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Dynamic MR Angiography of Upper Extremity Vascular Disease: Pictorial Review¹

¹ From the Department of Radiology, 560 First Avenue, TCH-HW-202, New York University Medical Center, New York, NY 10016 (F.S., E.M.H., R.R., B.T., M.K., V.S.L.), and Huntingdon Valley Orthopedics, Meadowbrook, Pa (L.E.H.). Presented as an education exhibit at the 2006 RSNA Annual Meeting. Received July 16, 2007; revision requested September 12; revision received and accepted September 27. Address correspondence to the author (email: hechte01{at}med.nyu.edu).

	Abstract

Top Abstract Introduction Imaging Techniques Imaging Protocols Basic Anatomy Upper Extremity Disease Hand Vasculitides Artifacts and Pitfalls Conclusion References

 
Unlike peripheral lower extremity vascular disease, upper extremity vascular disease is relatively uncommon. While atherosclerosis and embolic disease are the most common causes of upper extremity ischemia, a wide variety of systemic diseases and anatomic abnormalities can affect the upper extremity. Upper extremity ischemia poses a significant diagnostic and therapeutic challenge for both clinicians and radiologists. Although history and physical examination remain the mainstays of diagnosis, imaging can be vital in confirming suspected disease and guiding treatment planning. Digital subtraction angiography is often the preferred method for detection of upper extremity vascular disease, particularly for characterization of complex arteriovenous anatomy such as in vascular malformations and for evaluation of dialysis fistulas and grafts. However, this modality is invasive, requires iodinated contrast agents and radiation, and may fail to demonstrate significant extraluminal disease. More recently, magnetic resonance (MR) angiography techniques have made important advances, permitting higher temporal and spatial resolution that is preferable for diagnosing upper extremity vascular disorders. In this review, the authors present an overview of upper extremity MR angiography techniques and protocols, revisit the often variable vascular anatomy of the arm and hand, and offer examples of various pathologic entities diagnosed with MR angiography. Finally, several imaging pitfalls that one must be aware of for accurate diagnosis are illustrated and reviewed.

	Introduction

Top Abstract Introduction Imaging Techniques Imaging Protocols Basic Anatomy Upper Extremity Disease Hand Vasculitides Artifacts and Pitfalls Conclusion References

 
Vascular disorders of the hand and upper extremity encompass a broad spectrum of diseases ranging from acute limb-threatening ischemia to chronic disabling disease. Although less common than lower extremity vascular disease, upper extremity disease affects as much as 10% of the population (1). Familiarity with normal vascular anatomy, the common pathologic entities that affect the upper extremity, and pitfalls of magnetic resonance (MR) angiography of the upper extremity is important to ensure optimal image quality and accurate interpretation.

MR angiography, unlike digital subtraction angiography (DSA) or computed tomographic (CT) angiography, offers a noninvasive approach to diagnosis and treatment planning, eliminating the need for ionizing radiation and substantially decreasing the risks of allergic reactions to contrast agents and nephrotoxicity. Over the last few years, MR angiography has emerged as an alternative to DSA for diagnostic imaging in patients with upper extremity symptoms and for serial follow-up, particularly for younger patients. However, imaging small-caliber peripheral vessels, especially in the wrist and hand, presents a challenge. For optimal imaging, protocols should be tailored for specific clinical concerns and symptoms. Advances in MR hardware and software are also required to improve image quality.

The angiographic effect in MR imaging is created in a variety of ways, including techniques without contrast agent enhancement such as time-of-flight and phase-contrast angiography, or with contrast-enhanced MR angiography using a gadolinium chelate agent. The non–contrast agent techniques exploit the dynamic nature of flowing blood and produce bright-blood images. However, these techniques are time-consuming and often overestimate stenosis, especially in the setting of complex anatomy, tortuous vessels, and abnormal blood flow. Other non–contrast agent techniques are actively being explored, such as three-dimensional (3D) electrocardiograph-triggered half-Fourier fast spin echo, but are beyond the scope of this review article (2,3). Contrast-enhanced MR angiography has emerged as a robust and reliable alternative to flow-dependent imaging techniques and can be performed in seconds rather than minutes. Contrast between blood vessels and background is achieved by shortening the T1 relaxation time of blood with a paramagnetic contrast material. However, one of the greatest challenges of contrast-enhanced MR angiography is achieving optimal timing of the contrast agent bolus and limiting venous contamination. In the peripheral extremities, timing of the bolus is particularly challenging. Test bolus timing examinations and bolus tracking techniques may be limited because small vessel opacification may be obscured by inflow effects.

Recent advances in contrast-enhanced MR angiography techniques such as keyhole and parallel imaging permit higher temporal resolution. Multiple 3D volume data sets may be acquired sequentially, revealing not only conventional anatomic imaging but adding a fourth dimension (ie, temporal data to anatomic imaging). With four-dimensional MR angiography, the hemodynamics of complex upper extremity vascular disease may be revealed without compromising spatial resolution.

In this review, MR angiography techniques and protocols, normal vascular anatomy, and MR angiographic findings of common disease entities of the upper extremity are discussed along with pitfalls of MR angiography.

	Imaging Techniques

Top Abstract Introduction Imaging Techniques Imaging Protocols Basic Anatomy Upper Extremity Disease Hand Vasculitides Artifacts and Pitfalls Conclusion References

 
In this section, the most commonly used imaging sequences, time-of-flight (TOF) and contrast-enhanced MR angiography, are introduced together with a brief description of innovations that can be applied to upper extremity imaging, namely parallel imaging and time-resolved gadolinium contrast-enhanced MR angiography. Please note that the use of a gadolinium chelate for MR angiography is considered an "off label" use of this pharmaceutical.

TOF MR Angiography
TOF MR angiography is based on the principle that fresh blood flowing into an imaging section has higher signal intensity than the partially saturated stationary tissue within that section. This is known as the "inflow phenomenon." This mechanism of vascular enhancement is based on the time it takes for blood to flow into an imaging section (4). The signal difference between the protons in flowing blood and those in background tissue in these gradient-echo sequences is accentuated by increasing the flip angle of the radiofrequency pulse.

Advantages

Blood flow dependent.

No intravenous contrast agent required.

May be used to assess direction of blood flow. Selective imaging of arterial or venous blood vessels may be performed by placing a saturation band above or below the section plane.

Disadvantages

Long acquisition time.

Overestimates stenoses in regions of complex flow or in vessels flowing parallel to the section plane (in-plane saturation effect).

Obscures retrograde arterial flow when performed with venous saturation bands.

May be limited by artifacts such as the ghosting artifact caused by triphasic pulsatile flow.

May be limited by artifacts related to calcifications, metallic devices, and stents.

Contrast-enhanced MR Angiography
Unlike TOF MR angiography, contrast-enhanced MR angiography does not rely on blood flow but on the T1 shortening of blood by an intravenous gadolinium chelate agent. This allows considerably faster acquisition of data. Accurate timing of the contrast agent bolus is required to capture the arterial phase and reduce venous contamination (5). Fast interpolated 3D acquisitions permit near isotropic acquisitions that can improve depiction of complex vascular anatomy.

Advantages

Not dependent on blood flow.

High temporal and spatial resolution may be achieved.

Minimal flow-related artifacts.

Arteriography and venography may be performed, depending on the timing of the contrast agent bolus.

Disadvantages

Requires adequate intravenous access.

Risks associated with gadolinium administration (particularly in patients with underlying renal disease) (6).

May be limited by artifacts related to calcifications, metallic devices, and stents and by signal loss due to high gadolinium chelate concentrations at which T2* effects may dominate.

Parallel Imaging
In the past, to localize MR signal, only phase- and frequency-encoding gradients were used. However, the strength of a signal detected by one coil versus that detected by another can also be used for spatial localization. In parallel MR imaging, spatial information is determined by that method (7). Phase-encoding lines in k-space are undersampled and data is recovered by using coil sensitivity information. This requires multiple coils overlying the patient in the phase-encoding direction, each with a separate receiver channel. The most common techniques include sensitivity encoding (SENSE) (8) and simultaneous acquisition of spatial harmonics (SMASH) (9). Combining these techniques with 3D contrast-enhanced MR angiography can improve both temporal and spatial resolution. In addition, these techniques require a computer system that is able to handle reconstruction of large data sets in an efficient manner. Parallel imaging does result in lower image signal-to-noise ratios, and artifacts such as wraparound artifact may be seen, particularly when used with a rectangular field of view.

