CHAPTER 10

Upper Extremity Arterial Occlusive Disease

Phyllis Gordon
Nancy Shebel

First Edition Author: Theresa Glessner

OBJECTIVES

Introduction

Upper extremity arterial occlusive disease is much less common than lower extremity disease (Eskandari, 2012). Although upper extremity ischemia is less prevalent that lower extremity ischemia, upper extremity impairment can be significantly devastating to those patients affected by its sequelae. Humans depend more on their upper extremities to carry out the activities of daily life than their lower extremities; therefore, a lower extremity amputation can be less debilitating than an upper extremity amputation. Although only about 5% to 10% of all embolic events involve the upper extremities, prompt diagnosis and treatment of upper extremity ischemia is paramount for limb salvage (Soloway, 2013).

I. Anatomy (see Chapter 3, Anatomy and Physiology of the Vascular System)

A. Subclavian Artery

1. Major blood supply of the upper extremities

2. As it passes over the first rib, it becomes the axillary artery

B. Axillary Artery

1. 15 cm long

2. Six major branches which serve as collaterals for the shoulder girdle

C. Brachial Artery

1. Extends from lower border of the teres muscle to its bifurcation at the head of the radius

2. Branches into the radial, ulnar, and interosseous arteries at the antecubital fossa

D. Radial and Ulnar Arteries (Mowlavi, 2012)

1. Supply most of the hand circulation

2. Supply palmar arch which supplies the fingers via the digital arteries; incomplete palmar arch supplied by the radial artery only is present in 20%

II. Pathophysiology

A. Vasculitis Fibromuscular Dysplasia and Atherosclerosis produce symptoms by narrowing or occlusion of the arterial lumen (Eskandari, Rowe, & Pearce, 2012; Mitchell & Schoen, 2010)

1. Atherosclerosis: local accumulation of lipids, initially seen as fatty streaks that progressively develop fibrous plaque and local hemorrhage, and ulceration that involve the intima with calcification of the media and loss of arterial wall elasticity. Similar to lower extremity disease (see Chapter 9, Lower Extremity Arterial Disease)

a. Diameter reduction of 50% or a cross-sectional area reduction of 70% represents a hemodynamically significant lesion (Mowlavi, 2012)

b. Lesions cause a pressure drop across the stenosis and exercise-induced fatigue in which demand for blood flow exceeds supply

c. Cool extremity and decreased peripheral pulses are manifested by intermittent claudication or pain with arm use

2. Vasculitic and inflammatory arteritis disorders: severe, chronic inflammatory process of the vessel wall with cellular infiltrates and eventual necrosis (Mitchell & Schoen, 2010)

a. Large group of systemic diseases; pathologic changes vary depending on disorder; underlying cause is unknown

b. Involvement of upper extremities is rare

c. Vascular lesions caused by deposits of fibrin or complement; infiltration by inflammatory cells and fibrous obliteration of the vessel

d. Inflammation may involve entire vessel wall or only some of the layers which results in diffuse or focal changes

e. When a vessel is destroyed by the inflammatory process, vasculitis is termed “necrotizing”

f. Buerger disease (thromboangiitis obliterans) (see Chapter 16, Buerger Disease). Inflammation progresses to all layers of the artery; lumen contains thrombus with fibroblasts and giant cells and is associated with young male smokers (Arkkila, 2006; Espinoza, 2009). The intima, media, and adventitia have varying amounts of thickening and inflammatory changes

3. Fibromuscular dysplasia (FMD) (Rice & Armstrong, 2009)

a. Has been found in all peripheral arteries; it occurs rarely in the upper extremity, it is more common in internal carotid artery, but may affect the vertebral arteries

b. Long areas of smooth narrowing, intimal hyperplasia (not the usual ‘‘string of beads’’ as in renal FMD) with subtypes of either intimal, medial, or perimedial dysplasia; intimal hyperplasia most common

c. Usually asymptomatic but can lead to focal stenosis and dilation, may cause a variance in blood pressure between limbs, or ischemia

d. Limited data; seems to affect women more than men

e. Diagnosed by angiogram (Eskandari et al., 2012)

f. Treatment reserved for symptomatic patients

4. Vasospastic disorders (e.g., Raynaud disease): symptoms of pallor alternating with cyanosis and hyperemia of the fingers are related to episodic vasospasm (see Chapter 17, Raynaud Phenomenon)

