Management of the subclavian steal syndrome

Thorax (1966), 21, 347.

Management of the subclavian steal syndromeP. J. MOLLOY AND E. WYN JONES

From the Regional Cardio-thoracic Surgical Unit, Broadgreen Hospital, and the Regional CardiacCentre, Sefton General Hospital, Liverpool

Since the subclavian steal syndrome was firstdescribed by Contorni in 1960, numerous articleshave appeared indicating that it is commoner thanwas formerly realized. Reivich, Holling, Roberts,and Toole (1961) drew the attention of the Eng-lish literature with an account of two patientswho had features of cerebral ischaemia, and itsstriking title was coined in an editorial (1961) inthe New England Journal of Medicine. Thepresent paper describes five such patients andseeks to outline the steps in management and todiscuss problems arising therefrom.The underlying pathology in nearly all the

recorded cases is atherosclerotic occlusive vasculardisease, although arteritis, dissecting aneurysm,

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or syphilis may give rise to the condition. Diabetesmay be associated (Siekert and Millikan, 1955)with basilar artery insufficiency states.

In patients with the subclavian steal syndromeocclusion of the subclavian artery (or innominateartery) proximal to the vertebral artery on thatside gives rise to a pressure differential betweenthe two vertebral arteries. Blood from the contra-lateral vertebral artery is siphoned over at thebasilar junction and flows retrograde into thesubclavian artery on the occluded side, therebydepriving the basilar artery of some of its supply(Fig. 1). If the carotids are stenosed the brain stemcirculation may be imperilled by a lack of flowthrough the anastomotic channels at the circle of

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FIG. 1. The arrows show the direction ofblood flow when the left subclavian arteryorigin is occluded, indicating the site ofsubclavian stealing at the basilar arteryjunction.

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P. J. Molloy and E. Wyn Jones

Willis, as is evidenced in the third patient in this hospital with equal pressures in the two arms (160/100group. Rotation of the head may aggravate symp- mm. Hg). He survived a myocardial infarct six weekstoms due to occlusion of the prograde flowing later and has been maintained throughout on anti-vertebral artery. coagulants. He has had no further episodes of cerebralischaemia in 12 months of survey.

CASE REPORTS

CASE 1 J.H. aged 61, a right-handed ship's engineer.awoke in Hamburg in August 1964 with dysarthria anda left arm paresis. He had a controlled atrial fibrillationof unknown aetiology of 11 years' duration. Physicalexamination showed signs of generalized atheroma, withno other abnormality in the cardiovascular, respiratory,or alimentary systems. The left hand was colder thanthe right, in which arm the blood pressure was 165/105mm. Hg. The left arm pressure was 100/? mm. Hg.There were no bruits in the root of the neck. Aorto-graphy, using percutaneous femoral artery puncture bythe Seldinger technique, showed obstruction to the leftsubclavian artery with reversed flow down the leftvertebral artery (Fig. 2).On 17 February 1965 operation was performed

through a left fourth rib bed posterolateral incision.The aorta was taped, and the left subclavian arteryand its branches were dissected free and held in non-occlusive tapes. The subclavian artery was opened afterpartly occluding the aorta and the subclavian arteryorigin, and endarterectomy was performed. The plaqueextended into the aorta, and on opening the aorticclamp no prograde flow ensued. A 4 mm. disc of theoccluding plug was excised, but it was thought that the_flow was inadequate. A 8 in. (16 mm.) Teflon graftwas sutured end-to-side from the aorta to the distalend of the subclavian incision. Flow on releasing theaortic clamp was satisfactory. The patient's con-valescence was uneventful and he was dischargedfromo

FIG. 2. Case 1. Retrograde aortogram, left oblique view.(a) Shows normal innominate and left carotid arterieswith the right vertebral artery filled. There is only a shortstump of the left subclavian artery visible; (b) 1.5 sec.after (a) shows left vertebral artery filling retrogradely;(c) 0-5 sec. after (b) shows left vertebral artery still opaci-fied and filling the left subelavian artery.

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Comment This patient showed no hyper-tension and no arm claudication, nor were anyother symptoms provoked by arm exercise.