Time-resolved, or Four-dimensional, MR Angiography
Also known as keyhole imaging or time-resolved echo-sharing MR angiography, techniques such as time-resolved imaging of contrast kinetics (TRICKS)(10) help achieve high temporal resolution without compromising spatial information.Echo-sharing techniques save time by not sampling all the high spatial frequencies (periphery of k-space); instead they share k-space lines from one 3D data set to another. This results in a substantial increase in the frame rate of a multimeasurement acquisition.

How Is This Implemented in Clinical Practice? With contrast-enhanced approaches, a modified 3D spoiled gradient-echo sequence with parallel and/or keyhole imaging techniques is used to achieve a high temporal frame rate for four-dimensional MR angiography. An initial mask, a data set obtained before contrast agent administration, is obtained for subtraction from contrast-enhanced data sets. The sequence is then repeated multiple times after administration of contrast agent to get snapshots of the vascular system at multiple time points. This allows visualization of, for example, the gradual enhancement of small, diseased vessels or vessels that are reconstituted by collateral vessels.

Advantages

-Both morphologic and kinetic information are obtained.

-May obviate a test dose timing study, but also can be used to determine patient circulation time for subsequent pre- and postcontrast MR angiography.

-A low dose (<0.1 mmol/kg) of contrast agent can be used.

-Can combine echo-sharing techniques with parallel imaging to further reduce imaging time.

Disadvantages

-Adequate intravenous access and contrast agents are still necessary.

-Large volume of data is acquired.

-Imaging artifacts such as ringing can occur because of differences in concentration of contrast agent when the center and peripheral portions of k-space are acquired, leading to discontinuities in k-space.

-May be limited by the same artifacts as in routine contrast-enhanced MR angiography.

The Table summarizes the contrast mechanisms and advantages and disadvantages of the three imaging techniques.

	Imaging Protocols

Top Abstract Introduction Imaging Techniques Imaging Protocols Basic Anatomy Upper Extremity Disease Hand Vasculitides Artifacts and Pitfalls Conclusion References

Imaging techniques: Use parallel imaging and/or echo-sharing techniques to improve both temporal and spatial resolution. Breath-hold imaging is required for thoracic imaging.

Contrast agent: A 0.1–0.2 mmol/kg dose of gadolinium chelate is injected at 2 mL/sec. For studies requiring two separate injections, the dose for the first study should be less than that for the second; for example, 0.08 mmol/kg followed by 0.12 mmol/kg. If symptoms are unilateral, inject contrast agent into the contralateral arm to avoid artifacts due to high concentrations of gadolinium chelate during the initial infusion. For the same reason, when performing direct MR venography, dilution of the contrast agent is recommended. When performing time-resolved MR angiography, a shorter duration of contrast agent injection should be considered because there is no advantage to injecting over a longer period than the duration of the acquisition. This is most commonly achieved by using a lower dose of gadolinium chelate for time-resolved imaging or injecting at a higher rate, but the latter may be difficult to achieve in patients with limited venous access.

Positioning:

Mark site of clinical concern to ensure adequate coverage.

For upper arm imaging, the patient should be supine with arm to the side in anatomic position. If patient is thin, move patient to the side and try to position the arm of interest closer to the center of the magnet bore.

For imaging of the hand and forearm, a "Superman" position (patient prone with arms extended) may be preferable to avoid wraparound artifact, although the supine position may be satisfactory. Patient comfort is important to ensure that there is no motion and that the patient will complete the examination.

Postprocessing and image interpretation:

Subtraction is useful but can lead to overestimation of stenoses.

Complex subtraction of Fourier data is better than magnitude subtraction and should be used when available.

Always check source images rather than subtracted images for better assessment of degree of stenosis and for evaluation of extraluminal disease.

Cross-sectional imaging with a nonangiographic sequence such as a fat-suppressed two-dimensional or 3D T1-weighted gradient-echo sequence is important to exclude extraluminal or venous disease. .

Protocols
In the present study, all MR imaging was performed on a 1.5-T Symphony or Avanto system (Siemens Medical Systems, Erlangen, Germany) with eight or 32 radiofrequency receivers, a maximal gradient amplitude of 40 or 45 mT, and slew rates of 125 or 200 T/m/sec, respectively. A six-element body array coil was placed over the patient’s chest and arm of interest anteriorly, and posterior spine array coils were used on the Symphony system. Two six-element coils were used anteriorly to maximize the field of view, as well as multielement spine coils (up to eight elements).

The MR angiographic sequences included conventional coronal or coronal-oblique high-resolution imaging with a 3D spoiled gradient-echo sequence with a repetition time (msec)/echo time (msec) of 3.4–4.5/1.1–1.3, 25° flip angle, 400–500-mm rectangular field of view, 448 x 512 matrix; and parallel imaging using generalized autocalibrating partially parallel acquisition (GRAPPA) with an acceleration factor of 2–3 in the left-to-right direction, interpolated section thickness of 1.0–1.7 cm, and an acquisition time of 17–20 seconds. A timing run was performed at the level of the descending thoracic aorta using 1 mL of an intravenous gadolinium chelate followed by a 20-mL saline infusion at a rate of 1.5–2.0 mL/sec. Once the patient’s circulation time was determined, the imaging delay was calculated by using the patient’s circulation time, the rate and volume of contrast agent injection, and the time to reach the center of k-space (11).

Typical imaging parameters for the dynamic coronal or coronal-oblique time-resolved 3D spoiled gradient-echo sequence were as follows: 3.5/1.2, 25° flip angle, 300–500-mm field of view, 384–448 x 160–250 matrix, parallel imaging using GRAPPA with an acceleration factor of 2–3 in the left-to-right direction and/or echo sharing using a time-resolved echo-sharing angiographic technique (TREAT) or time-resolved angiography with interleaved stochastic trajectories (TWIST), 1.2–1.7-mm section thickness, and acquisition time of 3–9 seconds with 8–12 data sets acquired consecutively. No fat saturation was used to keep acquisition time to a minimum, but a mask unenhanced data set was acquired initially with matching parameters for subtraction. No timing run is needed, although an empiric 5–10-second delay may be useful to reduce the number of unenhanced data sets.

An axial 3D fat-suppressed gradient-echo sequence was also performed with the following parameters: 3.5/1.5, 12° flip angle, 400–500-mm field of view, 256–320 x 86–156 matrix, 2–3-mm interpolated section thickness, 350–480-mm slab thickness, a parallel imaging factor of 2 in the anteroposterior direction, and an acquisition time of 15–20 seconds.

Proximal Upper Extremity (eg, Subclavian) Disease Positioning: Place patient in supine position in magnet with arm at side.

Sequences:

• Axial single-shot fast-spin-echo (SSFSE) sequence through chest and upper extremity.
  
• Precontrast coronal 3D T1-weighted spoiled gradient-echo MR angiography sequence.
  • Timing run with single section placed at the level of the descending thoracic aorta, or automatic bolus tracking.
    
  • Postcontrast (two measures back to back for arterial and early venous imaging) coronal 3D T1-weighted spoiled gradient-echo MR angiography sequence.
    
  • Postcontrast axial 3D T1-weighted fat-saturated spoiled gradient-echo acquisition to exclude extraluminal disease.
    
  
  

If subclavian steal syndrome is suspected, a two-dimensional TOF sequence in the neck (five to six sections), with a saturation band placed above and then below the imaging slabs to assess direction of flow in the vertebral arteries, may be used. Alternatively, two-dimensional phase-contrast or time-resolved imaging may be used for this purpose.

If vasculitis is suspected, a fat-suppressed T2-weighted sequence such as an inversion-recovery fast-spin-echo sequence in addition to the postcontrast T1-weighted gradient-echo sequence is recommended to examine for mural disease.

