The lower-extremity arteries are a common site for vascular diseases. The legs have a relatively large muscle mass and a prominent role in basic daily activities. Lesions in this vascular bed produce troublesome symptoms at an early stage. Advanced disease frequently results in limb loss, although often the underlying systemic disease has the greatest impact on mortality. Interventions in the lower extremities are increasing in frequency as techniques and devices improve.

Anatomy

The blood supply to the lower extremities can be roughly divided into runoff vessels (inline flow to the foot) and musculoskeletal branches that terminate in the structures of the limb. In most instances, the status of the runoff vessels is the primary clinical concern. However, in the presence of occlusion of the runoff vessels, the musculoskeletal branches become the principal source of collateral blood supply.

The common femoral artery (CFA) is the continuation of the external iliac artery. This vessel is usually 6-9 mm in diameter and 5-7 cm in length, with frequent and variable small, unnamed muscular branches. The CFA extends from the inguinal ligament to the origins of the superficial femoral artery (SFA) and profunda femoris artery (PFA) just distal to the inferior margin of the femoral head ( Fig. 15-1 ). In 10% of individuals, the artery bifurcates while it is still anterior to the femoral head (termed high bifurcation ) ( Fig. 15-2 ). The CFA is contained within the femoral sheath, a continuation of the abdominal wall fascia. The sheath is funnel shaped, with the broad base opening toward the abdomen. In addition to containing the artery, the sheath also contains the femoral vein (medial to the artery) and the femoral canal (the most medial structure). The femoral canal contains lymphatic channels and often a lymph node. The femoral nerve lies lateral to the femoral sheath, within the femoral triangle formed by the sartorius muscle laterally, the adductor longus muscle medially, the inguinal ligament superiorly, and the iliacus, psoas major, pectineus, and adductor longus muscles posteriorly.

Figure 15-1, Drawing of lower-extremity arteries. 1, Common iliac artery. 2, External iliac artery. 3, Deep iliac circumflex artery. 4, Superficial circumflex iliac artery. 5, Inferior epigastric artery. 6, Common femoral artery. 7, Profunda femoris artery (PFA). 8, Medial femoral circumflex artery. 9, Lateral femoral circumflex artery. 10, Descending branch of PFA. 11, Superficial femoral artery. 12, Descending genicular artery. 13, Popliteal artery. 14, Lateral superior genicular artery. 15, Medial superior genicular artery. 16, Lateral inferior genicular artery. 17, Medial inferior genicular artery. 18, Sural arteries. 19, Anterior tibial artery. 20, Tibioperoneal trunk. 21, Posterior tibial artery. 22, Peroneal artery. 23, Perforating branches to anterior and posterior tibial arteries. 24, Dorsalis pedal artery.

Figure 15-2, Computed tomography angiogram of the pelvis showing high bifurcation of the left common femoral artery (arrow) anterior to the femoral head. Compare to the common femoral artery bifurcation on the right relative to the femoral head.

The origin of the PFA has a lateral and posterior orientation relative to the SFA (see Fig. 10-8 ). The PFA provides proximal branches to the hip (the lateral and medial femoral circumflex arteries) before descending deep in the thigh adjacent to the medial edge of the femur. There are multiple branches from the PFA to the muscles of the thigh before it terminates above the adductor canal. These muscular branches anastomose with muscular branches of the SFA and popliteal arteries. Variations in the branching pattern and origin of the PFA are present in 40% of individuals. The most common variants are independent origins of the medial (20%) or lateral (15%) circumflex femoral arteries from the CFA.

The SFA is remarkable for the almost complete lack of variability (rather boring for anatomists but appreciated by interventionalists) ( Table 15-1 ). The origin of the SFA from the CFA is anterior and medial to the PFA. The SFA runs beneath the sartorius muscle in the thigh, anterior to the femoral vein ( Fig. 15-3 ). The artery passes through the adductor canal in the distal thigh, where it becomes the popliteal artery. The SFA is usually 5-7 mm in diameter, with many muscular branches along its length. The last large medial branch is named the descending or supreme genicular artery . The muscular branches of the SFA become important collateral pathways in the setting of occlusive disease.

Table 15-1
Anatomic Variants of the Lower-Extremity Arteries
Variant Incidence (%)
Two or more PFA branches from CFA 2
Persistent sciatic artery 0.025
Duplication of SFA <0.001
High origin of a tibial artery 5
Peroneal origin from the anterior tibial artery 1
True popliteal artery trifurcation (no tibioperoneal trunk) 2
Hypoplastic posterior tibial artery 3.8
Hypoplastic anterior tibial artery 1.6
Hypoplastic anterior and posterior tibial arteries 0.2
CFA, common femoral artery; PFA, profunda femoris artery; SFA, superficial femoral artery.

