Subclavian Artery Thrombosis 

Updated: Aug 12, 2021
Author: Mary C Mancini, MD, PhD, MMM; Chief Editor: John Geibel, MD, MSc, DSc, AGAF 


Practice Essentials

Subclavian artery thrombosis is a condition in which the blood flow through the subclavian artery is obstructed.[1] The occlusion typically arises secondary to damage to the intima of the vessel. This damage can occur as a result of external muscular compression and repetitive stress to the artery or because of atherosclerotic changes to the vessel. Embolic phenomena and hypercoagulable states are also contributing factors.

Symptoms occur secondary to lack of blood flow to the affected extremity. To maintain blood supply to the extremity, blood is naturally rerouted from the vertebral, carotid, and internal mammary arteries, producing the various steal syndromes.

Subclavian artery thrombosis is common in young athletic individuals who exert a significant amount of upper body activity.[2]  Sudden occlusion from emboli followed by thrombosis of the artery is common in the population with signs of significant atherosclerotic disease.

The patient presenting with acute subclavian artery occlusion usually has a history of repetitive use of or stress injury to the upper extremity on the affected side. A history of upper-extremity claudication is common.

In situations where the occlusion is secondary to atherosclerosis, acute thromboses of the artery are generally asymptomatic. In fact, in 9% of autopsy series, the left subclavian artery was either stenotic or occluded. If symptoms are present, upper-extremity claudication on the affected side is most common. The patient may also present with dizziness, vertigo, imbalance, visual disturbances, or hemisensory dysfunction indicative of a subclavian steal syndrome.[3]  However, note that subclavian steal is observed on 2% of cerebral angiograms and causes no symptoms.

Therapeutic intervention is indicated in any symptomatic patient once the etiology of the symptoms has been defined. Contraindications for surgical intervention include the following:

  • Inadequate distal runoff
  • Inadequate vessel size
  • Marked collateralization of the occluded area
  • Concomitant medical problems that would endanger the patient during a surgical intervention

In any operative procedure for subclavian artery thrombosis, care must be taken to protect the thoracic duct from damage. Future therapy for subclavian artery thrombosis is likely to involve increasing use of endovascular stents.


In patients with subclavian artery occlusion secondary to variations in the thoracic outlet, two areas can undergo vascular compression during hyperabduction of the extremity. One site is where the axillary artery passes posterior to the pectoralis minor and beneath the coracoid process. The other point is where the artery courses between the clavicle and the first rib. Fibrous tissue proliferation in this area can impose extrinsic compression on the vessel. (See the image below.)

The anatomy of the subclavian artery in the thorac The anatomy of the subclavian artery in the thoracic outlet.

Aberrant origins of the subclavian artery off the aortic arch can be a cause of subclavian artery occlusion.[4]  In atherosclerotic disease, the carotid-subclavian and carotid-vertebral junctions are areas that appear to be predisposed to atheromata formation and calcification. Subsequently, this region is most likely to be involved in the occlusive process.[5]  Areas of the subclavian artery that are exposed to repeated forms of injury resulting in intimal damage are predisposed to occlusion.


The affected artery demonstrates detectable intimal damage, which is usually secondary to compressive forces exerted by the muscles of the shoulder girdle that compress the artery. Bony abnormalities in this area can also contribute to the process.[6] As these muscles enlarge secondary to physical activity, they exert pressure on the artery. This pressure, coupled with exertional activity of the upper extremity, can stretch and compress the intima, thereby disrupting its natural integrity. This disruption precipitates platelet deposition in the area, with resulting thrombosis.

Atherosclerotic changes in the vessel occur secondary to the flow characteristics in the area. These depositions are accelerated by all of the dietary and sociologic influences that affect the progression of atherosclerotic disease, including smoking, hypercholesterolemia, and hypertension. Occlusion secondary to atherosclerosis is more insidious and often causes no symptoms. At times, the symptom complex of claudication precedes the actual loss of blood flow.

Patients with hypercoagulable states, either intrinsic or secondary to dehydration complicated by concomitant cardiac arrhythmias and systemic inflammatory processes, make up a small subset of individuals who may exhibit this pathology.


The occlusion arises secondary to damage to the intima of the artery. This damage can occur as a result of external muscular compression and repetitive stress to the artery, atherosclerotic changes to the vessel, or inflammatory processes.

Embolic or thrombotic occlusion of the artery occurs, particularly in the presence of atherosclerotic stenoses. Hypercoagulable states contribute to this scenario.


Symptomatic lesions occur in less than 1% of the population. In autopsy series, 9% of the population demonstrate stenosis or occlusion of one subclavian artery, usually on the left. About 2% of cerebral angiograms demonstrate asymptomatic subclavian steal.


The results from stenting procedures on the subclavian artery have documented an 87% patency rate after 3 years. Karpenko et al, in a study assessing endovascular treatment of atherosclerotic steno-occlusive disease of the subclavian artery in 245 patients, reported 4-year patency rates of 89.8% in patients with stenosis (n = 125) and 87% in those with occlusion (n = 120).[7]

Outcomes from operative treatment of subclavian artery thrombosis have demonstrated a patency rate of approximately 90% after 5 years.