If thoracic outlet syndrome is suspected, the protocol should initially be performed with the patient’s arms up. If there is abnormal compression of the vasculature, repeat MR angiography with the arms down.

Aretriovenous Fistulas/Grafts or Vascular Malformations/Anomalies Positioning: Place patient in supine position in magnet with arm at side. If only the forearm or hand is to be imaged, Superman position should be considered.

Sequences:

• Axial SSFSE (half-Fourier acquisition single-shot turbo spin echo [HASTE]) sequence.
  
• Pre- and postcontrast coronal-oblique time-resolved 3D T1-weighted spoiled gradient-echo sequence.
  • No test bolus required.
    
  • Contrast agent dose of 0.1–0.2 mmol/kg (lower dose is preferable in the setting of renal insufficiency).
    
  • Acquisition time of less than 6 seconds is desirable to differentiate between high- and low-flow vascular malformations (12).
    
  • Large field of view required for hemodialysis grafts and fistulas. Include central vessels and tilt the imaging slab as needed to include arm and chest (elevating arm by propping up on towels may be helpful).
    
  • To limit wraparound artifact, a saturation band can be placed over contralateral arm or phase oversampling can be used.
    
  
  
• Postcontrast axial or coronal 3D fat-suppressed spoiled gradient-echo sequence.
  

For vascular malformations/anomalies, additional sequences are warranted and include precontrast fat-suppressed T2-weighted imaging to demonstrate the extent of disease. Gradient-echo imaging with variable echo time (T2*-weighted sequence) can be helpful when looking for blooming effects from calcifications-related phleboliths or hemosiderin.

Forearm/ Hand Emboli, Vasculitis, or Vascular Mass Positioning: Place patient in Superman position or supine with arm above head, with arm centered in magnet. If patient cannot tolerate such positioning, arm may be placed overlying the thigh in neutral anatomic position.

Sequences:

• Axial SSFSE (HASTE) sequence primarily used to locate the vessels and to detect any soft-tissue masses or collections that may need further assessment with additional sequences.
  
• Axial fat-suppressed T2-weighted sequence may be used to improve tissue characterization if a mass is present and to assess for inflammation as can be seen in vasculitis.
  
• Pre- and postcontrast coronal-oblique time-resolved 3D T1-weighted spoiled gradient-echo sequence.
  • No test bolus required.
    
  • To limit wraparound artifact, a saturation band can be placed over contralateral arm or phase oversampling can be used.
    
  • Contrast agent total dose of 0.1–0.2 mmol/kg, but dose may be split between initial time-resolved sequence and high-resolution MR angiography..
    
  • Imaging should be performed over 1–2 minutes to accommodate various circulation times.
    
  
  
• High-resolution conventional MR angiography (3D, not time resolved) may be performed for greater anatomic detail. Appropriate timing may be determined from the time-resolved data sets, as it may be impossible to visualize the small vessels of the wrist with a test bolus timing run. A dedicated hand coil, if available, is useful for obtaining small-field-of-view high-resolution images.
  
• Postcontrast axial or coronal 3D fat-suppressed spoiled gradient-echo sequence.
  

If central and proximal upper extremity MR angiography is also indicated, adjust patient positioning and proceed to conventional contrast-enhanced MR angiography as discussed in the subclavian steal protocol, and use a timing run or automatic triggering if available. Contrast agent dose should be split between the two studies, with a slightly lower overall dose for the first study. Unenhanced data sets should be acquired so that subtraction can be used to compensate for any potential venous contamination during the second study.

	Basic Anatomy

Top Abstract Introduction Imaging Techniques Imaging Protocols Basic Anatomy Upper Extremity Disease Hand Vasculitides Artifacts and Pitfalls Conclusion References

 
Arterial Supply of the Upper Extremity
The subclavian artery originates from the brachiocephalic trunk on the right and directly from the aorta on the left in most individuals. It continues as the axillary artery at the lateral border of the first rib. After giving off the thoracoacromial, lateral thoracic, and subscapular branches, the axillary artery terminates in the anterior and posterior circumflex humeral arteries and becomes the brachial artery as it passes the inferior margin of teres major. The brachial artery continues just distal to the elbow joint and gives rise to the radial and ulnar arteries, the branches of which provide the blood supply to the hand and forearm. The common interosseous artery arises from the ulnar artery just below the tuberosity of the radius and divides into the anterior and posterior interosseous arteries approximately 1 cm from its origin (Fig 1). Within the distal forearm, the anterior (volar) and posterior (doral) interosseous arteries form anastomoses with each other and with the volar and dorsal carpal networks.

View larger version (42K): [in this window] [in a new window] [Download PPT slide]   Figure 1.  Common upper extremity arterial anatomy: The ulnar artery supplies the superficial palmar arch, the major source of blood flow to the digits. The radial artery supplies the deep palmar arch, which in turn supplies the dorsal arches of the hand. (Reprinted with permission from reference 13.)

Upper Extremity Venous Drainage
Venous drainage of the arm is divided into superficial and deep systems. Superficial drainage begins in the dorsal venous plexus of the hand and ascends via the cephalic and basilic veins to form the axillary vein. Deep venous drainage is via veins that accompany their corresponding arteries and include the brachial vein, which joins the basilic vein at the level of the proximal humerus to become the axillary vein (Fig 2). The axillary vein drains into the subclavian vein, which extends from the outer border of the first rib to the sternal end of the clavicle. It then unites with the internal jugular vein to form the innominate vein. The innominate vein provides the upper extremity venous return to the right atrium via the superior vena cava.

View larger version (63K): [in this window] [in a new window] [Download PPT slide]   Figure 2.  Upper extremity venous drainage. Superficial system: The cephalic vein ascends the anterolateral forearm and courses in the deltopectoral groove to drain into the axillary vein. The basilic vein ascends the medial forearm, pierces the deep fascia, and joins the brachial vein to form the axillary vein. Deep system: This is composed of the venae comitantes, or veins that accompany corresponding arteries. (Reprinted with permission of Wesley Norman, PhD, from The Anatomy Lesson.)

View larger version (105K): [in this window] [in a new window] [Download PPT slide]   Figure 3.  The superficial palmar arch is formed mainly by the ulnar artery and is completed by the superficial branch of the radial artery. A complete arch is not always present. The superficial palmar arch provides the arterial supply to the digits via the digital palmar arteries. (Reprinted with permission of Wesley Norman, PhD, from The Anatomy Lesson.)

View larger version (101K): [in this window] [in a new window] [Download PPT slide]   Figure 4.  The deep palmar arch is supplied by the radial artery as it passes under the "snuff box" tendons and gives rise to the princeps pollicis and deep palmar arch. The deep palmar arch is more often complete than the superficial palmar arch. (Reprinted with permission of Wesley Norman, PhD, from The Anatomy Lesson.)

	Upper Extremity Disease

Top Abstract Introduction Imaging Techniques Imaging Protocols Basic Anatomy Upper Extremity Disease Hand Vasculitides Artifacts and Pitfalls Conclusion References

MR angiography provides a noninvasive means of making the correct diagnosis, assessing the severity of the primary lesion, and establishing the presence of flow reversal in the vertebral artery. Contrast-enhanced MR angiography helps confirm the presence and location of the vertebral arteries and demonstrates the stenosis of the proximal subclavian artery (Fig 5c). Two-dimensional TOF MR angiography with a saturation band above the section depicts cephalad flow. A flow void in the ipsilateral vertebral artery (Fig 5a) could reflect occlusion or flow reversal in the vertebral artery. Repositioning the saturation band below the section of imaging in the TOF sequence demonstrates blood flowing caudad toward the heart, confirming retrograde flow in the vertebral artery (Fig 5b). Alternatively, the test dose timing study can be used to detect asymmetry in blood flow in the vertebral arteries. Wu et al demonstrated that a delay of more than 2 seconds in time to peak flow in the vertebral artery was 100% specific for the diagnosis of subclavian steal (19).