Figure 15-3, Axial computed tomography image of the thigh during the venous phase. The calcified and occluded superficial femoral artery (white arrow) lies beneath the sartorius muscle (arrowhead) , slightly anterior and medial to the femoral vein (open arrow) . The bent arrow indicates an ePTFE surgical bypass graft.

One of the few variants of SFA anatomy is a persistent sciatic artery (0.025%). This vessel is a normal fetal branch of the internal iliac artery that continues into the lower-extremity posterior to the femoral head to supply the runoff vessels ( Fig. 15-4 ). This artery usually regresses as the external iliac artery becomes the arterial supply of the lower limb. When persistent, the sciatic artery may terminate in the posterior thigh, in which case the runoff is through the SFA, or continue to the popliteal artery with a discontinuous or absent SFA. Persistent sciatic arteries are bilateral in 25% of patients. The posterior course of the artery renders it subject to repetitive trauma, resulting in occlusive disease or aneurysm formation.

Figure 15-4, Bilateral persistent sciatic arteries. A, Axial image from a computed tomography angiogram showing small common femoral arteries (arrowheads) and bilateral persistent sciatic arteries posteriorly (open arrows) . B, Volume rendering of the same patient showing the persistent sciatic arteries (open arrows) originating from the internal iliac arteries ( arrowheads , common femoral arteries). This patient has occlusive disease in the left persistent sciatic artery that was symptomatic with claudication.

The popliteal artery is the continuation of the SFA from the adductor canal to the origins of the tibial vessels below the knee (see Fig. 15-1 ). In clinical practice the joint line of the knee divides the artery into above-knee and below-knee segments. Although these are not official anatomic terms, the popliteal artery should always be described in this manner because the type of intervention and subsequent outcome are influenced by the level of disease.

The average diameter of the popliteal artery is 4-5 mm. The blood supply of the knee joint is provided by the superior and inferior (medial and lateral), and middle genicular arteries. These arteries are recognizable by their horizontal course around the knee. The posterior calf muscles are supplied by the vertically oriented sural arteries arising from the posterior aspect of the popliteal artery. The most common anatomic variation of the popliteal artery is a high origin of one or more of the tibial arteries. Usually, the popliteal artery bifurcates into the anterior tibial artery and the tibioperoneal trunk at the distal edge of the popliteus muscle. In 5% of individuals, one of the tibial runoff vessels has an origin from the popliteal artery above this level ( Fig. 15-5 ).

Figure 15-5, Coronal maximum intensity projection of a three-dimensional gadolinium-enhanced magnetic resonance angiogram at the level of the knees, showing high origin of the right anterior tibial artery (arrow) and low origin of the right posterior tibial artery (arrowhead) . Compare with the normal left tibial artery origins.

The runoff vessels in the calf consist of the anterior tibial, posterior tibial, and peroneal arteries. The anterior tibial artery arises from the popliteal artery just distal to the popliteus muscle. This artery passes anteriorly through the interosseous membrane and then descends to the foot medial to the fibula in the anterior fascial compartment of the calf ( Fig. 15-6 ). In fewer than 1% of individuals, the peroneal artery originates from the anterior tibial artery. In most instances, the tibioperoneal trunk is a short artery of variable length that descends several centimeters beyond the anterior tibial artery origin before bifurcating into the posterior tibial and peroneal arteries. The posterior tibial artery courses deep to the soleus muscle to the medial malleolus. The peroneal artery descends to the ankle posterior and medial to the fibula (see Fig. 15-6 ). At the ankle, the peroneal artery terminates in a characteristic fork created by the anterior and posterior perforating branches (see Fig. 15-1 ). The posterior tibial and peroneal arteries are contained within the deep posterior fascial compartment of the calf.

Figure 15-6, Axial computed tomography image during the arterial phase at the level of the calf. ( Black arrowhead, anterior tibial artery; white arrowhead , peroneal artery; white arrow, posterior tibial artery.)

The anterior and posterior tibial arteries continue into the foot in 95% of individuals, while the peroneal artery terminates above the ankle in an equal percentage. In roughly 5% of individuals, one of the runoff vessels is absent. When either the anterior or posterior tibial artery is congenitally absent in the calf, the peroneal artery may continue into the foot in its stead.