The prognosis for the patient with atherosclerotic disease is directly dependent on the severity of the disease and on the willingness of the patient to make lifestyle modifications, including cessation of tobacco use and regulation of diet. If these modifications are made, the progression of the atherosclerotic process slows, and the risk of recurrence of thrombosis falls.

For the patient whose occlusion is secondary to thoracic outlet problems, the prognosis after therapy is excellent.



History and Physical Examination

A patient with an acute occlusion presents with a cold, painful, pulseless upper extremity. Axillary, brachial, and radial pulses are generally absent. When the occlusion is secondary to atherosclerotic changes, various prodromes and manifestations may be observed.

The patient may present with no symptoms or may have upper-extremity claudication secondary to exertion. If the condition has precipitated a steal syndrome, no symptoms are typically present.

The examining physician should be aware of the rare presentation of various neurologic symptoms and findings that may be associated with the steal syndromes, including syncope, vertigo, ataxia, sensory loss, visual changes, and stroke, depending on the vessels involved in the steal.

The affected upper extremity may or may not demonstrate diminished pulses. Blood pressure differences between affected and unaffected sides may be noted.


Potential complications of subclavian artery thrombosis secondary to atherosclerotic disease include distal embolization to the digits and neurologic symptoms, including stroke secondary to a steal syndrome. If the subclavian artery thrombosis is secondary to thoracic outlet problems, subclavian vein thrombosis can occur as well.[8]  Accompanying neurologic symptoms resulting from brachial plexus compression can also be associated with the syndrome.



Laboratory Studies

Laboratory studies that may be useful include the following:

  • Complete blood count (CBC), platelet count, and basic chemistry profile - Results should be within reference ranges; however, abnormalities in these parameters could be early indicators of dehydration or a hypercoagulable state
  • Prothrombin time (PT) and activated partial thromboplastin time (aPTT) - Again, results should be within reference ranges; however, they should be checked in order to assess the patient's coagulation profile
  • Antithrombin III level - In a hypercoagulable state, the antithrombin III level is low
  • Alpha-macroglobulin and plasminogen levels - Low levels indicate a prothrombotic state
  • Fibrinogen, factor VII, and factor VIII levels - Elevated levels indicate a prothrombotic state
  • Protein C and S levels - Abnormalities in these parameters indicate a chronic inflammatory state
  • Factor V Leiden and factor II C20210-a levels

Imaging Studies

Arteriography is a vital component of the evaluation process with regard to determining the anatomic aberrations of the arterial system and planning possible therapeutic interventions. A venous runoff should be included as well, because accompanying subclavian vein pathology should not be overlooked.

Computed tomography (CT) can help define bony pathology of the thoracic outlet that may contribute to occlusion of the subclavian artery. In particular, multidectector CT (MDCT) may be useful.[9]

Magnetic resonance arteriography (MRA) is a useful modality for defining subclavian artery anatomy and pathology.[10]

Echocardiography should be obtained in order to evaluate possible sources of arterial emboli.



Approach Considerations

Therapeutic intervention is indicated in any symptomatic patient once the etiology of the symptoms has been defined.

For instances of upper-extremity claudication or acute thrombosis in which the problem has been attributed to the subclavian artery, intervention should be planned and executed. For patients in whom cerebrovascular symptoms predominate, a careful neurologic evaluation must be undertaken in order to isolate the problem. Once the anatomic aberration has been defined, intervention is indicated if the subclavian artery is involved.

Surgery to correct subclavian artery thrombosis is the treatment of choice. Interventions include catheter-based procedures and formal operative procedures.[11] Contraindications for surgical intervention include the following:

  • Inadequate distal runoff
  • Inadequate vessel size
  • Marked collateralization of the occluded area
  • Concomitant medical problems that would endanger the patient during a surgical intervention

Future therapy for subclavian artery thrombosis will most likely involve increased use of endovascular stents.[12, 13, 14, 15] As technology improves and a better understanding of restenosis issues is achieved, stenting of these lesions will be more commonplace.[16, 17]  Stenting potentially allows successful treatment of patients with greater medical challenges; however, the presence of appropriate arterial runoff and adequate artery size are imperative for ensuring the success of the procedure.

In any operative procedure for subclavian artery thrombosis, care must be taken to protect the thoracic duct from damage.

Medical Therapy

Early diagnosis and therapy of subclavian artery thrombosis are indicated to prevent disabling upper-extremity ischemia and gangrene. As a temporizing measure, the use of catheter-directed thrombolytic therapy may be indicated for superimposed clot formation in an area of stenosis until definitive treatment of the obstruction can be undertaken.[18]

Prolonged anticoagulation therapy for an obvious mechanical problem is not indicated. Anticoagulation may be considered as supplemental therapy after surgical intervention.

Surgical Excision and Bypass

Subclavian artery occlusion secondary to thoracic outlet syndrome or muscular compression is treated by excision of the anatomic structure compressing the artery, whether muscle or bone.[19] The artery may or may not require additional reconstruction, depending on the presence or absence of intimal damage.