View larger version (73K): [in this window] [in a new window] [Download PPT slide]   Figure 5a.  Subclavian steal syndrome. (a) TOF sequence with a saturation band above the section demonstrates absence of signal in the left vertebral artery (arrow). (b) TOF sequence with a saturation band below the section demonstrates signal corresponding to retrograde flow in the left vertebral artery (arrow). (c) Coronal maximum intensity projection (MIP) image from contrast-enhanced MR angiographic study demonstrates occlusion of the proximal subclavian artery (arrow), with reconstitution distal to the origin of a patent left vertebral artery.

View larger version (62K): [in this window] [in a new window] [Download PPT slide]   Figure 5b.  Subclavian steal syndrome. (a) TOF sequence with a saturation band above the section demonstrates absence of signal in the left vertebral artery (arrow). (b) TOF sequence with a saturation band below the section demonstrates signal corresponding to retrograde flow in the left vertebral artery (arrow). (c) Coronal maximum intensity projection (MIP) image from contrast-enhanced MR angiographic study demonstrates occlusion of the proximal subclavian artery (arrow), with reconstitution distal to the origin of a patent left vertebral artery.

View larger version (81K): [in this window] [in a new window] [Download PPT slide]   Figure 5c.  Subclavian steal syndrome. (a) TOF sequence with a saturation band above the section demonstrates absence of signal in the left vertebral artery (arrow). (b) TOF sequence with a saturation band below the section demonstrates signal corresponding to retrograde flow in the left vertebral artery (arrow). (c) Coronal maximum intensity projection (MIP) image from contrast-enhanced MR angiographic study demonstrates occlusion of the proximal subclavian artery (arrow), with reconstitution distal to the origin of a patent left vertebral artery.

It is important to remember that not all patients with angiographic findings of subclavian steal are symptomatic. In fact, endovascular stenting of the thoracic aorta often requires placing the stent over the origin of the subclavian artery to achieve adequate fixation of the stent graft. Prior to intervention, complete assessment of arch anatomy, including intracranial and extracranial circulation, is needed to assess collateral supply and anatomic variants. Most often, coverage of the left subclavian artery origin with an endovascular stent graft does not lead to ischemic symptoms and can be managed expectantly (20,21). Revascularization procedures such as common carotid–to–subclavian artery bypass or transposition of the subclavian to the common carotid artery may be warranted in select cases.

Once the diagnosis of subclavian steal syndrome has been established on the basis of imaging findings and clinical symptoms, the goals of treatment are improvement of arterial perfusion of the upper extremity and restoration of antegrade vertebral artery flow. This is accomplished with endovascular techniques such as percutaneous transluminal angioplasty or by surgical revascularization, including the above-mentioned revascularization procedures, in severe longstanding disease.

Takayasu Arteritis
Takayasu arteritis is a rare, large-vessel granulomatous vasculitis of unknown etiology. It affects the major branches of the thoracic and abdominal aorta and pulmonary arteries. Takayasu arteritis is more frequently found in the Asian population and in women (80%–90%) (22) during the 2nd–3rd decade of life (23). However, it can rarely affect men and non-Asians. Takayasu arteritis affects the aorta and the great vessels but can also affect the renal, mesenteric, coronary, and pulmonary arteries. In one study of 47 patients by Park et al, the left subclavian artery was involved in 55%, abdominal aorta in 53%, right renal artery in 45%, right subclavian and left renal arteries in 38%, descending thoracic aorta in 32%, left common carotid artery in 30%, and coronary arteries in15% (22). Clinical presentation is classically divided into early and late stages, or the "prepulseless" and "pulseless" stages. The early stage manifests as systemic symptoms of low-grade fever, myalgias, weight loss, and fatigue, and the late stage by diminished or absent pulses, limb claudication, and renal, mesenteric, cardiopulmonary, and cerebrovascular ischemic symptoms (23,24). Unfortunately, diagnosis and assessment of disease activity can be challenging because laboratory data, including inflammatory markers such as erythrocyte sedimentation rate and C-reactive protein, are not reliable.

MR angiography can help establish the diagnosis and assess the extent of vascular involvement. Clinical diagnosis, staging, and treatment are in large part determined by the extent and severity of involvement of specific arteries, so that assessment of the entire aorta is required (22). Not only can MR angiography help assess the arterial lumen but it can also detect extraluminal features of the disease, which may be evident before significant luminal narrowing occurs. MR angiographic findings include segmental regions of arterial stenosis, dilatation, mural thrombi, and circumferential wall thickening. Although the markers of the disease are best depicted with contrast-enhanced MR angiography (Fig 6), T2-weighted imaging may reveal hyperintensity related to surrounding edema and perivascular inflammatory changes prior to the development of stenosis. Enhancement of the vessel walls with gadolinium chelate agents is seen in active disease with delayed postcontrast fat-suppressed T1-weighted sequences (23,25,26).

View larger version (46K): [in this window] [in a new window] [Download PPT slide]   Figure 6a.  Takayasu arteritis. (a) Coronal MIP image from contrast-enhanced MR angiographic study reveals a normal aortic arch, brachiocephalic trunk, and left common carotid artery, with bilateral long-segment subclavian and axillary artery stenoses. (b) Magnified image of the right subclavian artery again demonstrates high-grade stenoses and occlusions (arrows), with collateral reconstitution of the axillary artery. Note that patient was injected with contrast agent on the right, accounting for mild venous opacification. (c) Coronal-oblique MIP image of the aortic arch and left subclavian artery proximal to the vertebral artery origin demonstrates mild and moderate stenoses (arrow), but the more distal subclavian and axillary arteries demonstrate severe long-segment stenoses.

View larger version (140K): [in this window] [in a new window] [Download PPT slide]   Figure 6b.  Takayasu arteritis. (a) Coronal MIP image from contrast-enhanced MR angiographic study reveals a normal aortic arch, brachiocephalic trunk, and left common carotid artery, with bilateral long-segment subclavian and axillary artery stenoses. (b) Magnified image of the right subclavian artery again demonstrates high-grade stenoses and occlusions (arrows), with collateral reconstitution of the axillary artery. Note that patient was injected with contrast agent on the right, accounting for mild venous opacification. (c) Coronal-oblique MIP image of the aortic arch and left subclavian artery proximal to the vertebral artery origin demonstrates mild and moderate stenoses (arrow), but the more distal subclavian and axillary arteries demonstrate severe long-segment stenoses.

View larger version (117K): [in this window] [in a new window] [Download PPT slide]   Figure 6c.  Takayasu arteritis. (a) Coronal MIP image from contrast-enhanced MR angiographic study reveals a normal aortic arch, brachiocephalic trunk, and left common carotid artery, with bilateral long-segment subclavian and axillary artery stenoses. (b) Magnified image of the right subclavian artery again demonstrates high-grade stenoses and occlusions (arrows), with collateral reconstitution of the axillary artery. Note that patient was injected with contrast agent on the right, accounting for mild venous opacification. (c) Coronal-oblique MIP image of the aortic arch and left subclavian artery proximal to the vertebral artery origin demonstrates mild and moderate stenoses (arrow), but the more distal subclavian and axillary arteries demonstrate severe long-segment stenoses.

Giant Cell Arteritis
Giant cell arteritis, also known as temporal arteritis, is a systemic inflammatory vasculitis that affects medium-large arteries and is often associated with polymyalgia rheumatica. Giant cell arteritis affects older patients (>50 years), with peak incidence in the 6th–8th decades of life and with a predominance in women (27, 28). Neurologic and ophthalmologic complications predominate because the disease most commonly involves the extracranial carotid artery and its branches, including the superficial temporal, vertebral, and ophthalmic arteries. Symptoms include jaw claudication, headache and visual disturbances, including sudden-onset blindness. However, any artery of the body containing an internal elastic lamina may be affected. Aortic aneurysms, dissections, and peripheral lower extremity and cervical arterial stenoses have all been reported in patients with the disease (29). Evans et al reported that these patients are 17.3 times more likely to develop thoracic aneurysms and 2.4 times more likely to develop isolated abdominal aortic aneurysms than the general population (30).