There is much variability of the arterial supply to the foot, similar to the hand. Rather than memorize minutiae, it is best to be familiar with the classic anatomy described and use it as a basis when interpreting imaging studies. The anterior and posterior tibial arteries provide the bulk of the arterial supply to the foot ( Fig. 15-7 ). The anterior tibial artery continues into the foot below the level of the ankle joint as the dorsalis pedis artery. The medial and lateral tarsal arteries are large branches that arise from the proximal dorsalis pedis artery. At the level of the proximal metatarsals, the dorsalis pedis bifurcates into a deep plantar branch and the arcuate artery. The arcuate artery curves toward the lateral edge of the foot along the dorsal aspect of the metatarsal bone bases, supplying the dorsal metatarsal arteries to the distal foot before anastomosing with distal branches of the plantar arteries. The posterior tibial artery passes posterior and inferior to the medial malleolus, and then bifurcates into the medial and lateral plantar arteries. The lateral plantar artery is usually the larger of the two, with a course diagonally across the plantar aspect of the foot. The lateral plantar artery forms a second, deep plantar arch that supplies the plantar metatarsal arteries. This arch anastomoses with the deep plantar branch of the dorsalis pedis artery between the first and second metatarsals. The medial plantar artery travels inferior to the first metatarsal bone to supply the great toe.

Figure 15-7, Pedal artery anatomy. A, Lateral digital subtraction angiogram (DSA) of the ankle and forefoot. 1, Distal peroneal artery with anterior and posterior communicating branches. 2, Posterior tibial artery . 3, Medial plantar artery. 4, Lateral plantar artery. 5, Dorsalis pedis artery. 6, Lateral tarsal artery. 7, Medial tarsal artery. 8, Anterior tibial artery. B, DSA of the forefoot. 4, Lateral plantar artery. 5, Dorsalis pedal artery. 9, Arcuate artery. 10, Dorsal metatarsal artery. 11, Plantar metatarsal artery.

The blood supply of the foot can be considered in terms of three-dimensional anatomic units called angiosomes . These include skin as well as the underlying structures ( Table 15-2 ). An understanding of angiosomes can help direct revascularization procedures when there is tissue loss in the foot.

Table 15-2
Angiosomes of the Foot
Artery Arterial branches Angiosome
PT Medial calcaneal Heel
Medial plantar Instep
Lateral plantar Lateral foot and forefoot
Peroneal Anterior perforating Lateral anterior upper ankle
Lateral Calcaneal Plantar heel
AT Multiple branches Anterior ankle
Dorsalis pedis Dorsum of the foot
AT, Anterior tibial artery; PT, posterior tibial artery.

Key Collateral Pathways

The PFA is critically important in the collateral supply of lower-extremity arteries ( Fig. 15-8 ). Occlusion of the CFA results in collateralization from the abdomen, pelvis, and the contralateral extremity to the PFA, which in turn reconstitutes the SFA ( Box 15-1 and Fig. 15-9 ). These are the same collateral pathways that reconstitute the PFA when it is severely stenotic or occluded at its origin.

Figure 15-8, Diagram of collateral pathways to the lower-extremity arteries. Shaded areas are levels of obstruction. 1, Superior mesenteric artery. 2, Inferior mesenteric artery. 3, Lumbar artery. 4, Common iliac artery. 5, Internal iliac artery. 6, Deep iliac circumflex artery. 7, External iliac artery. 8, Common femoral artery. 9, Medial femoral circumflex artery. 10, Lateral femoral circumflex artery. 11, Profunda femoris artery. 12, Superficial femoral artery. 13, Second perforator. 14, Descending branch of lateral femoral circumflex artery. 15, Descending genicular artery. 16, Popliteal artery. 17, Anterior tibial artery. 18, Peroneal artery. 19, Posterior tibial artery. 20, Dorsalis pedis artery.

Box 15-1
Collateral Pathways in Common Femoral Artery Occlusion

  • Lumbar artery → circumflex iliac artery → PFA → SFA

  • Common iliac artery → internal iliac artery → PFA → SFA

  • Contralateral PFA → transpubic collaterals → PFA → SFA

PFA, Profunda femoris artery; SFA, superficial femoral artery.

Figure 15-9, Collateralization around chronic left common femoral artery occlusion (white arrowheads) in an adolescent due to cardiac catheterization as an infant. The only symptom was leg-length discrepancy. There are well-developed collaterals from ipsilateral hypogastric branches (black arrowhead) and contra lateral external pudendal arteries (black arrow) .

Proximal occlusion of the SFA results in hypertrophy of PFA branches, which in turn reconstitute the SFA via muscular branches in the thigh ( Fig. 15-10 ). This can be an extremely effective collateral pathway, so much so that patients may have palpable distal pulses. When the distal SFA is occluded, the descending trunk of the PFA provides collateral flow to the popliteal artery through the lateral genicular arteries. Occlusion of the above-knee popliteal artery can be collateralized from both the distal SFA (via the descending genicular artery) and the PFA. In the presence of a below-knee popliteal artery occlusion, the sural and genicular arteries can reconstitute the tibial arteries.

