Subclavian steal syndrome
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| Subclavian steal syndrome Classification and external resources | |
| ICD-10 | G45.8 |
|---|---|
| ICD-9 | 435.2 |
| DiseasesDB | 31525 |
| MeSH | D013349 |
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In medicine, subclavian steal syndrome (SSS), also subclavian steal phenomenon and subclavian steal steno-occlusive disease, is a constellation of signs and symptoms that arise from retrograde (reversed) vertebral artery (blood) flow or retrograde internal thoracic artery flow due to a proximal subclavian artery stenosis (narrowing) and/or occlusion.
Pathophysiology
Classically, SSS is a consequence of a redundancy in the circulation of the brain[1][1] and hemodynamics (the physics of blood flow).
SSS results when the short low resistance path (along the subclavian artery) becomes a high resistance path (due to narrowing) and blood flows around the narrowing via the arteries that supply the brain (left and right vertebral artery, left and right internal carotid artery). The blood flow from the brain to the upper limb in SSS is considered to be stolen as it is blood flow the brain must do without.
As in vertebral-subclavian steal, coronary-subclavian steal may occur in patients who have received a coronary artery bypass graft using the internal thoracic artery (ITA).[1] As a result of this procedure, the distal end of the ITA is diverted to one of the coronary arteries (typically the LAD), facilitating blood supply to the heart. In the setting of increased resistance in the proximal subclavian artery, blood may flow backward away from the heart along the ITA causing myocardial ischemia. Vertebral-subclavian and coronary-subclavian steal can occur concurrently in patients with an ITA CABG.[1]
Hemodynamics
Blood, like electrical current, flows along the path of least resistance. If blood is presented with two paths a short one that is very narrow (with a high overall resistance) and a long one that is wide (with a low overall resistance) it will take the long and wide path (the one with the lower resistance).
Vascular anatomy
The blood vessels supplying the brain arise from the vertebral arteries and internal carotid arteries and are connected to one another by communicating vessels that form a circle (known as the cerebral arterial circle).
Path of the blood (normal versus SSS)
Normally, blood flow from the aorta into the subclavian artery and then some of that blood leaves via the vertebral artery to supply the brain.
In SSS a reduced quantity of blood flows through the proximal subclavian artery. As a result, blood travels up one of the other blood vessels to the brain (the other vertebral or the carotids) goes around the cerebral arterial circle and via the (ipsilateral) vertebral artery to the subclavian (with the proximal blockage) and feeds blood to the distal subclavian artery (which supplies the upper limb and shoulder).
Etiology
Signs and symptoms
- Presyncope (sensation that one is about to faint)
- Syncope (fainting)
- Neurologic deficits
- Blood pressure differential between the arms
Associated with other stigma to vascular disease (e.g. vascular insufficency ulcers of the foot).
Differential diagnosis
Diagnostic tests
- Doppler ultrasound
- CT angiography
- Angiogram
Treatment
- Stenting and balloon angioplasty
- Endartertectomy
See also
References
External links
- Subclavian Steal Syndrome - emedicine.com
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