Temporal artery biopsy remains the reference standard for diagnosis of giant cell arteritis, but MR angiography may be used to assess the extent of large vessel involvement and help guide clinicians to alternative biopsy sites when initial results are negative. High-resolution imaging of the wall of the superficial temporal artery is another promising method for directing biopsy and diagnosing giant cell arteritis (28). MR angiography findings include segmental smooth arterial stenoses alternating with normal caliber or dilated segments, producing a beaded appearance of the arterial lumen (Fig 7). The stenoses are smooth and tapered without evidence of the plaque or ulceration that is typically present in the setting of atherosclerosis. Extraluminal findings include wall thickening, hyperintensity in the vessel wall on fat-suppressed T2-weighted images and wall enhancement on delayed imaging (23). Treatment is usually with long-term high-dose steroids, unless severity of symptoms mandates surgical revascularization.

View larger version (99K): [in this window] [in a new window] [Download PPT slide]   Figure 7.  Giant cell arteritis. Coronal MIP image from a contrast-enhanced MR angiographic study demonstrates multifocal beading, with alternating segments of stenosis and normal luminal caliber (arrows) involving the entire length of the subclavian artery bilaterally.

View larger version (70K): [in this window] [in a new window] [Download PPT slide]   Figure 8a.  Thoracic outlet syndrome (venous subtype). (a) Coronal MIP images from a contrast-enhanced MR angiographic study performed with arms up positioning demonstrate normal-caliber patent subclavian arteries bilaterally in the arterial phase image on the left and stenosis of the distal right subclavian vein (arrow) in the venous phase image on the right. (b) Axial MIP image from contrast-enhanced MR angiographic study performed with arms up positioning again demonstrate a severe distal right subclavian vein stenosis (arrow). (c) Coronal MIP image from the same study performed with patient’s arms in neutral position shows that the right subclavian vein has returned to normal caliber (arrow), demonstrating the dynamic changes at the thoracic outlet that can elicit clinical symptoms and different imaging findings.

View larger version (76K): [in this window] [in a new window] [Download PPT slide]   Figure 8b.  Thoracic outlet syndrome (venous subtype). (a) Coronal MIP images from a contrast-enhanced MR angiographic study performed with arms up positioning demonstrate normal-caliber patent subclavian arteries bilaterally in the arterial phase image on the left and stenosis of the distal right subclavian vein (arrow) in the venous phase image on the right. (b) Axial MIP image from contrast-enhanced MR angiographic study performed with arms up positioning again demonstrate a severe distal right subclavian vein stenosis (arrow). (c) Coronal MIP image from the same study performed with patient’s arms in neutral position shows that the right subclavian vein has returned to normal caliber (arrow), demonstrating the dynamic changes at the thoracic outlet that can elicit clinical symptoms and different imaging findings.

View larger version (110K): [in this window] [in a new window] [Download PPT slide]   Figure 8c.  Thoracic outlet syndrome (venous subtype). (a) Coronal MIP images from a contrast-enhanced MR angiographic study performed with arms up positioning demonstrate normal-caliber patent subclavian arteries bilaterally in the arterial phase image on the left and stenosis of the distal right subclavian vein (arrow) in the venous phase image on the right. (b) Axial MIP image from contrast-enhanced MR angiographic study performed with arms up positioning again demonstrate a severe distal right subclavian vein stenosis (arrow). (c) Coronal MIP image from the same study performed with patient’s arms in neutral position shows that the right subclavian vein has returned to normal caliber (arrow), demonstrating the dynamic changes at the thoracic outlet that can elicit clinical symptoms and different imaging findings.

View larger version (72K): [in this window] [in a new window] [Download PPT slide]   Figure 9.  Thoracic outlet syndrome (arterial subtype). Coronal MIP images from a 3D T1-weighted spoiled gradient-echo MR angiographic sequence. In the left image, during the arterial phase of enhancement with the patient’s arms elevated, severe stenosis of the right subclavian artery (arrow) and mild stenosis of the left subclavian artery (arrowhead) are seen. In the right image, the stenoses resolve after the patient’s arms are placed in the neutral position.

MR angiography with dynamic positioning is particularly useful in the diagnosis of vascular subtypes of thoracic outlet syndrome. It allows localization of the stenotic lesion and confirmation of its positional cause. The Wright maneuver is performed during MR angiography with the patient supine in the magnet to permit visualization of compression of the vasculature, if present. If there is compression or symptoms, MR angiography is repeated with the patient’s arms down in neutral position to see if vessel diameter changes. MR imaging can provide additional diagnostic information about the specific anatomic cause with careful scrutiny of the source data or supplemental imaging with a sagittal T1-weighted turbo spin-echo sequence.

Once the diagnosis of arterial thoracic outlet syndrome is established, surgical intervention is required to treat or prevent acute thromboembolic events.

Treatment of venous thoracic outlet syndrome, also referred to as thoracic "inlet" syndrome, depends primarily on the presence and extent of associated venous thrombosis and may include anticoagulation, thrombolysis, or surgical decompression.

Paget-Schroetter Syndrome
Paget-Schroetter syndrome refers to thrombosis of the axillary and subclavian veins (Fig 10a, 10b) usually caused by anatomic compression in the costoclavicular space of the thoracic outlet (Fig 10c). This syndrome is also termed "effort" thrombosis because of its common association with exertion and mechanical stress, namely repetitive hyperabduction and external rotation of the upper extremity. Patients are often young, otherwise healthy adults who participate in activities associated with repetitive shoulder-arm motion such as weightlifting, wrestling, tennis, or baseball pitching. In the past, upper extremity deep venous thrombosis accounted for only 1%–2% of all cases of deep venous thrombosis. However, more recently, the incidence has been on the rise, likely because of improvements in imaging diagnosis, usually with ultrasonography or direct venography, and because of the increasing use of central venous catheterization for vascular access, the increase in the placement of pacemakers, and intravenous drug abuse (33,34).

View larger version (91K): [in this window] [in a new window] [Download PPT slide]   Figure 10a.  Paget-Schroetter syndrome in young weightlifter. (a) Coronal postcontrast 3D T1-weighted fat-suppressed spoiled gradient-echo images with dynamic positioning (arm up in left image and down in right image) demonstrate a long segment of occlusive venous thrombus extending from the basilic vein into the right subclavian vein (arrowheads), with wall enhancement. (b) Axial postcontrast 3D T1-weighted fat-suppressed spoiled gradient-echo image again demonstrates that the right axillary and subclavian veins are completely occluded and distended with thrombus. (c) Sagittal unenhanced T1-weighted turbo spin-echo image supplements the angiographic images and demonstrates the severely compressed subclavian vein (solid arrow) in the costoclavicular space, interposed between the clavicle (black arrowhead) and the anterior scalene muscle (white arrowhead). The subclavian artery (open arrow) is seen as a flow void posterior to the anterior scalene muscle.

View larger version (83K): [in this window] [in a new window] [Download PPT slide]   Figure 10b.  Paget-Schroetter syndrome in young weightlifter. (a) Coronal postcontrast 3D T1-weighted fat-suppressed spoiled gradient-echo images with dynamic positioning (arm up in left image and down in right image) demonstrate a long segment of occlusive venous thrombus extending from the basilic vein into the right subclavian vein (arrowheads), with wall enhancement. (b) Axial postcontrast 3D T1-weighted fat-suppressed spoiled gradient-echo image again demonstrates that the right axillary and subclavian veins are completely occluded and distended with thrombus. (c) Sagittal unenhanced T1-weighted turbo spin-echo image supplements the angiographic images and demonstrates the severely compressed subclavian vein (solid arrow) in the costoclavicular space, interposed between the clavicle (black arrowhead) and the anterior scalene muscle (white arrowhead). The subclavian artery (open arrow) is seen as a flow void posterior to the anterior scalene muscle.

