Subclavian Artery Thrombosis 

Subclavian artery thrombosis is a condition in which the blood flow through the vessel is obstructed. The condition usually occurs secondary to some form of antecedent injury to the vessel, hypercoagulable state, or atherosclerotic changes. The condition is common in young athletic individuals who exert a significant amount of upper body activity.^[1] 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 and/or stress injury to the upper extremity on the affected side. A history of upper extremity claudication is common.

In situations in which 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. However, note that subclavian steal is observed on 2% of cerebral angiograms and causes no symptoms.

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 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.

Frequency

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. Two percent of cerebral angiograms demonstrate asymptomatic subclavian steal.

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.

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.^[2] 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, thus 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 sociological 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, comprise a small subset of individuals who may exhibit this pathology.

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 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 neurological 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 the affected and unaffected sides may be noted.

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 neurological evaluation must be undertaken in order to isolate the problem. Once the anatomical aberration has been defined, intervention is indicated if the subclavian artery is involved.

In patients with subclavian artery occlusion secondary to variations in the thoracic outlet, 2 areas can undergo vascular compression during hyperabduction of the extremity. One site is where the axillary artery passes posterior to the pectoralis minor muscle 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. The image below illustrates the relevant anatomy.

Aberrant origins of the subclavian artery off the aortic arch can be a cause of subclavian artery occlusion.^[3]

In atherosclerotic disease, the carotid-subclavian junction or 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.^[4]

Areas of the subclavian artery that are exposed to repeated forms of injury resulting in intimal damage are predisposed to occlusion.

Contraindications to surgical intervention include inadequate distal runoff, inadequate vessel size, and marked collateralization of the occluded area. Concomitant medical problems that would endanger the patient during a surgical intervention are also contraindications to surgery. With the advent of stenting, patients with greater medical challenges can be treated successfully; however, the presence of appropriate arterial runoff and adequate artery size are imperative in order to ensure success of the procedure.