the extracranial cerebral arterial circulation, however, surgical correction of the lesion appears warranted and can result in amelioration of the symptoms. Surgical therapy cannot justifiably be urged for the prevention of stroke under these circumstances, because subclavian steal alone does not appear to cause stroke. ⁽¹²⁾ When the subclavian steal syndrome occurs in association with other extracranial arterial lesions, it is evident that the other significant lesions should be repaired as well. It appears likely that concomitant correction of the subclavian steal syndrome in certain of these patients should be undertaken; however, there are a number of reports of symptomatic relief in patients with subclavian steal in whom only the other arterial lesions were corrected. ⁽⁹⁾

Operative Technique.

A variety of surgical procedures have been recommended for correction of subclavian steal, including simple ligation of the ipsilateral vertebral artery, aorta-subclavian artery bypass graft, or subclavian endarterectomy using a mediastinal or transthoracic approach. ⁽⁴⁾ ⁽⁵⁾ ⁽²⁹⁾ As the intrathoracic procedures were initially associated with impressive morbidity, several supraclavicular procedures emerged. By the late 1960s, most surgeons had adopted the carotid-to-subclavian artery bypass graft carried out through a cervical incision as the procedure of choice. ⁽⁴⁾ ⁽⁹⁾ Subsequent experimental observations and widespread clinical application of this approach have demonstrated that significant reduction of internal carotid artery flow does not occur unless there is concomitant stenosis of the proximal common carotid artery. ⁽¹⁾ ⁽¹⁹⁾ Under such circumstances, this operation is clearly not advisable, because a significant reduction in total cerebral flow may result from an associated carotid steal.

The optimal approach for carotid-subclavian bypass is through a transverse cervical incision superior and parallel to the clavicle (Fig. 50-77) . The clavicular head of the sternocleidomastoid muscle is divided, and the exposed scalene fat pad swept inferiorly to expose the phrenic nerve coursing from lateral to medial over the anterior surface of the anterior scalene muscle. With gentle medial traction of the phrenic nerve, the scalene muscle is divided near its insertion on the first rib, exposing the mid-segment of the subclavian artery. The subclavian artery is then mobilized from the origin of the vertebral and mammary arteries to the lateral border of the first rib. The common carotid artery just deep to the sternal head of the sternocleidomastoid muscle and medial to the internal jugular vein is mobilized for a sufficient distance to accommodate a short arteriotomy and catheter tourniquets, in the rare event that an indwelling shunt is required. Although many surgeons prefer never to use a shunt, and others employ it routinely, some prefer to carry out this procedure with electroencephalographic monitoring, using the shunt on a selective basis. Whereas the choice of conduit is a subject of much debate, most surgeons prefer a short

Figure 50-77 Diagrammatic illustration of the technique of carotid-to-subclavian bypass grafting. The incision is placed at the base of the neck. The clavicular portion of the sternocleidomastoid muscle is divided, exposing the anterior scalene muscle and phrenic nerve. The phrenic nerve is carefully spared and the anterior scalene is divided, exposing the fascia overlying the subclavian artery, which can be freed from the vertebral origin laterally beyond the margin of the first rib. The common carotid artery is exposed through the same incision as it lies beneath the sternocleidomastoid muscle posteromedial to the jugular vein. A graft of autogenous saphenous vein is sutured end-to-side to the common carotid artery. An internal shunt (inset) may be used to preserve flow in the carotid artery while the anastomosis is performed. The shunt is removed just before completion of the suture line. The vein graft is then trimmed to size and sutured end-to-side to the subclavian artery.

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Figure 50-78 Diagrammatic illustration of the technique of subclavian-carotid artery transposition carried through the exposure described for Figure 50-77 . The subclavian artery is transected distal to the stenotic or occlusive lesion and sutured directly end-to-side to the common carotid arteriotomy.

prosthetic graft. ⁽³⁰⁾ A 6- to 8-mm. graft is sutured end-to-side to the common carotid artery, delivered deep to the internal jugular vein, and anastomosed end-to-side to the subclavian artery. Thirty-day operative mortality is generally in the range of 2%, and 5-year graft patency rates approach 95% with relief of symptoms in the vast majority. ⁽⁷⁾ ⁽⁹⁾ ⁽²⁰⁾ ⁽²⁶⁾ ⁽²⁷⁾ ⁽²⁸⁾

The subclavian steal syndrome may also be corrected by a subclavian-subclavian artery bypass graft through bilateral supraclavicular incisions ⁽¹⁰⁾ ⁽¹¹⁾ or by an axillary-axillary bypass graft carried out through two infraclavicular incisions. ⁽¹⁶⁾ Patency rates of these grafts have in general been favorable, and both avoid interfering with the anterior cerebral circulation. However, more extensive and therefore more time-consuming dissection is required: bilateral phrenic nerve palsy is a potential serious complication; and the axillary-axillary graft procedure places the graft in the undesirable superficial location as it crosses the sternum in the midline.