View larger version (99K): [in this window] [in a new window] [Download PPT slide]   Figure 10c.  Paget-Schroetter syndrome in young weightlifter. (a) Coronal postcontrast 3D T1-weighted fat-suppressed spoiled gradient-echo images with dynamic positioning (arm up in left image and down in right image) demonstrate a long segment of occlusive venous thrombus extending from the basilic vein into the right subclavian vein (arrowheads), with wall enhancement. (b) Axial postcontrast 3D T1-weighted fat-suppressed spoiled gradient-echo image again demonstrates that the right axillary and subclavian veins are completely occluded and distended with thrombus. (c) Sagittal unenhanced T1-weighted turbo spin-echo image supplements the angiographic images and demonstrates the severely compressed subclavian vein (solid arrow) in the costoclavicular space, interposed between the clavicle (black arrowhead) and the anterior scalene muscle (white arrowhead). The subclavian artery (open arrow) is seen as a flow void posterior to the anterior scalene muscle.

Arteriovenous Fistulas/Grafts for Hemodialysis
Hemodialysis requires well-functioning vascular access to allow sufficient blood flow for adequate clearance and dialysis dosing. This is achieved temporarily by central vein catheterization and subsequently by surgical creation of an arteriovenous fistula or graft for more permanent and durable access. An upper extremity arteriovenous fistula is created by surgical end-to-side anastomosis of the radial or brachial artery to an adjacent basilic, cephalic, or medial antecubital vein (36)(Fig 11). In cases where the adjacent vein is not suitable for access, a piece of prosthetic or autogenous saphenous vein graft may be interposed. One advantage to synthetic grafts is that they need less time to mature, but they have a higher rate of complications and inferior patency rates (36,37). Although preferred over central venous catheters for their durability and lower rate of infection, surgically created arteriovenous fistulas are prone to significant complications that increase long-term morbidity and mortality in end-stage renal failure patients. It has been estimated that approximately 20% of hospitalizations of dialysis patients are related to vascular access complications (38). Complications include venous stenosis, thrombosis, infection, aneurysms, and, rarely, arterial steal syndrome (Fig 12). Thrombosis is the most common cause of dysfunction and is usually associated with venous stenosis at or near the anastamotic site due to neointimal hyperplasia (39). However, stenoses can occur anywhere along the arteriovenous circuit, and diagnostic imaging of the entire graft and central vasculature therefore may be required to determine the underlying problem (Fig 12b).

View larger version (63K): [in this window] [in a new window] [Download PPT slide]   Figure 11.  Diagrams of the three types of upper arm arteriovenous fistulas used for hemodialysis. A, Normal anatomy of the right antecubital fossa, showing the cephalic vein (CV), median antecubital vein (MACV), basilic vein (BV), brachial artery (BA), radial artery (RA), and ulnar artery (UA). B, Brachiocephalic arteriovenous fistula. C, Brachiobasilic arteriovenous fistula. D, Brachial artery–to–median antecubital vein arteriovenous fistula (36).

View larger version (141K): [in this window] [in a new window] [Download PPT slide]   Figure 12a.  Hemodialysis arteriovenous fistula complications. (a) Time-resolved contrast-enhanced MR angiographic images at 6 seconds per frame demonstrate a left-side brachiobasilic hemodialysis fistula with multiple venous stenoses(arrows). (b) Coronal postcontrast 3D T1-weighted fat-suppressed spoiled gradient-echo images reveal an additional significant finding: multiple intraluminal venous thrombi (arrowheads). (c) Time-resolved contrast-enhanced MR angiograms in two patients with arteriovenous hemodialysis fistula complications; the patient in the left image has two venous aneurysms (arrows), and the patient in the right image has complete venous occlusion with collateral vessels present (arrowhead).

View larger version (72K): [in this window] [in a new window] [Download PPT slide]   Figure 12b.  Hemodialysis arteriovenous fistula complications. (a) Time-resolved contrast-enhanced MR angiographic images at 6 seconds per frame demonstrate a left-side brachiobasilic hemodialysis fistula with multiple venous stenoses(arrows). (b) Coronal postcontrast 3D T1-weighted fat-suppressed spoiled gradient-echo images reveal an additional significant finding: multiple intraluminal venous thrombi (arrowheads). (c) Time-resolved contrast-enhanced MR angiograms in two patients with arteriovenous hemodialysis fistula complications; the patient in the left image has two venous aneurysms (arrows), and the patient in the right image has complete venous occlusion with collateral vessels present (arrowhead).

View larger version (123K): [in this window] [in a new window] [Download PPT slide]   Figure 12c.  Hemodialysis arteriovenous fistula complications. (a) Time-resolved contrast-enhanced MR angiographic images at 6 seconds per frame demonstrate a left-side brachiobasilic hemodialysis fistula with multiple venous stenoses(arrows). (b) Coronal postcontrast 3D T1-weighted fat-suppressed spoiled gradient-echo images reveal an additional significant finding: multiple intraluminal venous thrombi (arrowheads). (c) Time-resolved contrast-enhanced MR angiograms in two patients with arteriovenous hemodialysis fistula complications; the patient in the left image has two venous aneurysms (arrows), and the patient in the right image has complete venous occlusion with collateral vessels present (arrowhead).

It should be noted that despite the previously held belief that MR contrast agents were safe in patients with renal insufficiency, recent reports of nephrogenic systemic fibrosis (6) indicate that MR contrast agents may cause serious complications and should probably be avoided in patients with renal insufficiency unless deemed medically necessary. While not proven to reduce the risk of nephrogenic systemic fibrosis, dialysis within 24 hours of gadolinium chelate injection has been advocated (43).

Congenital and Developmental Vascular Anomalies
Vascular anomalies are common soft-tissue masses most often seen in the pediatric population. These congenital and developmental anomalies may be divided into two major categories: proliferative vascular anomalies and vascular malformations. Proliferative vascular anomalies demonstrate abnormal mitotic activity and cellular hyperplasia and are true neoplasms; the classic example is infantile capillary hemangioma. Vascular malformations are nonneoplastic lesions resulting from abnormal vascular morphogenesis and are divided into subcategories based on the predominant vascular channel: capillary, venous, arterial, lymphatic, or mixed (44). Vascular malformations are far more common in adults, adolescents, and children more than 1 year of age. Lesions with a predominantly arterial component are termed high-flow vascular lesions (45).

Imaging is used to assess the extent of the lesions, differentiate between high- and low-flow lesions, and identify the predominant vascular channel and its arterial supply and venous drainage. Perhaps most importantly, MR imaging is useful for allowing distinction between benign vascular anomalies and congenital vascular malformations due to aggressive or malignant vascular neoplasms. Associated anomalies can also be detected (45).

Proliferative Vascular Anomalies Infantile hemangiomas are the most common vascular tumor of infancy and are most often found in the head and neck region (60%); the extremities are the third most common site (15%) after the trunk (25%). The presence of multiple cutaneous infantile hemangiomas (ie, six or more) should raise suspicion of visceral involvement. These lesions are more common in girls and premature infants and classically have distinct proliferative and involutive phases. They are usually identified within the first few weeks of life during their proliferative phase, but by definition are not evident at birth. Many spontaneously regress over time, with the involutive phase lasting on average between 1 and 7 years. During this phase, the hemangioma becomes progressively less vascular and undergoes fibrofatty replacement (46,47)

Congenital hemangiomas, by definition, are present at birth and are clinically and histologically distinct from their infantile counterparts. These benign vascular tumors are fully formed at birth and come in two varieties: rapidly involuting congenital hemangiomas and noninvoluting congenital hemangiomas. No postnatal growth is described in these lesions; instead they either rapidly decrease in size over 1 year (involuting) or, less commonly, fail to involute altogether (48,49).

The MR imaging appearance of infantile and congenital hemangiomas is a solid, well-defined lobulated mass with prominent flow voids. These tumors are markedly and homogeneously hyperintense on T2-weighted images and have intermediate intensity on T1-weighted images; uniform homogeneous contrast enhancement is also the norm. Should these features not be present, other entities including infantile fibrosarcoma and hemangioendothelioma should be considered, and biopsy is recommended. Distinction of these high-flow lesions from high-flow vascular malformations lies in the identification of a discrete tumor mass, which is not classically seen in arteriovenous malformations.