Figure 15-10, Collateralization of a superficial femoral artery (SFA) occlusion by enlarged profunda femoris artery (PFA). Coronal maximum intensity projection of a computed tomography angiogram showing an enlarged left PFA (curved arrow) that reconstitutes an occluded SFA in the midthigh (straight arrow). Note the focal SFA stenosis (arrowhead) on the right.

Occlusion of the tibioperoneal trunk and the proximal tibial arteries results in collateral supply from the sural and genicular arteries. Each of the tibial arteries has the potential to provide collateral supply to the others. The peroneal artery is the most common source of collateral supply, in that it is frequently spared in occlusive disease and occupies a central location in the calf. At the ankle the peroneal artery has a constant bifurcation that can collateralize to the distal anterior or posterior tibial arteries (see Fig. 15-7 ).

Occlusion of either the dorsalis pedis or posterior tibial artery distal to the medial malleolus is well tolerated if the plantar arches are intact. Occlusion of both the proximal dorsalis pedis and the inframalleolar posterior tibial artery is collateralized by tarsal and metatarsal arteries.

Noninvasive Physiologic Evaluation

Evaluation of lower-extremity arterial occlusive disease requires determination of physiologic impact as well as imaging. The severity of an obstructive lesion does not always correlate with the severity of the symptoms. Knowledge of the patient’s past surgical history is important for accurate interpretation of physical examination and any test. Noninvasive physiologic testing provides an objective measure of disease that can be used to follow patients and document outcomes of interventions ( Box 15-2 ).

Box 15-2
Noninvasive Tests of Lower-Extremity Arterial Supply

  • Physical examination

  • Ankle-brachial index (ABI)

  • Segmental limb pressures

  • Doppler waveforms

  • Plethysmography (volume or photo)

The most basic physiologic assessment is the physical examination. Important information can be obtained from the patient history and by examining the limbs in question. The lower extremities should be evaluated for skin integrity, capillary refill, temperature, and palpable pulses. In diabetic patients, it is important to inspect between the toes for early skin breakdown and infection. The femoral, popliteal, dorsalis pedis, and posterior tibial arterial pulses should be checked in both legs, regardless of the laterality of symptoms. In addition, the carotid and radial pulses should be assessed.

The ratio of the systolic blood pressures of the ankle to the upper arm (the ankle-brachial index, ABI) is a basic measure of the status of the peripheral arteries. An appropriately sized blood pressure cuff and a Doppler ultrasound probe are used to determine the systolic blood pressure at the ankle (dorsalis pedis or posterior tibial artery) and the brachial artery. The blood pressure in both arms should be obtained, and the highest used to calculate the ratio. Ratios are often slightly greater than 1 in normal individuals. In patients with occlusive disease, the ABI correlates roughly with the extent of disease and degree of ischemia ( Table 15-3 ). This is a simple test that can be performed at the bedside or the procedure table before and after an intervention.

Table 15-3
Resting Ankle-Brachial Indices
ABI Severity of Disease Typical Symptoms
≥0.95 None None
0.75-0.95 Mild, single segment None, claudication
0.5-0.75 Moderate Claudication
0.3-0.5 Moderate severe, usually multilevel Severe claudication
<0.3 Critical, multilevel or acute occlusion Rest pain, tissue loss
ABI, Ankle-brachial index (ratio of ankle systolic blood pressure and brachial systolic blood pressure).

The ABI can be falsely elevated in patients with diabetes with noncompressible vessels due to calcific medial sclerosis. The digital arteries are not as severely affected by this process. In these patients, toe pressures are an important indicator of the severity of occlusive disease. The normal systolic blood pressure in the toe is greater than 50 mm Hg, with a toe-brachial index of at least 0.6. Toe pressures less than 30 mm Hg are incompatible with healing of ulcers or surgical incisions.

One of the major limitations of the ABI is that it does not provide any information about the level of the obstruction. A useful and simple modification is to obtain blood pressures at three or four different levels in the leg (“segmental limb pressures”). A Doppler probe is positioned over a pedal artery as cuffs over the thigh, calf, and ankle are inflated and deflated. The pressure at which signal reappears in the foot is noted as each cuff is deflated. Appropriately sized cuffs are used for each segment of the leg. The variability in limb circumference of the leg results in slightly higher pressure measurements with the thigh cuffs, especially in obese patients. In addition, diabetic patients may have falsely normal pressure measurements for reasons noted earlier. A drop in pressure of more than 20-30 mm Hg at any level suggests hemodynamically significant occlusive disease in that vascular segment. In addition, a difference in pressures from side to side of more than 20 mm Hg indicates occlusive disease at that level or proximal in the affected limb.