CASE 2 M.P. aged 61, a right-handed school-teacher,had an 11 months' history of dizziness, loss of speech,weakness in the left arm, and occasional syncopalattacks. Turning the head to the left or using the leftarm induced dizziness. An electrocardiogram showedchanges of left ventricular hypertrophy. She had beenmaintained on anticoagulants and hypotensive drugsfor some time before admission.An arch aortogram (femoral route, Seldinger tech-

nique) showed occlusion of the left subclavian arteryfrom its origin to the origin of the vertebral artery,which was filled retrograde from the right vertebralartery. The other arch vessels showed changes ofatherosclerosis. In February 1965 the left subclavianartery was explored through a left fourth rib bedincision. Because of the widespread atherosclerosis anaorto-subclavian graft using X in. (16 mm.) Teflonwas performed by side-to-side anastomosis. There wasgood flow on releasing the clamp, and convalescencewas uneventful. Adequate anticoagulation control wasdifficult to obtain due to an idiosyncrasy until warfarinwas substituted for phenindione, but she was relievedof symptoms and has maintained equal pressure in eacharm (190/100 mm. Hg).

Comment This patient showed limb claudica-tion and symptoms related to exercise and posturein a known hypertensive.

CASE 3 T.A. aged 58, a social worker, also right-handed, had had intermittent dysphagia for two weeksand visual disturbances for two years. She had had aknown systemic hypertension for five years (B.P. 180/100 mm. Hg). She presented when she had a dropattack at the school of the previous patient's husband,who made the correct diagnosis! There was no limbclaudication, but the syncopal attack had been pre-ceded by loss of power in the left arm. She showedpulse differences (R. 100/0; L. 185/105 mm. Hg) withno neurological signs in the limb. There were, however,right and left carotid bruits, a to-and-fro murmur overthe right subclavian origin, and bruits over each renalartery. An electrocardiogram showed minor changesof left ventricular hypertrophy. An arch aortogram(percutaneous femoral artery, Seldinger technique)showed the left subclavian artery to be patent, the leftvertebral artery narrowed at its origin, the left carotidartery occluded, and the right subclavian artery blockedto the origin of the right vertebral artery, in whichblood flow was retrograde. The right internal carotidartery was also occluded. This patient's cerebral circu-lation depended on a stenosed left vertebral artery(Fig. 3). After the aortogram she had three dizzyattacks interpreted as a portent of worsening cerebralischaemia and therefore had an emergency operation.The innominate artery was approached through a

low transverse neck incision, and, although a little2E

cramped by the medial end of the clavicle, exposurewas adequate for proximal control. The innominate-subclavian artery junction was opened, and an occlud-ing plaque of atheroma was removed up to the originof the vertebral artery. Since the right common carotidartery was patent above the innominate artery bifurca-tion, the carotid bifurcation was exposed through ahigher crease incision and a right internal carotidendarterectomy was performed. There was surprisinglygood back-bleeding down the internal carotid artery.After closure of the incisions there was good progradeflow in both vertebral and carotid arteries.

It was elected to continue with anticoagulants. Shewas well for two days with equal pressures of 200/110mm. Hg in each arm; 72 hours post-operatively shehad an epileptic seizure and became comatose andhe-miplegic. Her blood pressure was noted to be 270/180 mm. Hg. She failed to regain consciousness anddied 76 hours after operation. Post-mortem examina-tion showed the sites of endarterectomy to be patent,and the cause of death was massive subarachnoid andintracerebral haemorrhage occasioned by the hyper-tension and possibly aggravated by the anticoagulants.

Comment This patient showed no limbfeatures other than pulse difference, but was aknown hypertensive. More adequate control ofthe acute hypertension while she was on anti-coagulants might have averted the loss of thispatient.

CASE 4 A.M. aged 48, a clerical worker, had hadvertiginous attacks for two and a half years anddiplopia for seven to eight months. There was no limbclaudication nor neurological disturbance. There wasa pulse discrepancy (blood pressure R. 80/60,L. 130/70 mm. Hg) and a loud systolic bruit on theright at the root of the neck. An arch aortogram (per-cutaneous femoral, Seldinger technique) showedmarked atheromatous narrowing of the innominateartery with early poor filling of the right subclavianartery. The later films showed retrograde flow throughthe right vertebral artery and later refilling of theright subclavian artery.The aortic arch was explored through a median

sternotomy which gave excellent exposure. A rightinnominate and subclavian endarterectomy was per-formed with restoration of prograde flow. During theprocedure the right carotid circulation was supportedby a femoro-carotid bypass. Hypothermia was notused. Convalescence was uneventful and at dischargethe patient was symptom free with equal pressures ineach arm (140/90 mm. Hg).

Comment This patient had progressive symptomsof vertebral ischaemia and was not hypertensive.Although there was some prograde flow in theright subclavian artery, the pressure differentialwas sufficient to permit retrograde filling of theright vertebral artery and subclavian stealing.