Vascular Malformations Venous and lymphatic malformations typically have intermediate signal intensity on T1-weighted images and are markedly hyperintense on fat-saturated T2-weighted images. These lesions usually have lobulated contours, occasionally with internal septations; venous malformations can also demonstrate tubular morphology, with calcified phleboliths that may be more apparent with long-echo-time sequences. Fluid-fluid levels may be present in both types of lesions, owing to proteinaceous or hemorrhagic components. Distinction of venous from lymphatic malformations rests with the demonstration of the patchy progressive tubular enhancement of venous malformations during the venous phase of imaging; lymphatic malformations show septal but no central enhancement on delayed images. Capillary malformations can be difficult to see at MR imaging given their superficial location (45); the utility of imaging these lesions lies in the possible detection of associated underlying vascular anomalies.

Arteriovenous malformations are uncommon, high-flow vascular malformations composed of a tangle of abnormal communications between the arterial and venous systems, with absence of a normal capillary bed. This complex nidus distinguishes an arteriovenous malformation from an arteriovenous fistula, with the latter representing a single anomalous arteriovenous communication. These lesions are prone to serious complications including high-output cardiac failure, paradoxical emboli, hemorrhage, and ischemia of regional tissues due to the steal phenomenon. As a result, high-flow tissue overgrowth may occur and lead to limb length discrepancy. Typically, there is no associated soft-tissue mass. Optimal therapy requires a comprehensive evaluation of feeding and draining vessels and the effect of the nidus on and its relationships with adjacent structures. MR imaging features include a complex network of flow voids on noncontrast images, dilated supplying arteries, and draining veins with tortuous disorganized vascular channels (Fig 13). Arterial enhancement is rapid, as is early enhancement of the draining veins (45,50).

View larger version (97K): [in this window] [in a new window] [Download PPT slide]   Figure 13.  Congenital arteriovenous malformation. Time-resolved MR angiography of the left arm in a young child demonstrates a high-flow arteriovenous malformation characterized by a dilated, ectatic arterial system, a complex vascular nidus in the hand and forearm (arrow), and early filling of markedly dilated and tortuous basilic and cephalic veins (arrowheads). Associated hypertrophy of the left arm is seen, as well as diffuse infiltration of the muscular and subcutaneous compartments by the vascular nidus, which was best seen on T2-weighted images (not shown).

Treatment options depend on the anatomic extent and hemodynamics of the malformation and range from conservative therapy for asymptomatic lesions to superselective embolization of the nidus or surgery. Transarterial embolization currently plays a role in high-flow arteriovenous malformations; larger lesions, however, frequently require complex surgical treatment (52).

Hypothenar Hammer Syndrome
Hypothenar hammer syndrome is a posttraumatic cause of vascular insufficiency to the hand that may ultimately result in embolic occlusion of the digital arteries and digital ischemia. Symptoms may be similar to those of the Raynaud phenomenon in the ulnar digits. Although this syndrome has been reported in the past as an occupational disease occurring in workers using hammers and screwdrivers, it may be seen in any case of repetitive compression or blunt trauma to the hypothenar eminence. Such trauma results in injury to the terminal segment of the ulnar artery or proximal superficial palmar arch. The ulnar artery is most vulnerable as it passes over the hook of the hamate in the Guyon canal. A blunt or repetitive adequate force in this location may cause significant damage to the arterial wall and may compromise flow to the superficial palmar arch. Hypothenar hammer syndrome may lead to vascular stenosis, thrombotic occlusion (Fig 14), arterioarterial thromboembolism, and aneurysms (Movies 2, 3 radiographics.rsnajnls.org/cgi/content/full/e28/DC1.) (53). Given the variation in palmar anatomy among individuals, therapeutic stratification is based on assessment of adequate digital blood supply.

View larger version (80K): [in this window] [in a new window] [Download PPT slide]   Figure 14.  Ulnar artery occlusion. Time-resolved MR angiography of the hand demonstrates occlusion of the distal ulnar artery (arrow) 8 cm proximal to the wrist. The radial artery is patent and the superficial palmar arch and common digital arteries of the third to fifth fingers are filled via deep palmar arch collateral vessels (arrowheads).

View larger version (126K): [in this window] [in a new window] [Download PPT slide]   Figure 15.  Posttraumatic pseudoaneurysm. Time-resolved MR angiography of the hand demonstrates a pseudoaneurysm (arrow) at the level of the fifth metacarpophalangeal joint, arising from a branch of the third common palmar artery. In addition to the clinical history of prior trauma, the absence of a draining vein indicates that this is unlikely to represent a hemangioma.

MR angiography can be used to evaluate the integrity of the ulnar artery and its branches, define the extent of vessel injury, and provide valuable information about the distribution pattern of hand vasculature, including the presence of collateral vessels. Angiography in hypothenar hammer syndrome may demonstrate a "corkscrew" appearance, with arterial stenoses alternating with ectasias, segmental ulnar artery occlusion, and, in 50% of cases, occlusions due to emboli (54,55). A corkscrew appearance is also present in the contralateral asymptomatic hand in 92% of cases (56).

Embolic Disease of Distal Extremity
Peripheral embolic disease is caused by embolization of atherosclerotic debris into the distal arterial vasculature. Upper extremity emboli account for 15%–20% of all emboli to the extremities (57). This may occur spontaneously or as a result of mechanical manipulation (eg, endovascular procedures). In spontaneous upper extremity embolic disease, as many as 70% of emboli arise from a cardiac source and are usually due to mural thrombi that develop in the setting of a cardiac arrhythmia such as atrial fibrillation (58). The subclavian artery secondary to thoracic outlet compression and the superficial palmar arch are also common sources.

In the upper extremity, microemboli may occlude the distal vasculature of the hand, thereby compromising blood flow to the digits (Fig 16a). Presenting symptoms are related to vascular compromise and include paresthesias, pallor, blue coloration, petechiae, ulceration, and gangrene. When the clinical suspicion for acute embolic disease is high, patients are usually evaluated with conventional angiography because it can offer high-resolution images for rapid diagnosis and permit immediate intervention. If symptoms are more chronic or less severe, MR angiography is an excellent alternative in looking for underlying causes and extent of disease. MR imaging can be used to not only establish a possible source of emboli but to evaluate overall atherosclerotic plaque burden. Both the distal extremity and central vasculature should be assessed (Fig 16b). If echocardiography is suboptimal, cardiac MR imaging may be useful for assessing a potential cardiac source.

View larger version (84K): [in this window] [in a new window] [Download PPT slide]   Figure 16a.  Distal extremity embolic disease. (a) Time-resolved MR angiography of the hand in a patient presenting with sudden onset pallor and paresthesias of the digits demonstrates an abrupt occlusion of the second digital palmar artery (arrow) without collateral vessels, consistent with an acute distal arterial embolism. (b) Coronal MIP image from a contrast-enhanced MR angiographic study demonstrates a normal-caliber aortic arch and bilateral subclavian, axillary, and brachial arteries without any evidence of atherosclerosis or other vascular disease. Since no arterial embolic source was demonstrated, a cardiac source must be considered, which was the cause in this case.

View larger version (121K): [in this window] [in a new window] [Download PPT slide]   Figure 16b.  Distal extremity embolic disease. (a) Time-resolved MR angiography of the hand in a patient presenting with sudden onset pallor and paresthesias of the digits demonstrates an abrupt occlusion of the second digital palmar artery (arrow) without collateral vessels, consistent with an acute distal arterial embolism. (b) Coronal MIP image from a contrast-enhanced MR angiographic study demonstrates a normal-caliber aortic arch and bilateral subclavian, axillary, and brachial arteries without any evidence of atherosclerosis or other vascular disease. Since no arterial embolic source was demonstrated, a cardiac source must be considered, which was the cause in this case.

