eMedicine Specialties > Vascular Surgery > Medical Topics
Upper Extremity Occlusive Disease
Updated: Apr 5, 2007
Introduction
History of the Procedure
Symptomatic upper extremity arterial occlusive disease is uncommon because of the abundant collateral network and the infrequency of atherosclerosis in the upper extremity. Patients who present with upper extremity ischemia range from young adults with nonatherosclerotic causes to elderly patients with atherosclerosis.
Problem
Arterial occlusive disease of the upper extremity may represent either local or systemic disease. The pattern of arterial disease varies according to etiology. Diseases that affect the brachiocephalic vessels include atherosclerosis, arteritis, congenital anomalies, trauma, and fibromuscular dysplasia. In the United States, atherosclerosis is the most common cause of subclavian artery stenosis. Outside of the United States, Takayasu arteritis is more common. The axillary and brachial arteries are common sites of injury. One third of peripheral emboli lodge in the upper extremity, producing acute arterial occlusion. Radiation therapy of the chest or breast may induce subclavian artery disease.
Frequency
Brachial artery occlusion occurs in 0.9-4% of cardiac catheterizations. The brachial artery is also the most commonly injured artery in civilian trauma (30% of all arterial injuries). Digital gangrene is a frequent manifestation of connective-tissue disease or a hypercoagulable state. Buerger disease manifests with multiple digital artery occlusions caused by heavy smoking and is rare. Many patients with upper extremity arterial disease have associated Raynaud syndrome or significant cold sensitivity.
Etiology
- Large-vessel occlusion (eg, subclavian, brachial, forearm arteries)
- Atherosclerosis
- Trauma (eg, thoracic outlet syndrome, penetrating, blunt, iatrogenic)
- Arteritis (eg, Takayasu arteritis, giant cell)
- Irradiation
- Embolic (eg, cardiac or thoracic outlet in origin, including bacterial endocarditis, microemboli from ascending aorta, paradoxical emboli)
- Fibromuscular dysplasia
- Digital artery occlusion (see Image 1)
- Connective-tissue disease - Scleroderma; chondrocalcinosis, Raynaud phenomenon, esophageal motility disorder, sclerodactyly, and telangiectasia (CREST); and mixed connective-tissue disease
- Buerger disease
- Hypersensitivity angitis
- Hematologic - Hypercoagulable states, hyperviscosity, malignancy
- Traumatic - Occupational (eg, hypothenar hammer syndrome, vibratory tools), iatrogenic, recreational (baseball palmar artery injuries)
- Infection - Infection from injection of drugs, infection from arterial procedures
- Flow phenomenon - Vascular steal related to dialysis access graft or fistula placement
Pathophysiology
Vasculitis, fibromuscular dysplasia, and atherosclerosis produce symptoms related to progressive narrowing of the arterial lumen. A diameter reduction of 50% or a cross-sectional area reduction of 70% represents a hemodynamically significant lesion. These lesions produce a pressure drop across the stenotic area. The distal arterial bed is supplied by collateral blood vessels. Symptoms include exercise-induced fatigue as the demand for blood exceeds the supply.
In patients with acute arterial occlusions, collateral blood vessels have not formed, and perfusion drops rapidly below a critical threshold level, which results in persistent pain and tissue necrosis. Limb pressure is generally less than 30 mm Hg. Doppler tones cannot be heard in the digital vessels.
The pathophysiology of Raynaud syndrome is unknown. Precapillary smooth muscle cells constrict in an abnormal response to cold stimulation. The sympathetic nervous system adrenoreceptor function and number are believed to be altered. The distinction between Raynaud disease and Raynaud phenomenon is arbitrary and is best divided into patients with normal digital arteries (Raynaud disease) and patients with obstructed arteries (Raynaud phenomenon). The two are easily distinguished using noninvasive blood flow testing (see Diagnostic Procedures).