B. Acute Arterial occlusion caused by embolus, thrombus, or trauma causes tissue perfusion to drop below a critical threshold level, which in turn causes persistent pain and tissue necrosis

1. Limb pressure <30 mm Hg

2. No Doppler signal in the digital vessels (Eskandari et al., 2012)

C. Neurovascular compression of neurovascular bundle supplying the upper extremity and/or compression of the subclavian vasculature (arterial or venous) is referred to as thoracic outlet syndrome (see Chapter 18, Thoracic Outlet Syndrome)

D. Aneurysms of Axillosubclavian Systems and Distal Arteries in the forearm or hand (Magishi, Izumi, & Shimizu, 2010)

1. Rare; data limited but have common features

2. Rupture rare, but usually fatal when rupture occurs

3. Depending on size, rate of expansion, and location of aneurysm, may have symptoms of nerve, tracheal, esophageal, or venous compression

4. Treated to prevent distal embolization and thrombosis. Most threatening aspect of aneurysms is the tendency for emboli or thrombus to cause end-organ ischemia and infarction

E. Congenital or Acquired Arteriovenous Fistulae or Malformations; direct communication between an artery and vein tend to enlarge over time

1. Congenital malformations; several types of lesions

a. Arteriovenous fistulae

b. Tumor-like growths (e.g., hemangiomas: arterial, venous, capillary, or mixed; also termed cavernous hemangioma)

c. Angiodysplasias: various forms of abnormal growth of vessels

d. Benign and malignant tumors: hemangiosarcomas, lymphosarcomas, and any large vessel tumors

2. Acquired arteriovenous fistulae: hemodialysis fistulae or trauma, including iatrogenic injuries (see Chapter 15, Vascular Access)

F. Degenerative Arteriopathies: Congenital or Acquired

1. Abnormalities in collagen or elastic tissue of vessel wall

2. May result in aneurysm formation or dissection of arteries in upper extremity (e.g., Marfan syndrome)

III. Etiology/Precipitating

A. Emboli/Thrombus: thromboemboli of the upper extremity can occur from a variety of sources (Mowlavi, 2012; Weinberg, 2011); however, Licht, Balezantis, Wolff, Baudier, and Røder (2004) found that in 37% of acute ischemic cases, the cause was unknown

1. Most often originate from the heart or great vessels

2. Site can be left atrium, as in atrial fibrillation, or from injured ventricular endothelium after myocardial infarction

3. Other cardiac conditions predisposing to emboli: cardiomyopathy, congestive heart failure (CHF), rheumatic valvular disease, cardioversion, prosthetic valves, cardiac surgery or catheterization, vegetations associated with endocarditis and atrial myxoma

4. May be precipitated by progressive arterial atherosclerosis similar to lower extremity disease

5. Other noncardiac etiologies of emboli: aneurysm of ascending aorta, arch, subclavian artery, complicated aortic plaques, sepsis, peripherally inserted arterial lines, or percutaneous procedures

B. Atherosclerosis

1. Similar etiology to lower extremity or cerebrovascular atherosclerosis

2. Exact cause remains undefined but related to known risk factors: smoking, hypertension, hyperlipidemia, sedentary life style, obesity, diabetes mellitus, age, male gender, and heredity

3. Considerably less common than in lower extremities (Eskandari, 2012)

4. Confined predominantly to the origins of the vessels

5. Lesions may be stenotic or occlusive

6. Symptomatic upper extremity arterial occlusive disease is present in less than 5% due to the abundant collateral network and the infrequency of atherosclerosis in the upper extremity (Eskandari, 2012). Upper extremity claudication may manifest as tired, heavy or painful limb, with or without cyanosis of digits (see IV Assessment, C. Patient History, 1. Subjective findings)

7. Most common site of occlusion is the left subclavian artery, causing a subclavian steal

a. Blood flow to arm is maintained via reversal of flow through left vertebral artery

b. Right vertebral flow enters Circle of Willis; blood is directed to basilar artery and then into vertebral on left

c. Patients seldom have cerebral symptoms (vertigo, visual disturbances or drop attacks) unless there is co-existing carotid stenosis

d. Collateral flow to left arm usually limits ischemic symptoms but patients are at risk for embolization to digits