Segmental limb pressures are frequently combined with Doppler waveform analysis at each level ( Fig. 15-11 ). This greatly enhances the utility of the study by providing an assessment of flow in addition to pressure. Changes in the shape and amplitude of the waveform reflect increasing severity of disease ( Fig. 15-12 ). Precise identification of the insonated vessel is essential for accurate testing.

Figure 15-11, Schematic of changes in lower-extremity arterial Doppler waveforms with different levels of ischemia. Note that the normal pattern is triphasic (high peripheral resistance).

Figure 15-12, Normal and abnormal lower-extremity Doppler waveforms. A, Normal examination showing excellent waveforms and pressures at all levels. The pedal waveforms typically lose the triphasic pattern. B, Examination in a patient with severe ischemia. The arm/thigh blood pressures ratios were 0.53 on the right and 0.43 on the left, indicating bilateral inflow disease. The arm/calf pressure indices dropped to 0.35 on the right and 0.28 on the left, indicative of bilateral superficial femoral artery disease as well. The ankle-brachial index (ABI) was 0.28 on the right and 0.24 on the left. The waveforms are barely biphasic proximally and are essentially flat in the toes. These findings are consistent with severe bilateral multilevel disease.

Additional noninvasive examinations for peripheral vascular disease are volume and photoplethysmography. These techniques measure the global perfusion of the extremity by recording the minute changes in the volume of the extremity that occur throughout the cardiac cycle. The terms volume plethysmographic recordings (VPRs) or pulse volume recordings (PVRs) are essentially interchangeable. A series of blood pressure cuffs are applied to the extremity, and sequentially inflated to 60-65 mm Hg. The pressure in the cuff changes slightly as the volume of blood changes with systole and diastole. These changes are displayed as a waveform ( Fig. 15-13 ). Abnormalities in the waveform indicate occlusive disease in the vascular segment proximal to the cuff. For example, an abnormal tracing at the thigh is not caused by SFA disease, but disease in the aorta, common iliac artery, or CFA. Medial sclerosis does not affect plethysmography, but patient motion does degrade the study.

Figure 15-13, Schematic of volume plethysmographic waveforms in relationship to degree of inflow disease. As disease progresses, the waveform becomes blunted and diminished in amplitude.

The plethysmographic waveform can be analyzed for both contour and amplitude. The contour of the waveform is determined by the status of the arterial blood supply. As the degree of stenosis becomes more severe, the dicrotic notch is lost and the overall slope is flattened. The amplitude of the waveform reflects the underlying muscle mass. Fat and bone are relatively avascular, and contribute little to the change in volume during the cardiac cycle. This accounts for why the amplitude increases slightly at the calf in normal individuals owing to the lower amount of adipose tissue. Photoplethysmography can be used in the evaluation of vasospastic disorders by testing before and after temperature stimuli.

Patients with claudication and normal or near-normal pulse examinations and physiologic tests should undergo exercise testing. Occlusive lesions that are well compensated at rest may be unmasked by hyperemia created in the distal muscular bed during exercise. Testing is performed before and after walking on a treadmill at a grade of 10-12 degrees for 5 minutes at 1.5-2 miles per hour. The time to onset and features of the symptoms are recorded. Normally, the ABI remains unchanged or even increases with exercise, and the amplitude of the volume recording increases with preservation of the contour. An abnormal response indicates hemodynamically significant occlusive disease.

Imaging

A wide variety of imaging modalities can be applied to the lower-extremity arteries. Availability of a technique at a particular institution depends upon the presence of appropriate equipment and expertise. Regardless of the imaging modality, it is essential to know the patient’s symptoms, past surgical history, and results of noninvasive testing before performing and interpreting a study.

Color-flow Doppler ultrasound can be used to image the lower-extremity arteries and surgical bypass grafts. A variety of criteria have been promoted to categorize occlusive lesions ( Table 15-4 ). Careful inspection of each abnormal vascular segment with gray-scale, color, and Doppler ultrasound is necessary to precisely localize abnormalities. Bypass grafts are particularly well suited to ultrasound imaging when they are superficial in location.

Table 15-4
Duplex Criteria for Native Lower-Extremity Arterial Stenosis
Stenosis PSV (Sample Value) Poststenotic Turbulence
None Normal (100 cm/sec) None
<50% <2 × normal (<200 cm/sec) Minimal
50%-75% 2-4 × normal (>200 cm/sec) Moderate
76%-99% >4 × normal (≥400 cm/sec) Severe
100% No flow Not applicable
PSV, Peak systolic velocity.