Presentation
- The patient’s history may include the following:
- Arm fatigue upon exercise (ie, subclavian artery occlusion)
- Vertebrobasilar insufficiency (ie, subclavian steal)
- Rest pain that involves hand and digits
- Digital gangrene
- Raynaud syndrome (eg, color changes—white, blue, red or white, red, blue)
- Smoking history
- Occupational and recreational history (eg, baseball pitcher, tennis player, handballer, carpenter)
- Drug ergots (peripheral vasoconstrictors used in the treatment of shock [eg, dopamine, adrenaline])
- The results of physical examination include the following:
- Fever (if an associated vasculitis is present)
- Unequal arm pressures (>20 mm Hg difference)
- Supraclavicular or infraclavicular bruit
- Adson maneuver (loss of radial pulse upon abduction and external rotation of the upper extremity)
- Supraclavicular pulsatile mass (associated with a subclavian aneurysm or cervical rib)
- Palpation of pulses (axillary, brachial, radial, ulnar)
- Digital gangrene
- Color and capillary refill of the digits
- A positive Allen test result: An abnormal result on the Allen test demonstrates an incomplete palmar arch. In this test, the ulnar and radial arteries are occluded with the fist clenched. The hand is then opened, releasing one of the arterial occlusions (radial or ulnar); prompt capillary refill should result. The same maneuver should then be performed with the release of the other artery. If the palmar arch is not intact, the release of the affected artery produces a sluggish capillary refill. Alternatively, a Doppler stethoscope is used to map these collateral flow patterns in the hand by manually occluding, one at a time, the radial and ulnar arteries.
Indications
- Arm fatigue - Carotid-subclavian bypass (see Image 2), percutaneous transluminal angioplasty (PTLA), and stent
- Vertebrobasilar insufficiency - Carotid subclavian bypass and possible vertebral artery transposition to carotid artery
- Subclavian aneurysm and thoracic outlet injuries with distal embolization - Resection of subclavian artery aneurysm and venous bypass and rib resection with thoracic outlet (see Image 3)
- Acute arterial occlusion - Embolectomy for embolus and repair for trauma (blunt or penetrating)
- Chronic arterial occlusion with pain at rest, ulcer, or gangrene - Bypass using the autogenous vein for distal segments and prosthetic material for larger proximal segments, amputation (digital or forearm), and sympathectomy (controversial)
Relevant Anatomy
See Image 4.
Right subclavian artery: This artery originates from the innominate artery. Rarely, the origin of the right subclavian is distal to the left subclavian, passing behind the esophagus and producing dysphagia lusoria (ie, difficulty swallowing). An aberrant right subclavian artery is also prone to aneurysm degeneration (ie, Kommerell diverticulum).
Vertebral artery: This is the first branch of the subclavian and a major collateral for proximal subclavian artery stenosis (retrograde vertebral artery blood flow). The distal vertebral artery also provides blood flow to the anterior spinal artery.
Internal mammary artery: The internal mammary artery (IMA) is the second branch of the subclavian artery and is used for coronary artery bypass grafting (CABG). Occasionally, progressive subclavian stenosis produces angina in patients who have undergone CABG.
Brachial artery: This branches at the elbow into the ulnar, radial, and interosseous arteries. Rarely, the ulnar and radial arteries arise from the axillary or subclavian arteries.
Ulnar and radial arteries: These connect in the hand to form the superficial and deep palmar arches. Palmar arch anatomy varies. In most patients, the ulnar artery is the dominant blood supply of the hand.
Contraindications
Few contraindications for surgical intervention exist in the presence of significant cerebrovascular symptoms or gangrene of the hand.
Arterial reconstruction may not be feasible if too many of the outflow target arteries are destroyed.
Asymptomatic subclavian artery stenosis, even with radiographic evidence of subclavian steal (retrograde vertebral flow), should not be treated.
Severe coexisting life-threatening illness may prevent surgical intervention.
More on Upper Extremity Occlusive Disease |
 Overview: Upper Extremity Occlusive Disease |
| Workup: Upper Extremity Occlusive Disease |
| Treatment: Upper Extremity Occlusive Disease |
| Follow-up: Upper Extremity Occlusive Disease |
| Multimedia: Upper Extremity Occlusive Disease |
| References |
| Next Page » |
References
Dennis JW, Frykberg ER, Crump JM. New perspectives on the management of penetrating trauma in proximity to major limb arteries. J Vasc Surg. Jan 1990;11(1):84-92; discussion 92-3. [Medline].