C. Traumatic Vessel Wall Injury: leading cause of upper extremity ischemia

1. Result of acute trauma or repetitive motion trauma: penetrating or blunt injuries, crush injuries, frostbite, procedures that require an arterial puncture

a. Penetrating injuries: gunshot or knife wounds, lacerations

b. Blunt injuries: clavicular fractures, shoulder or elbow dislocations, humeral fractures

c. Crutches: prolonged use may lead to axillary artery trauma, thrombosis, or aneurysm formation

2. Acute traumatic vessel injuries need to be rapidly diagnosed and treated to prevent limb loss or death secondary to hemorrhage (Higgin & McClinton, 2010)

a. Compartment syndrome: elevated intracompartmental pressures caused by acute swelling within osteofascial compartments in response to sudden injury or reperfusion following intervention (see Chapter 9, Lower Extremity Arterial Disease)

3. Chronic vibration trauma secondary to prolonged use of vibratory tools (e.g., jackhammer or chainsaw) (Eskandari et al., 2012)

a. Pathologic changes in small arteries: hypertrophy of the intima and media, smooth muscle cells, sympathetic overactivity, and endothelial damage (Shepherd, 2005)

b. Increased blood viscosity (reason unclear)

c. Changes result in vessel narrowing, lumen obstruction, vasospasm, and thrombosis

d. Similar small vessel problems are also seen in typists, piano players, baseball and hockey players, or any occupation or hobby that requires excessive use of hands

4. Hypothenar hammer syndrome: use of heel of hand to hammer, push, or twist objects leads to ulnar artery thrombosis or aneurysm formation with embolization and ischemia of digits (Mowlavi, 2012; Nitecki, Anekstein, Karram, Peer, & Bass, 2008)

5. Iatrogenic trauma to subclavian, axillary, brachial, or radial artery during diagnostic or therapeutic interventions (Soloway, 2013)

a. Arterial thrombosis, hemorrhage, or embolization may result

b. Cardiac catheterization by way of the brachial artery is common if patient has significant lower extremity atherosclerosis

c. Bleeding into axilla following arteriography may lead to nerve compression

d. May result from cannulation of the radial or brachial artery in the presence of an incomplete palmar arch

e. Hand ischemia caused by dialysis access grafts: surgical injury, embolization, pseudoaneurysm formation, infection or mycotic aneurysm at anastomosis sites

6. Post-traumatic pain syndrome and neuropathies (Gradl & Rommel, 2007)

a. Reflex sympathetic dystrophy (RSD) and post-traumatic pain syndrome

1) Severe pain syndrome following trauma, often with peripheral nerve injury and/or ischemia as inciting event. Exact cause may be difficult to identify

2) Three stages of RSD (symptoms vary and do not always progress):

a) Acute stage: burning, redness, swelling, sweating, and extreme tenderness; reversible; may resolve spontaneously

b) Dystrophic stage: coolness, cyanosis, brawny edema, continuous pain

c) Atrophic stage: increased severity of pain affecting other limbs or body areas, skin atrophy, muscle wasting, digital ulcerations, advanced demineralization of bones with joint contractures and ankylosis

3) Mimics nerve entrapments, Raynaud syndrome, arterial ischemia, thoracic outlet syndrome

4) May respond to sympathetic nerve block, antidepressants (amitriptyline) or antiseizure medication (gabapentin)

b. Ischemic monomelic neuropathy: rare; pain syndrome associated with acute ischemic injury to arm manifested as ‘‘multiple axon-loss mononeuropathies distally in the limb without muscle necrosis’’ (Andary, Mahal, & O’Conner, 2011)

1) Most often seen in diabetic renal failure patients after insertion of hemodialysis graft

2) Symptoms: numbness, dysesthesias, burning continuous pain with mild motor weakness and loss of coordination; symptoms persist even after correction of cause for ischemia

D. Inflammatory or Immune Arteritis (see Pathophysiology)

1. Classified according to small, medium, or large vessel involvement

2. Small vessel arteritis (Mitchell & Schoen, 2010)

a. Etiology thought to be autoimmunity for most disorders

b. Frequently associated with rheumatoid disorders (e.g., systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis, mixed connective tissue disorders, scleroderma)

c. Erythema nodosum or hypersensitivity angiitis may develop spontaneously or be related to other systemic disorders

d. Medications or circulating factors such as cryoglobulins, hepatitis A or B antigens, or tumor antigens may precipitate vasculitis manifested by arterial thickening, connective tissue swelling, and vascular occlusion

e. Skin and joints most often involved; fingers and hands most often affected but entire limb may be symptomatic

f. Signs and symptoms: urticaria, rashes, livedo, purpura, Raynaud phenomenon, hemorrhage, infarction, ulceration, gangrene