The occluded artery may require a bypass procedure, depending on the location of the occlusion or the presence of a subclavian steal syndrome. The bypass options include subclavian-carotid, subclavian-subclavian, and axillary-axillary bypasses. Another possible bypass option is transposition of the subclavian artery to the ipsilateral carotid artery.

Careful assessment of patients with thoracic outlet syndrome will be required because of the complexity of this problem, the multiple structures involved, and the high-profile medicolegal issues that arise with treatment of these patients. Operative treatment of the arterial complications of the thoracic outlet syndrome should be performed. However, careful evaluation of the potentially associated venous and neurologic pathologies should be undertaken prior to any operative therapy.

Preparation for surgery

After the appropriate diagnostic studies have been performed to define the problem, operative preparation should be carried out. Administer preoperative prophylactic antibiotic therapy in the form of a first-generation cephalosporin. Perform appropriate preoperative medical screening to assess for evidence of other atherosclerotic disease, such as coronary, carotid, or peripheral vascular occlusions.[18]


For patients in whom the occlusion is secondary to atherosclerotic disease, perform a bypass of the area. For subclavian steal syndrome, a carotid-subclavian bypass using a ribbed synthetic tube graft is the procedure of choice (see the image below).

Carotid-subclavian bypass for subclavian steal syn Carotid-subclavian bypass for subclavian steal syndrome.

Depending upon the location of the occlusion, subclavian-subclavian or axillary-axillary bypass can be undertaken using a ribbed synthetic conduit (see the image below).

Subclavian-subclavian or axillary-axillary bypass Subclavian-subclavian or axillary-axillary bypass for subclavian artery occlusion.

Because of the position of the graft and the necessity of crossing bony structures in some cases, autologous vein conduits have limited patency.

Rib resection

For patients in whom thoracic outlet compression is the cause of the thrombosis, cervical rib resection via a supraclavicular incision appears to be adequate treatment.[20, 21, 22] Resection of the midportion of the clavicle is sometimes needed for exposure. Undertake arterial resection because the intima of the vessel is damaged.

Graft interposition may or may not be required. Redundancy of the normal adjacent artery may allow end-to-end reconstruction. If a graft is required for arterial reconstruction, a large autogenous saphenous vein or expanded polytetrafluoroethylene or Dacron fabric grafts may be used. First-rib resection may be indicated in these instances as well, depending on the size of the thoracic outlet.[23]

Angioplasty and Stenting

Angioplasty and stenting of stenotic and even occluded arteries have been undertaken successfully with adequate patency rates and minimal morbidity.[24]  These interventions are particularly appropriate for atherosclerotic arteries.

A study to determine if stenting alone is superior proved inconclusive.[25]  A study from Germany found that endovascular therapy was safe and effective for treating stenosis and occlusion of the subclavian artery and yielded excellent long-term patency.[26]  A large-scale multicenter study from Japan found that primary endovascular therapy for subclavian artery disease yielded good outcomes with regard to perioperative complication and long-term patency rates.[27]

Newer ultrasonic therapies have shown promising results when applied to clot disruption in both the arterial and the venous system.[28]

Postoperative Care

Check distal upper-extremity pulses immediately after the operative procedure, while the field is still sterile. Maintain careful observation for the development of muscular compartment syndromes, and perform compartment measurements if indicated. Concomitant fasciotomies may be indicated, depending on the length of ischemia suffered by the extremity prior to revascularization.

Postoperative pleural effusions should be promptly evaluated for the presence of chyle, which would be indicative of thoracic duct injury. Prompt therapeutic measures should be undertaken if this complication occurs.


Complications of the procedure can include injury to the thoracic duct. Complications from surgical interventions to address the arterial occlusion can include graft occlusion (acute and chronic), stent migration, stent occlusion, bleeding, and infection.

Although postoperative bleeding is rare, the possibility that it may occur should be reviewed with the patient before the operative intervention.  Bleeding complications should be promptly addressed by means of reoperation in order to correct the problem.

Long-Term Monitoring

Postprocedural angiography should be performed at prescribed times after the operative intervention in order to assess the patency of the graft or stent. One suggested timing sequence for the studies is at 1 month and 6 months, provided that the patient remains asymptomatic. In the interim, noninvasive Doppler imaging can be used to assess distal flow to the extremity.



Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.


Class Summary

These agents dissolve recent clots promptly by activating a plasma proenzyme, plasminogen, to its active form, plasmin. Plasmin degrades fibrin to soluble peptides. The potential benefits of thrombolytic therapy for the treatment of thrombosis include fast dissolution of physiologically compromising emboli, faster recovery, prevention of recurrent thrombus formation, and rapid restoration of hemodynamic disturbances.

The use of catheter-directed thrombolytic therapy may be indicated for superimposed clot formation in an area of stenosis until definitive treatment of the obstruction can be undertaken.

Alteplase (Activase, Cathflo Activase)

Alteplase, or tissue plasminogen activator (tPA), exerts an effect on the fibrinolytic system to convert plasminogen to plasmin. Plasmin degrades fibrin, fibrinogen, and procoagulant factors V and VIII. The serum half-life of alteplase is 4-6 minutes but is lengthened when the drug is bound to fibrin in clot.