Magnetic resonance angiography (MRA) can detect luminal stenoses greater than 50% in the lower-extremity arteries with sensitivity and specificity that exceed 95%. The first technique to produce reliable imaging was two-dimensional time-of-flight (2-D TOF) MRA. This appeared to have the ideal quality of imaging blood flow rather than contrast enhancement, so that timing issues were nonexistent. However, overestimation of stenoses, saturation of inplane flow, and the long time span (1.5-2 hours) needed for a complete examination were among several serious limitations of 2-D TOF MRA. Gadolinium-enhanced three-dimensional (3-D) acquisitions have replaced 2-D TOF MRA in most instances. Stepping table technology permits true gadolinium-enhanced MRA runoffs. Bolus chase or multiple injections of gadolinium (usually no more than 30-40 mL in total) provide excellent images from the renal arteries to the ankle (see Fig. 3-12 ). Time-resolved techniques allow dynamic imaging of the blood flow in the extremity (see Fig. 3-13 ). Dedicated foot sequences are useful in the foot due to small vessel size ( Fig. 15-14 ). An entire runoff from the renal arteries to the foot can now be acquired in a few minutes. In patients with renal insufficiency at high risk for nephrogenic systemic fibrosis from gadolinium, noncontrast MRA techniques are used.

Figure 15-14, Dedicated three-dimensional gadolinium-enhanced magnetic resonance angiogram of the foot in a patient with severe tibial artery disease demonstrates a patent lateral plantar artery (arrow) .

Computed tomography angiography (CTA) of the lower-extremity arteries is widely available due to multirow detector technology. As the number of rows increases, the imaging of lower-extremity arteries improves. Depending upon the number of detector channels, reconstructed images of 0.5-2 mm thickness can be obtained from the renal arteries to the calf in less than 20 seconds (see Fig. 15-10 ). Contrast is injected at 3-5 mL/sec for a total volume of approximately 100-150 mL, although the volume needed decreases as the number of detector rows increases. Opacification is generally excellent from the renal to the tibial arteries. Venous enhancement and heavy calcification of small vessels are limitations in the calf and foot, but can sometimes be overcome by focused examinations ( Fig. 15-15 ). Streak artifact from joint replacements can make interpretation of the adjacent arteries impossible. Postprocessing is necessary to remove bone and soft tissues.

Figure 15-15, Volume rendering of a CTA at the level of the foot showing a reconstituted distal posterior tibial (arrow) and plantar arteries.

The role of conventional angiography in the diagnosis of lower-extremity arterial disease has changed substantially with the improvement in noninvasive imaging techniques. Angiography was once obtained uniformly in all patients before surgery or intervention. Currently angiography is a secondary diagnostic imaging modality (used to resolve conflicting noninvasive test results or when CTA or MRA are not adequate), but the primary imaging modality during interventions.

Angiographic evaluation of the lower extremities includes, as a minimum, the aortic bifurcation to the ankle. In most patients, an abdominal aortogram with a pigtail or other high-flow nonselective catheter is performed before imaging the lower extremities, particularly when renovascular or visceral artery occlusive disease is suspected (see Fig. 10-7 ). The catheter should be positioned with the side holes in the visceral segment when the celiac artery and SMA are to be included. Pelvic arteriography is performed with the same catheter just proximal to the aortic bifurcation. Anteroposterior and bilateral oblique views should be obtained whenever iliac artery pathology is suspected (see Fig. 10-8 ). Typical pelvic angiographic injection parameters are 8-10 mL/sec of contrast injected for 2-3 seconds, with imaging at 2-4/sec. Pressure gradients should be obtained across any suspicious stenosis (see Fig. 4-8 ).

Positioning of the legs is an important consideration during runoff angiograms. The legs should be held as close together and as stationary as possible without tight straps or tape that could compress vessels and create artifactual occlusions. The latter is most likely to occur at the ankles and feet. Even though optimum positioning of the feet varies among departments, it is not critical because dedicated foot imaging can and should always be added when indicated.

Bilateral lower-extremity runoffs are obtained with the catheter at the aortic bifurcation using two basic strategies. The simplest is stationary imaging of overlapping areas of the legs. Small (10-20 mL) contrast injections are performed with filming at 1-2 frame/sec until all vessels are fully opacified at the level being imaged. Rapidly filling normal arteries and slowly filling reconstituted arteries are both easily imaged. The overall volume of contrast necessary is dependent upon the severity of disease; as the length and number of occlusions increase, more contrast is needed to opacify reconstituted distal vessels. This technique allows runoff imaging even with very basic C-arms and tables.