3. Medium vessel arteritis (Mitchell & Schoen, 2010)

a. Polyarteritis nodosa: idiopathic and autoimmune focal, transmural inflammation of small and medium vessels which may lead to necrosis, thrombosis, and aneurysm formation; predominately affects renal and visceral vessels such as hepatic and mesenteric circulation; affects older patients; affects males twice as often as females (Mitchell & Schoen, 2010)

b. Other diseases which rarely affect upper extremity: Wegener granulomatosis, Kawasaki disease, Churg–Strauss syndrome cause necrosis and gangrene of skin and may be associated with neuropathy

4. Large vessel and giant cell arteritis (Mitchell & Schoen, 2010)

a. Takayasu arteritis: focal granulomatous and nongranulomatous inflammation involving entire vessel wall thickness with disruption of elastic fibers; usually involves aorta and branches; both stenoses and aneurysms common, subclavian artery most common site of stenosis; affects younger (<40 years) Asian women with 6:1 female:male ratio (Roberts, Rossmann, & Ahmed, 2011)

b. Temporal or systemic giant cell arteritis: similar pathology to Takayasu but generally less severe; most commonly involves branches of carotid but can affect any vessel; usually affects women >50 years (Mowlavi, 2012; Ramachandran & Ramachandran, 2012)

c. Usual symptoms: arm claudication, rest pain, skin breakdown; aneurysm of brachiocephalic vessels

d. Other conditions: Behcet syndrome, Cogan syndrome, relapsing polychondritis, and other arthropathies

E. Buerger Disease (Thromboangiitis Obliterans): disease entity with features of severe atherosclerosis and inflammatory changes of distal vessels (Arkkila, 2006; Higgin & McClinton, 2010) (see II, Pathophysiology, and Chapter 16, Buerger Disease)

1. Initially affects small and medium vessels, then large vessels, as well as veins and nerves

2. Rarely has systemic manifestations; only affects blood vessels of extremities

3. Superficial thrombophlebitis and venous changes usually only involve lower extremities

4. Clinical features of atherosclerosis but more severe; gangrene with amputation (both surgical and auto-amputation) of digits, hands, and arms not unusual

5. Cause is unknown but tobacco use plays a critical role

6. Affects predominately young men of 35 years or below

F. Aneurysms (Menard & Belkin, 2009)

1. Relatively rare

2. Brachiocephalic: atherosclerosis, trauma or infection

a. Prior to antibiotics, mycotic aneurysms related to syphilis were the most common type; now source of infection is IV drug use or infected arterial puncture

b. Less common etiologies: FMD, medial degeneration, arteritis, congenital

3. Axillosubclavian: etiology predominately from atherosclerotic changes or traumatic injury, especially first rib trauma; remainder related to lesser causes

a. Chronic injury from cervical rib or fibrous band at thoracic outlet

b. Improper crutch use

c. Aberrant right subclavian artery

d. Other less common etiologies: FMD, arteritis, infection, medial degeneration, arteritis, congenital anomalies

e. 30% to 50% of patients with axillary aneurysms have other associated aneurysms

4. Other distal sites: rare and related to trauma, infection, or dialysis access

G. Genetic Degenerative Arteriopathies result from an imbalance of elastin and the lack of collagen in the vessel walls as the aneurysm grows (Mitchell & Schoen, 2010)

1. Marfan syndrome

a. High incidence of aortic dilatation, dissection, and rupture; high mortality without early surgical intervention

b. Aneurysms of proximal major upper extremity vessels may occur

2. Ehlers–Danlos syndrome: rare; arteries occlude by rupture with thrombosis or aneurysm with embolization; affects younger patients; diagnosed by clinical presentation involving skin, eyes, and musculoskeletal defects

3. Pseudoxanthoma elasticum: rare; chronic occlusion of the forearm, thigh, and calf arteries with skin changes

H. Hypercoagulable State (see Chapter 19, Superficial Thrombophlebitis and Deep Vein Thrombosis)

1. Most commonly an inherited disorder that causes intravascular coagulopathy (Factor V Leiden mutation or prothrombin gene mutation) or dysproteinemia (Protein C or S); also problematic for patients with thrombocytosis or polycythemia (Mitchell, 2010)