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Management of the subelavian steal syndrome

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FIG. 4. Case 5. Retrograde aortogram, semi-oblique view.(a) Shows the innominate, right subclavian and vertebral,and left carotid arteries well filled, with absent left sub-clavian artery; (b) 2-5 sec. after (a) shows the left vertebralartery filling retrogradely with early opacification of theleft subclavian artery; (c) 05 sec. after (b) shows the leftsubclavian artery strongly opacified, indicating a signifi-cant degree of 'steal.' Note the small stump of subclavianartery proximal to the origin of the vertebral artery onthe left.

CASE 5 R. McD. aged 56, an electrician, noticed numb-ness of the left arm, paraesthesia, and pain broughton by working overhead with his left arm. He hadhad vertigo off and on for four years. He had coldnessof the fingers in the left hand and occasional numbness.Turning his head to the left brought on dizziness andaggravated his symptoms. Examination showed a coldleft hand with diminished pulse (blood pressure: right150/70 mm. Hg, left 100/? mm. Hg). The left sub-clavian artery could not be felt. There were no bruits.The remainder of the examination was uninformative.An aortogram (right transfemoral route) showed anabsent left subclavian artery with late retrograde flowdown the left vertebral artery (Fig. 4). Operation wasperformed on 18 January 1966. On exposing the leftsubelavian artery through a left third rib bed incisionit was clear that the vessel was blocked right to itsorigin. Accordingly, an aorto-subclavian bypass graft

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was performed. There was good prograde flow onreleasing the clamps. Convalescence was uneventful.He has been relieved of his symptoms, and bloodpressure is equal in each arm at 160/100 mm. Hg.

Comment This patient was not hypertensivebut had limnb claudication and a postural exacer-bation of symptoms.

DISCUSSION

The problems that arise in the management ofthis condition are those of diagnosis, treatment,and post-operative care.

DIAGNOSIS Symptoms are non-specific unless armclaudication or postural changes worsen them.The neurological features may suggest many non-vascular and vascular cerebral lesions, such asdisseminated sclerosis, pseudobulbar palsy, neuro-vascular syphilis, cervical vertebral spondylitis,scalenus anticus syndrome, diabetic neuropathy,basilar artery sclerosis, or cerebral vascularsclerosis. Many of these patients are in an agegroup in which degenerative disease is common,and unless the examiner is aware of the sub-clavian steal syndrome as a cause of these symp-toms the diagnosis will be overlooked.

Hypertension is not necessarily a feature andwas not present in our cases 1, 4, and 5. In a studyof 54 patients with vertebrobasilar insufficiency,Bradshaw and McQuaid (1963) noted that 37 werehypertensive. The ipatients may have otherfeatures of occlusive vascular disease as manifestby leg claudication, myocardial ischaemic symp-toms, or temporal arteritis.The critical points of diagnosis (apart from

awareness of the condition) are differentiation ofthe pulses in the two arms and adequate radio-graphy. Bruits should be sought, and Peart andRob (1960) have emphasized the value of listen-ing over the sites of division of vessels for evidenceof partial occlusion. A totally occluded vessel willof course, give rise to no flow murmur. Bothradial and brachial pulses on each side shouldbe compared by palpation, as there may be only20 to 30 mm. Hg difference. The blood pressureshould be taken in each arm. The finding of apulse discrepancy is the most useful clinical signin the diagnosis of subclavian obstruction, and, ifassociated with symptoms of cerebral ischaemia,the diagnosis of a subclavian steal syndromeshould be entertained. Williams, Scott, andTakaro (1963) have shown that the pulse in thesubclavian artery on the affected side may beobliterated 'by pressing on the origin of the ver-

tebral artery in the neck on that side. They alsoemphasize the relation of postural changes of thearm and neck to the onset of symptoms.

Accurate anatomical localization of the site ofobstruction and demonstration of the reversedvertebral flow is only possible by performingaortography. It is not enough to visualize thecarotid artery on the affected side, as all the archvessels must be seen. Sufficient late films must betaken to show filling of the vertebral vessels andthe direction of their flow. After the initialdescriptions of this condition, radiologists con-firmed the patho-physiological circulation andestablished it as a radiological entity (Simon,Rabinov, and Horenstein, 1962; Philp, Samuel,and Duncan, 1963; Ashby, Karras, and Cannon,1963; Steinberg and Halpern, 1963; Fischer andMattey, 1963). Great care, especially in the elderly(Williams and Wilson, 1962), must be taken, andretrograde percutaneous femoral artery punctureis to be preferred to the brachial route, as post-angiogram thrombosis of the subclavian arteryon the non-affected side may provoke bilateralvertebral, and consequent basilar, artery throm-bosis as well as upper limb ischaemia. Using aSeldinger technique, gentle advancement of theguide wire will permit the catheter to advance tothe aortic arch.