The second, more common approach is to image sequential overlapping levels of the pelvis and legs during a long continuous contrast injection using motorized tables, C-arms, or both. Although less overall contrast is typically used compared to stationary runs, the likelihood of underfilling of vessel segments is greater. A test injection of a small amount of contrast (10-20 mL) at the aortic bifurcation with imaging at the knees allows assessment of the symmetry of flow. The imaging stations, technique, and patient positioning are then set. Scout images of the legs are obtained followed immediately by contrast injection and digital subtraction imaging ( Fig. 15-16 ). Manually activated changes in table position (“bolus chase”) are based on real-time assessment of vascular opacification. Single-phase injections use a constant rate of contrast injection, whereas dual phase injections use one rate in the pelvis followed by a lower rate during imaging of the extremities to increase the overall duration of the injection. A typical single-phase injection would be full-strength or diluted low osmolar contrast injected at 6-10 mL/sec for 10-12 seconds. A dual-phase injection might use 10 mL/sec when imaging the pelvis followed by 6 mL/sec during filming of the legs.

Figure 15-16, Bilateral lower-extremity runoff using bolus-chase digital subtraction angiogram technique. Each level was carefully programmed to have several centimeters of overlap with the previous level. The levels were changed during the acquisition by the angiographer who monitored arterial opacification on a live image during the injection. Contrast was diluted to two-thirds strength and injected at a rate of 10 mL/sec for a total duration of 10 seconds. A, Station 1, pelvis. A pigtail catheter has been positioned in the distal abdominal aorta. There are stents in both common iliac arteries and occlusion of the left internal iliac artery. The arrow is on a distinctive branch of the left profunda femoris artery (PFA). B, Station 2, thighs. The distinctive branch of the left PFA (arrow) is seen at the top of the image, confirming adequate overlap with the previous station. The superficial femoral arteries are diseased but patent. C, Station 3, knees. There is focal severe stenosis of the above-knee popliteal artery on the left. D, Station 4, proximal calves. Both anterior tibial arteries are occluded proximally. E, Station 5, distal calves. On the right, the anterior tibial artery reconstitutes distally but the dorsalis pedis artery is occluded. The right posterior tibial artery is occluded distally, and the plantar artery is reconstituted from the peroneal artery. On the left, the peroneal and posterior tibial arteries are diseased but continuous. F, Station 6, feet. On the right, the medial and lateral plantar arteries are filled from a posterior terminal branch of the peroneal artery. The dorsalis pedis artery is not visualized. On the left, the posterior tibial artery is continuous with the plantar arteries, but the dorsalis pedis artery is not visualized.

When there is a big disparity in the time that it takes contrast to reach both knees, reactive hyperemia effectively decreases the transit time on the slower side by half. This simple maneuver is performed by inflating a blood pressure cuff to a suprasystolic pressure at the ankle for 2-3 minutes. The cuff is then released and removed just before contrast injection.

Selective single-limb angiography provides excellent filling of vessels with less dilution of contrast. The inflow vessels should first be examined with pelvic (or aortic and pelvic) arteriography. Subsequently, when the access is from the ipsilateral CFA, a 5-French straight multiple side-hole or a tightly recurved end-hole catheter can be withdrawn into the external iliac artery. When the access is from the contralateral CFA, an end-hole catheter such as an Sos or Cobra-2 can be positioned over the aortic bifurcation in the common or external iliac artery. Contrast injection rates of 4 mL/sec provide excellent opacification using bolus chase or standing runs (see Fig. 15-7 ).

The origins of the SFA and PFA are usually best viewed from an ipsilateral anterior oblique projection (see Fig. 10-8 ). These views should be obtained when the vessel origins are not clearly seen in anteroposterior projections. Additional oblique and even lateral views of specific abnormalities are not usually obtained, but can be important to accurately grade stenoses, particularly in the tibial arteries where overlying bone can obscure vessels or create subtraction artifacts ( Fig. 15-17 ).

Figure 15-17, Importance of careful limb positioning and multiple views during angiography. Popliteal artery stenosis obscured by total knee prosthesis. A, Digital subtraction angiogram in the anteroposterior projection showing the above-knee popliteal artery obscured by the knee prosthesis (arrows) . B, Lateral view of the same patient showing a focal stenosis (arrow) in the above-knee popliteal artery that was treated successfully with angioplasty.

Whenever there is pathology present in the foot, dedicated views are necessary. A single lateral view that includes the malleolus to the toes is usually sufficient, although an anteroposterior projection may be necessary for specific indications (see Fig. 15-7 ). Positioning the catheter tip in the external iliac artery or SFA maximizes the delivery of contrast to the foot. The foot should be carefully taped in position (with special attention to delicate skin and pressure points). Extreme plantar flexion of the foot should be avoided to prevent artifactual occlusion of the dorsalis pedis artery ( Fig. 15-18 ). In the presence of extensive proximal occlusive disease, it is important to use reactive hyperemia, prolonged image acquisition, and injection of full-strength low-osmolar contrast at 5 mL/sec for 4-6 seconds.