	Hand Vasculitides

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Raynaud Phenomenon and Scleroderma
The Raynaud phenomenon refers to the clinical presentation of peripheral arterial vasospasm of the digital arteries, causing pallor and dysesthesia of the digits, exacerbated by exposure to cold temperatures or psychologic stressors. Classically, the digits turn white (ischemia), then blue (deoxygenation), then red (reperfusion) (60). The Raynaud phenomenon can be primary (idiopathic and referred to as Raynaud disease) or secondary to a number of different diseases, including rheumatologic diseases such as scleroderma and a variety of other conditions, including extrinsic vascular obstruction as in thoracic outlet syndrome, paraproteinemias, and the presence certain drugs and chemicals (eg, β-blockers, polyvinyl chloride) (61). The pathogenesis therefore varies according to the underlying cause. As the vascular defect in the Raynaud phenomenon is primarily functional, the utility of imaging studies lies in the exclusion of other possible causes of similar clinical findings, including distal embolic disease and hypothenar hand syndrome. Intrinsic intravascular structural abnormalities, however, do exist in secondary Raynaud phenomenon, particularly in the setting of scleroderma. The pathogenesis involves dysfunction in vascular regulatory mechanisms that progresses to structural abnormalities, including intimal lesions and thrombosis that may ultimately lead to vessel occlusion.

Once the diagnosis of secondary Raynaud phenomenon is suspected clinically, it may be confirmed with conventional angiography by findings such as stenosis and vessel occlusion. However, the use of vasodilators is often necessary to evaluate vasospastic disorders with conventional angiography to minimize catheter-induced vasospasm (62). MR angiography, however, does not require vasodilators and therefore may provide a more accurate assessment of the true extent of vasospasm than conventional angiography (63). MR angiography findings that may be observed include digital hyperemia, severe arterial stenosis, and complete vessel occlusion (Fig 17, Movie 5 radiographics.rsnajnls.org/cgi/content/full/e28/DC1).

View larger version (84K): [in this window] [in a new window] [Download PPT slide]   Figure 17.  Scleroderma. Coronal MIP images from a contrast-enhanced MR angiographic study of the left hand reveal a patent radial artery from the proximal forearm to the wrist. At the level of the wrist, the radial artery becomes severely stenotic (arrowhead). Severe ulnar artery stenosis is also noted at the level of the wrist. The superficial palmar arch is not visualized. The deep arch is supplied by a collateral vessel from the radial artery (arrow). The second digit is hyperemic relative to the other digits. (The patient is status post resection of the distal phalanx of the third digit.)

	Artifacts and Pitfalls

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Recent developments in gadolinium-enhanced MR angiography including time-resolved and parallel imaging have made it possible to image the vasculature dynamically to assess the hemodynamics of vascular disease and to bring MR angiography closer to the DSA reference standard. Time-resolved imaging can be combined with high-resolution MR angiography for more detailed depiction of small vessels of the upper extremity. As with all technologic advances, however, accurate image interpretation requires familiarity with artifacts and potential pitfalls, as an awareness of their causes can suggest better imaging strategies (66).

One of the most demanding aspects of contrast-enhanced MR angiography is proper timing of image acquisition. Incorrectly timed studies can result in variable degrees of venous contamination during arteriography and decreased diagnostic accuracy. To ensure precise timing of image acquisition, various techniques such as the test-bolus method and automatic triggering to bolus arrival can be used. In the event the latter techniques are unreliable, time-resolved acquisitions can be used to circumvent the problem.

One must also be aware of the imaging pitfalls associated with interpreting postprocessed images, including subtracted or MIP images. Stenosis may be overestimated and assessment of intraluminal views alone is inadequate because the latter may lead to underestimation of the size of aneurysms and will not reveal extraluminal disease such as perivascular inflammation seen in vasculitides and inflammatory aneurysms. Evaluation of the source data and additional anatomic imaging is therefore necessary for complete assessment.

Overestimation of stenotic lesions is another significant problem encountered in MR angiography, often caused by partial-volume effects and spin dephasing due to turbulent flow at a stenosis. Although less common in gadolinium-enhanced MR angiography, MIP reconstructions can exacerbate this problem, again underscoring the importance of source data assessment (67).

Susceptibility artifacts are also a well-known problem in MR imaging. In the evaluation of angiographic images in particular, they may result in several interpretive pitfalls. One example is arterial pseudostenosis. In proximal upper extremity vasculature, this may be caused by the T2* effect of a high concentration of gadolinium in the central veins ipsilateral to the contrast agent injection site (66). The consequence is signal loss in the adjacent artery that may be interpreted as a true stenosis (Fig 18). This common pitfall is easily avoided by injecting the contrast agent contralateral to the side of clinical concern. Dilution of contrast agent or use of larger volumes of saline flush can also alleviate the problem. Alternatively, delayed images can be obtained to confirm patency and diminish susceptibility artifacts.

View larger version (78K): [in this window] [in a new window] [Download PPT slide]   Figure 18.  Subclavian artery pseudostenosis. Coronal MIP images from a contrast-enhanced MR angiographic study demonstrate apparent stenosis of the distal right subclavian artery (arrow) ipsilateral to the side of contrast agent injection. Delayed imaging demonstrates a normal-caliber subclavian artery, indicating that the finding was artifactual and secondary to signal loss caused by the high concentration of gadolinium in the adjacent vein.

View larger version (163K): [in this window] [in a new window] [Download PPT slide]   Figure 19a.  Metallic stent artifact: (a) Coronal MIP image from a time-resolved contrast-enhanced MR angiographic study demonstrates an arteriovenous fistula with two apparent severe stenoses involving the left brachiocephalic vein (arrow) and axillary vein (arrowheads). The margins of these stenoses are unusually abrupt and collateral vessels are present in the upper arm. (b) Axial (left) and coronal (right) reformations of the 3D T1-weighted fat-suppressed spoiled gradient-echo data demonstrate blooming artifacts at the sites of the two indwelling stents. The presence of the collateral vessels still raised the suspicion of possible stent occlusion, and DSA was recommended, which confirmed patency of the venous system. (c) Anteroposterior chest radiograph shows the presence of two stents (arrows) corresponding to the regions of suspected venous stenoses.

View larger version (63K): [in this window] [in a new window] [Download PPT slide]   Figure 19b.  Metallic stent artifact: (a) Coronal MIP image from a time-resolved contrast-enhanced MR angiographic study demonstrates an arteriovenous fistula with two apparent severe stenoses involving the left brachiocephalic vein (arrow) and axillary vein (arrowheads). The margins of these stenoses are unusually abrupt and collateral vessels are present in the upper arm. (b) Axial (left) and coronal (right) reformations of the 3D T1-weighted fat-suppressed spoiled gradient-echo data demonstrate blooming artifacts at the sites of the two indwelling stents. The presence of the collateral vessels still raised the suspicion of possible stent occlusion, and DSA was recommended, which confirmed patency of the venous system. (c) Anteroposterior chest radiograph shows the presence of two stents (arrows) corresponding to the regions of suspected venous stenoses.

View larger version (129K): [in this window] [in a new window] [Download PPT slide]   Figure 19c.  Metallic stent artifact: (a) Coronal MIP image from a time-resolved contrast-enhanced MR angiographic study demonstrates an arteriovenous fistula with two apparent severe stenoses involving the left brachiocephalic vein (arrow) and axillary vein (arrowheads). The margins of these stenoses are unusually abrupt and collateral vessels are present in the upper arm. (b) Axial (left) and coronal (right) reformations of the 3D T1-weighted fat-suppressed spoiled gradient-echo data demonstrate blooming artifacts at the sites of the two indwelling stents. The presence of the collateral vessels still raised the suspicion of possible stent occlusion, and DSA was recommended, which confirmed patency of the venous system. (c) Anteroposterior chest radiograph shows the presence of two stents (arrows) corresponding to the regions of suspected venous stenoses.

	Conclusion

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	Footnotes

 

Abbreviations: DSA = digital subtraction angiography, 3D = three-dimensional, TOF = time of flight, MIP = maximum intensity projection

	References

Top Abstract Introduction Imaging Techniques Imaging Protocols Basic Anatomy Upper Extremity Disease Hand Vasculitides Artifacts and Pitfalls Conclusion References

 

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