Subclavian artery thrombosis is more seriousthan femoral artery thrombosis, which must alsobe recognized as a possible complication as thelimb circulation will be endangered. As in case 3,the cerebral circulation may be so imperilled thatthe hypertonic contrast medium may provokeischaemic symptoms. If these patients are beinginvestigated, facilities for rapid surgical treatmenteither of the lesion itself or of complications ofthe investigation must be available.

TREATMENT Recognition of the presence of thecondition is not sufficient indication for treatment.The patients should have progressive symptomssufficient to alter their normal way of life andshould not be frail or elderly, since operativemanagement inflicts a major hazard, especially inthe left-sided lesions. In patients whose symptomsdo not warrant operative treatment, or whosecondition does not permit it, there is aplace for prolonged anticoagulant treatment withdicoumarol derivatives, bearing in mind the riskof cerebral or other haemorrhage, especially if thepatient is hypertensive. Bradshaw and McQuaid(1963) noted a poor prognosis in their series ofcases with vertebro-basilar insufficiency especiallyin those patients denied anticoagulants. These

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authors found an 8% mortality in 101 patients onanticoagulants, but a 50% mortality in a smallerseries of similar patients not so treated.

Operative procedures should aim at dis-obliterating the obstructed segment or bypassingit. There is little place for simple vertebral arteryligation, except perhaps in the frail or elderlywith severe symptoms which progress in spite ofanticoagulant therapy. There is a high risk ofbasilar artery thrombosis, which is always fatal(French and Haines, 1950).On the left side the subclavian artery is

approached via the left fourth rib bed. This givesgood access to the aortic arch, the subclavianartery origin, and its first branches. The aortashould be taped above and below the subclavianartery to allow control of haemorrhage. If theorigin of the vessel is patent, as determined byaortogram, palpation, and aspiration of blood, itcan be clamped at its origin, and an endarter-ectomy can be performed through a small (1 in.;25 mm.) incision.

If the lumen appears narrowed a vein patch orwoven material patch can be inserted to widen it.Care must ibe taken that the proximal limit of theendarterectomy does not extend into the aorticlumen, as not only may this act as the site of adissecting aneurysm but the atheromatous aorticwall may disintegrate and result in an uncontrol-lable haemorrhage.

If the subclavian artery is totally obliterated atits origin and the aortic wall as seen on theaortogram is atheromatous, it is better to bypassthe obstruction with a graft from the aorta distalto.the subclavian artery to the region of the sub-clavian branches. A localized endarterectomy maybe necessary distally in the subclavian artery togive an adequate lumen proximal to the vertebralartery, but too much intimal removal need not beattempted.On the right side, if the innominate artery is

blocked the arch of the aorta should beapproached by a median sternotomy using thefull length of the sternum. There is less risk ofopening the pleura, healing is as good and post-operative discomfort a good deal less than a T-shaped incision in the sternum. If access overthe subclavian artery is desired, the upper endof the incision can be extended across the neck1 in. (25 mm.) above the clavicle with or withoutthe detachment of the sternal and clavicular headsof sternomastoid. There is little place for excisingthe medial end of the clavicle. The aorta andinnominate artery can be dissected free and con-trolled. The innominate vein should be dissected

free along its full visible length and gentlyretracted to expose the innominate artery bifurca-tion: good exposure is obtained by this method.As on the left, endarterectomy or bypass graftcan then be performed to restore the lumen.

If the segment of the subclavian artery betweenthe innominate artery bifurcation and the vertebralartery origin alone is blocked, the obstruction maybe approached by a simple neck incision fromthe left of the suprasternal notch to the junctionof the outer and middle thirds of the clavicle.The cervical pleura should be carefully retractedto avoid inducing a pneumothorax after elevatingthe heads of the sternomastoid. After taping theinnominate, subclavian, and carotid arteriesendarterectomy can be performed. It must be notedthat side clamping of the innominate-carotid junc-tion is necessary to allow carotid artery flow. If thisis not practicable, facilities for femoro-carotid by-pass or hypothermia should be available. The useof hypothermia adds considerably to the risks ofthe operation and should not 'be employedroutinely, as it has its own hazards (Cooper andRoss, 1960). If necessary, a carotid endarterectomycan be performed at the same time, as in case 3.