Durham JR, Yao JS, Pearce WH. Arterial injuries in the thoracic outlet syndrome. J Vasc Surg. Jan 1995;21(1):57-69; discussion 70. [Medline].
Eskandari MK, Yao JST. Occupational Vascular Problems. In: Rutherford RB, ed. Vascular Surgery, 6th ed. Philadelphia, Pa:. WB Saunders;2005, in press.
Halpin DP, Moran KT, Jewell ER. Arm ischemia secondary to giant cell arteritis. Ann Vasc Surg. - Moran KT;2(4):381-4. [Medline].
Kaar G, Broe PJ, Bouchier-Hayes DJ. Upper limb emboli. A review of 55 patients managed surgically. J Cardiovasc Surg (Torino). Mar-Apr 1989;30(2):165-8. [Medline].
Kline RM Jr, Hertzer NR, Beven EG. Surgical treatment of brachial artery injuries after cardiac catheterization. J Vasc Surg. Jul 1990;12(1):20-4. [Medline].
Landry GJ, Edwards JM, McLafferty RB. Long-term outcome of Raynaud''s syndrome in a prospectively analyzed patient cohort. J Vasc Surg. Jan 1996;23(1):76-85; discussion 85-6. [Medline].
McCroskey BL, Moore EE, Pearce WH. Traumatic injuries of the brachial artery. Am J Surg. Dec 1988;156(6):553-5. [Medline].
Mesh CL, McCarthy WJ, Pearce WH. Upper extremity bypass grafting. A 15-year experience. Arch Surg. Jul 1993;128(7):795-801; discussion 801-2. [Medline].
Nomura M, Kida S, Yamashima T. Percutaneous transluminal angioplasty and stent placement for subclavian and brachiocephalic artery stenosis in aortitis syndrome. Cardiovasc Intervent Radiol. Sep-Oct 1999;22(5):427-32. [Medline].
Peterson BG, Resnick SA, Morasch MD. Aortic arch vessel stenting: a single-center experience using cerebral protection. Arch Surg. 2006;141:560-564.
Peterson BG, Resnick SA, Morasch MD. Aortic arch vessel stenting: a single-center experience using cerebral protection. Arch Surg. 2006;141:560-564.
Phipp LH, Scott DJ, Kessel D. Subclavian stents and stent-grafts: cause for concern?. J Endovasc Surg. Aug 1999;6(3):223-6. [Medline].
Rodriguez-Lopez JA, Werner A, Martinez R. Stenting for atherosclerotic occlusive disease of the subclavian artery. Ann Vasc Surg. May 1999;13(3):254-60. [Medline].
Safran MR, Bernstein A, Lesavoy MA. Forearm compartment syndrome following brachial arterial puncture in uremia. Ann Plast Surg. May 1994;32(5):535-8. [Medline].
Yao JST, Flinn WR, McCarthy WJ. Upper extremity revascularization. In: Bergan JJ, Yao JST. Techniques in Arterial Surgery. Philadelphia, Pa:. WB Saunders, Co;1990:328-336.
Ziomek S, Quinones-Baldrich WJ, Busuttil RW. The superiority of synthetic arterial grafts over autologous veins in carotid-subclavian bypass. J Vasc Surg. Jan 1986;3(1):140-5. [Medline].
Further Reading
Keywords
upper extremity occlusive disease,upper extremity arterial disease, atherosclerosis, arteritis, fibromuscular dysplasia, Raynaud syndrome, cold sensitivity, Raynaud disease, subclavian artery stenosis, Takayasu arteritis, subclavian artery disease, acute arterial occlusion, brachial artery occlusion, digital gangrene, Buerger disease, fibromuscular dysplasia, digital artery occlusion, scleroderma, chondrocalcinosis, esophageal motility disorder, sclerodactyly, telangiectasia, CREST syndrome, mixed connective-tissue disease, hypersensitivity angitis, hypothenar hammer syndrome