2. May have history of DVT or other manifestations of clotting disorder

3. Increased risk in patients with malignancy; cause uncertain

IV. Assessment

A. Risk Factors (usually related to risk of inflammation and/or thrombus production)

1. Personal history of atrial fibrillation, CHF, recent myocardial infarction, recent cardiac surgical intervention

2. Recent arterial diagnostic or monitoring procedure

3. History of atherosclerosis, previous graft problems, or infections

4. Cardiac valve prosthesis

5. Social history of injection of drugs

6. Occupational history of repetitive trauma to the hand by blunt or vibratory mechanisms or high-risk occupations for limb trauma (e.g., farmer or lumberjack)

7. Risk factors for atherosclerosis: tobacco use, hypertension, diabetes, lipid disorders, male gender, advancing age, heredity, obesity

8. Sensitivity to cold, familial history of connective tissue disorders or hypercoagulable disorders

9. Hemodialysis with upper extremity arteriovenous fistula

10. Personal history of irradiation

B. Primary Prevention

1. Smoking cessation

2. Blood pressure and lipid control

3. Public education

a. Awareness of risk factors

b. Promotion of a healthy lifestyle; weight management, exercise

c. Risks of occupational exposure to blunt or vibratory mechanisms of trauma

4. Professional college education: appropriate technique for arterial puncture and care of catheters, as well as cannulation of dialysis access grafts

5. Assess for presence of risk factors

6. Familial coagulation studies if positive family history

C. Patient History

1. Subjective findings: influenced by level and severity of stenosis and occlusion and presence of arterial collaterals

a. Claudication: arm fatigue, pain or cramping with exercise

b. Rest pain involving the hand or digits

c. Color changes in arm or hand

d. Acute or chronic arm pain

e. Arm and/or hand feel cold intermittently or continuously

f. History of trauma

2. Objective findings

a. Fever

b. Unequal blood pressures in arms

c. Signs of trauma to arm or hand

d. Family history of hypercoagulable state

e. Recent MI, CHF, coronary or valve surgery

f. Medication history: use of vasoconstrictors, ergot alkaloids, dopamine

3. Social history

a. Occupation: repetitive lifting, use of vibratory equipment, high risk for traumatic injury

b. Tobacco use: duration, amount per day, type

c. Illicit drug use

d. Social support system and living situation, especially if at risk for amputation

D. Physical Examination

1. Inspection of affected upper extremity

a. Skin: cool, mottled, blanching, erythema or purple discoloration of arms and or fingers; fingers may have ulcerative lesions or gangrene; punctate lesions on fingertips; tight, shiny, or atrophic skin on fingers and arms

b. Cardiovascular: prominent arm veins, supra- or infraclavicular pulsatile mass; if there is trauma bleeding will be observed and must be controlled

c. Neuro: loss of sensation and movement in affected extremity

d. Upper extremity: muscle atrophy, swelling, or edema

e. Measurement of upper arm circumferences

2. Palpation of the upper extremity

a. Pulses in the carotid, axillary, brachial, radial, and ulnar arteries should be palpated; assess for pulsatile mass or enlarging hematoma over vessel

b. Note pulse strength, tortuosity of the vessel, and any aneurysmal dilation of the artery

c. An Allen test will indicate patency of the palmar arch: radial and ulnar arteries are compressed while patient clenches fist to empty blood from hand; hand is opened and appears pale and mottled. If palmar arch patent, release of pressure over one vessel restores normal color immediately; if radial artery diseased, color does not return until ulnar artery released; if ulnar artery diseased, color returns when radial artery released

d. Adson maneuver (loss of radial pulse upon abduction and external rotation of the upper extremity and/or rotation of the head to the ipsilateral side) for thoracic outlet obstruction. Maybe used in assessing for thoracic outlet syndrome; however, not a strong indicator (see Chapter 18, Thoracic Outlet Syndrome) (Eskandari et al., 2012)

e. Presence and amount of edema

f. Skin color, temperature, capillary refill of the digits

g. Tight, swollen upper extremity may be an indication of compartment syndrome; compartment pressure may need to be measured

3. Auscultation

a. Blood pressure measurements in both upper extremities

b. Should be performed over the subclavian, axillary, and brachial arteries to reveal bruits which indicate areas of stenosis (Eskandari et al., 2012)

c. Cardiac: murmur, rub, arrhythmia

d. Pulmonary: breath sounds; rales, diminished lung sounds, pleural friction rub

e. Dialysis grafts: presence of appropriate bruit

4. Complete physical examination (especially cardiac and lower extremity) to assess for presence of systemic atherosclerosis, infection, or inflammatory disease as indicated