Since the mid-1980s an alternative procedure, the subclavian-carotid transposition, has become the procedure of choice for many surgeons. Initially recommended by Mehigan and associates in 1978 for patients exhibiting embolic complications from subclavian stenosis, the procedure is carried out through the supraclavicular approach. ⁽¹⁵⁾ The subclavian artery is divided just distal to its proximal stenosis or occlusion and the proximal end oversewn. The distal end is transposed and sutured end-to-side to the common carotid artery, converting the proximal common carotid vessel to a new innominate, perfusing both the subclavian and vertebral systems (Fig. 50-78) . Although the procedure requires more extensive mobilization of the proximal subclavian vessel, it obviates the need for a graft and shortens the operating time considerably. Overall patency rates after 5 years approach 99%, with minimal operative morbidity and mortality. ⁽⁶⁾ ⁽⁷⁾ ⁽²⁰⁾ ⁽²⁴⁾ ⁽²⁶⁾

SELECTED REFERENCES

Crawford, E. S., Stowe, C. L., and Powers, R. W., Jr.: Occlusion of the innominate, common carotid and subclavian arteries: Long-term results of surgical treatment. Surgery, 94:781, 1983.
Report of the experience of the senior author with reconstructions for obstruction of the brachiocephalic arteries in 142 patients over a 23-year period points out that transthoracic and extrathoracic operations in recent years have carried an equally low mortality. In fact, 89% of all patients survived operation, including early deaths when new techniques were being applied. Nevertheless, for single-vessel occlusions on one side of the neck, the authors still prefer the simplicity of the carotid-subclavian bypass and report that extrathoracic operations were performed in this large series in 69% of their patients. Eighty-three per cent of the patients remained asymptomatic over a follow-up period that averaged 7.5 years.

Edwards, W. H., Tapper, S. S., Edwards, W. H., Sr., Mulherin, J. L., Martin, R. S., and Jenkins, J. M.: Subclavian revascularization: A quarter-century experience. Ann. Surg., 219:673, 1994.
The authors report their experience with subclavian-carotid transposition in 178 procedures. The mortality rate associated with the isolated subclavian-carotid transposition was 1.1%, and all but one remained patent after a mean follow-up of 46 months. A thorough discussion addresses the risks and benefits of both carotid-subclavian bypass and subclavian-carotid transposition and argues for the latter as the procedure of choice for routine subclavian carotid occlusive disease.

Mehigan, J. T., Buch, W. S., Tipkin, R. D., and Fogarty, T. J.: Subclavian-carotid transposition for the subclavian steal syndrome. Am. J. Surg., 136:15, 1978.
This paper was one of the first to describe the direct anastomosis of the divided distal subclavian artery to the side of the common carotid artery to correct cerebral symptoms of the subclavian steal syndrome and to relieve symptoms of arm claudication, which are often associated with proximal subclavian occlusive disease. The technique as described has the advantage of not requiring a graft to correct the subclavian steal and of eliminating the possibility of embolization of clot or atherosclerotic debris from the proximal subclavian stenosis, which theoretically can occur after repair of the subclavian steal by carotid-subclavian bypass.

Reivich, M., Holling, H. E., Roberts, B., and Toole, J. F.: Reversal of blood flow through the vertebral artery and its effect on cerebral circulation. N. Engl. J. Med., 265:878, 1961.
This is the classic report describing the subclavian steal syndrome clinically and experimentally. Two patients were studied who had neurologic symptoms and reversal of flow in the left vertebral artery secondary to proximal subclavian stenosis, as demonstrated by angiography. Reversal of flow in the ipsilateral vertebral artery was demonstrated for the first time in humans at the time of operation in one of these patients by application of an electromagnetic flowmeter to the subclavian artery distal to the vertebral origin. The authors also report animal studies in which reversal of vertebral flow was demonstrated following subclavian artery occlusion. In the animal experiments, they conclude that total cerebral blood flow was markedly diminished by the subclavian steal.

REFERENCES

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6. Edwards, W. H., and Mulherin, J. L., Jr.: The surgical reconstruction of the proximal subclavian and vertebral artery. J. Vasc. Surg., 2:634, 1985.

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