POST-OPERATIVE CARE It is the authors' practiceto give 50 mg. heparin (5,000 units) once vascularincisions are closed and any leak controlled, andthis is repeated after six hours in the belief thatheparin anticoagulation minimizes platelet de-position on the vascular suture line in the earlypost-operative thrombotic phase. If there is nogood evidence of widespread vascular disease, asin case 5, anticoagulants are, stopped forthwith.If atheroma is widespread, long-term anti-coagulation should be continued for the rest ofthe patient's life, with exact and adequate control.If laboratory facilities are not adequate it is prob-ably safer to rely on the flow through the restoredvessels. Irvine, Luck, Sutton, and Walpita (1963)advise against anticoagulants early because of thedanger of bleeding from suture lines, but note thatcomplications are seldom serious in patients on

long-term therapy.If the patients are hypertensive great care must

be exercised in controlling this feature, especiallyin the anticoagulated patient. In case 3, failure todo this resulted in loss of the patient. Chlor-promazine or ganglion-blocking agents in smalldoses intravenously give the best control duringthe acute phase.

Drainage is not used in the neck incisionroutinely, but, if necessary, suction drainage for24 hours only is employed.

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SUMMARY

Five patients with the subclavian steal syndromeare described.Problems arising in diagnosis, management, and

post-operative care are discussed with particularreference to the need for controlling post-operative hypertension in an anticoagulatedpatient.

The authors wish to thank Dr. E. J. Epstein, who.referred case 1, and Mr. Raymond Helsby, whoreferred cases 4 and 5. The central Photographic Unitof the University of Liverpool and Mr. D. Allen madethe photographic copies of the aortograms.

REFERENCESAshby, R. N., Karras, B. G., and Cannon, A. 14. (1963). Clinical and

roentgenographic aspects of the subclavian steal syndrome.Amer. J. Roentgenoi., 90, 535.

Bradshaw, P., and McQuaid, P. (193). The syndrome of vertebro-basilar insufficiency. Quart. J. Med., 32, 279.

Contorni, L. (1960). Il circelo colletrale vertebro-vertebrale nellaobliterazione dell'arteria subclavia alla sua origine. Minervachir., 15, 268.

Cooper, K., and Ross, D. N. (1960). Hypothermia. In Surgical Prac-tice. Cassell, London.

Editorial (1961). A new vascular syndrome-'the subclavian steal'.New Engl. J. Med., 263, 912.

Fischer, M. J., and Mattey, W. E. (1963). The subclavian steal syn-drome. Amer. J. Roentgenol., 90, 532.

French, L. A., and Haines, G. L. (1950). Unilateral vertebral arteryligation. Report of a case ending fatally with thrombosis of thebasilar artery. J. Neurosurg., 7, 156.

Irvine, W. T., Luck, R. J., Sutton, D., and Walpita, P. R. (1963).Intrathoracic occlusion of great vessels causing cerebrovascularinsufficiency. Lancet, 1, 1177.

Peart, W. S., and Rob, C. (1960). Arterial auscultation. Ibid., 2, 219.Philp, T., Samuel, E., and Duncan, J. G. (1963). Reversed vertebral

artery blood flow in subclavian artery obstruction. Clin. Radiol.,14, 310.

Reivich, M., Holling, H. E., Roberts, B., and Toole, J. F. (1961).Reversal of blood flow through the vertebral artery and itseffect on cerebral circulation. New Engl. J. Med., 265, 878.

Siekert, R. G., and Millikan, C. H. (1955). Some clinical aspects ofthrombosis of the basilar artery. Proc. Mayo Clin., 30, 93.

Simon, M., Rabinov, K.. and Horenstein, S. (1962). Proximal sub-clavian artery occlusion and reversed blood flow to the arm.Clin. Radiol., 13, 201.

Steinberg, I., and Halpern, M. (1963). Roentgen manifestations of thesubclavian steal syndrome. Amer. J. Roentgenol., 90, 528.

Williams, C. L., Scott, S. M., and Takaro, T. (1963). Subclavian steal.Circulation, 28, 14.

Williams, D., and Wilson, T. G. (1962). The diagnosis of the majorand minor syndromes of basilar insufficiency. Brain, 85, 741.

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Management of the subclavian steal syndrome