E. Considerations Across the Lifespan

1. Young adulthood: contact sports, illicit drug injection, congenital anomalies, cardiomyopathy, CHF

2. Women of childbearing age: hypercoagulable disorder, cardiac arrhythmias, illicit drug use, planned pregnancy if using warfarin for anticoagulation, pregnancy-induced CHF or cardiomyopathy, increase in autoimmune diseases in this age group

3. Elderly: cardiac arrhythmias, subtherapeutic warfarin doses secondary to poor nutritional status or multiple drug interactions, trauma from falls, incidence of atherosclerosis increases with advancing age (Eskandari et al., 2012)

V. Pertinent Diagnostic Testing

A. Laboratory Tests

1. Chest x-ray

a. Important to identify enlarged heart, heart failure

b. Prominent lung markings

c. Atelectasis, infiltrates or effusions associated with CHF

d. Bony structure anomalies or injuries causing vascular compression

2. Electrocardiogram

a. Assesses for arrhythmia or MI

b. If arrhythmia new, will need to be evaluated for possible MI

3. Echocardiogram: assesses for valve disease, cardiac enlargement and chamber function

4. Transesophageal echocardiography (TEE) is performed in patients with a peripheral embolus suspected of originating from a cardiac source. TEE can be used to assess plaque in the ascending aorta as a source of the emboli or determine the presence of a right-to-left shunt through which paradoxical emboli might travel (Eskandari et al., 2012)

5. Complete blood cell count (CBC), platelet count, sedimentation rate, antinuclear antibody (ANA), rheumatoid factor for possible inflammatory or infectious origin, disease-directed laboratories as appropriate

6. Preoperative laboratories for acute ischemia or trauma: CBC, electrolytes, type and crossmatch, consider troponin, creatine kinase, and urine myoglobin if patient has been immobile for a prolonged period of time

7. Hypercoagulable workup: CBC with platelet count, fibrinogen, prothrombin level, partial thromboplastin level, protein C deficiency, protein S deficiency, factor V Leiden mutation, prothrombin gene mutation, antithrombin III deficiency, antiphospholipid antibody/anticardiolipin antibody, and homocysteine level

8. Laboratory evaluation for atherosclerosis: glucose, lipid profile, creatinine and blood urea nitrogen, electrolytes, urinalysis, calcium, phosphorus, possibly homocysteine, high-sensitivity C-reactive protein

B. Noninvasive Vascular Laboratory Studies; perform on both arms for comparison (Gerhard-Herman et al., 2006)

1. Segmental arterial pressures

a. Pressures taken in the brachial, radial, ulnar, and palmar arch vessels

b. Pressure in one arm compared to pressure in opposite arm

c. An abnormally large pressure gradient (>20 mm Hg) between any two segments indicates disease (Eskandari et al., 2012)

d. Wrist/brachial Index <0.65 begin to be symptomatic

2. Finger pressures

a. Finger cuff used, with a Doppler probe to measure systolic pressure

b. An absolute finger pressure <70 mm Hg is considered abnormal (Mowlavi, 2012)

3. Doppler flow studies

a. Subclavian, axillary, brachial, radial, ulnar, and digital arteries may be examined and analog waveforms recorded at each site

b. Waveforms will change from triphasic to blunted or monophasic at the level of obstruction

c. May perform Allen test while obtaining waveforms to document palmar arch status and vessel dominance or evidence of thoracic outlet obstruction respectively (see IV Assessment, palpation)

d. Duplex scanning will aid in diagnosis of the more proximal vessels.

4. Duplex and color flow scanning

a. Color flow scanning facilitates more accurate identification and location of vessels as well as visualization of aneurysms, pseudoaneurysms, or arteriovenous malformations

b. Arterial flow is normally red; venous flow is blue

c. Absence of color in an artery clearly visualized on B-mode scanning is diagnostic of occlusion; a color shift from red to white identifies stenotic sites with turbulent flow (Eskandari, 2012) (see Fig. 10-1)

d. Hemodialysis graft flow with Doppler velocity recordings from the proximal anastomosis to the distal and measurements of vein diameter. Assessment of the inflow and outflow vessels and allows anatomic visualization (Eskandari, 2012)

FIGURE 10.1  Arterial duplex.