Figure 15-18, Artifactual stenosis of dorsalis pedis artery due to positioning of the foot (“ballerina sign”). A, Lateral digital subtraction angiogram of the foot in plantar flexion (“en pointe” like a ballerina) showing focal stenosis (arrow) of the dorsalis pedis artery. B, The angiogram was repeated with the foot in neutral position. The dorsalis pedis stenosis is now gone (arrow) . This same artifact can also be caused by tight straps or tape on a limb.

Chronic Occlusive Disease

There are many causes of peripheral arterial occlusions ( Box 15-3 ). This section focuses on atherosclerotic disease, which is the most common chronic pathology encountered in lower-extremity arterial circulation.

Box 15-3
Etiologies of Chronic Peripheral Vascular Occlusions

  • Atherosclerosis

  • Thromboangiitis obliterans (Buerger’s disease)

  • Popliteal entrapment syndrome

  • Adventitial cystic disease

  • Radiation

  • Vasculitis

  • Ergotism

  • Trauma

  • Chronic embolism

The prevalence of atherosclerotic peripheral arterial disease increases with age, from 3% in individuals aged 40-59 years to 20% in adults older than 70 years. Until age 65 years, men are affected more often than women. Fewer than half of people with atherosclerotic peripheral arterial disease are symptomatic, most commonly with atypical leg pain. Classic pain with ambulation (claudication) occurs in 10%-35%. Only 1%-2% have rest pain, tissue loss, or gangrene (critical limb ischemia; CLI) at presentation. Smoking, diabetes, hyperlipidemia, homocystinemia, advanced age, ethnicity, and hypertension are important risk factors.

Peripheral arterial disease is a marker of systemic atherosclerosis and increased risk of death from stroke and myocardial infarction. The estimated rate of nonfatal cardiovascular events in patients with confirmed peripheral arterial disease is 2%-4% per year. Approximately 65% of patients with lower-extremity arterial disease have abnormal cardiac stress tests, and 25% have carotid artery stenoses greater than 70%. The underlying cause of death in 60% of patients with peripheral vascular disease is a cardiac event. A diagnosis of peripheral vascular disease confers a mortality rate that is almost triple that of age-matched controls ( Table 15-5 ).

Table 15-5
Survival in Patients with Peripheral Vascular Disease
Parameter (%)
5-year survival, all patients 70
10-year survival, all patients 50
15-year survival, all patients 30
5-year survival, claudication managed conservatively 87
5-year survival, claudication requiring surgery 80
5-year survival, limb-threatening ischemia treated with surgery 48
5-year survival, reoperation for limb-threatening ischemia 12

The symptoms of chronic peripheral arterial occlusive disease are related to the level of the occlusion and the presence of comorbid conditions such as diabetes. Symptoms are typically manifested in the limb segment distal to the occlusive process. The classic chronic complaint is claudication, which is consistently described by patients as onset of muscular tightening or cramping with exertion. This should resolve within minutes with rest. Patients may often report atypical symptoms such as nonspecific leg weakness and numbness with exercise that also resolves with rest. As chronic ischemia progresses, skin changes such as scaling, hair loss, and atrophy occur.

Critical limb ischemia is manifested as rest pain, ulceration, and tissue necrosis. Rest pain in CLI is aggravated by elevation of the limb and relieved when the limb is dependent. The foot may be noticeably red when dependent, and pale when elevated. Ulceration is painful and usually occurs in the foot and toes following minor trauma. Spontaneous posterolateral lower leg ulceration can be seen with small vessel arterial disease. Severe ischemic changes can develop in diabetic patients in the presence of palpable pedal pulses, owing to extensive microvascular pathology. To facilitate communication about patients with peripheral vascular disease, the classification devised by Rutherford and associates should be used ( Table 15-6 ).

Table 15-6
Rutherford Categories of Chronic Limb Ischemia
Grade Category Clinical Description Objective Criteria
0 0 Asymptomatic Normal treadmill or reactive hyperemia test
1 Mild claudication Completes treadmill test; ankle pressure after exercise > 50 mm Hg but at least 20 mm Hg lower than brachial pressure
I 2 Moderate claudication Between categories 1 and 3
3 Severe claudication Cannot complete treadmill test; ankle pressure < 50 mm Hg after exercise
III 4 Ischemic rest pain Resting ankle pressure < 60 mm Hg; flat or severely dampened ankle or metatarsal pulse volume recording; toe pressure < 40 mm Hg
III 5 Minor tissue loss; nonhealing ulcer, focal gangrene with diffuse pedal ischemia Resting ankle pressure < 40 mm Hg; flat or barely pulsatile ankle or metatarsal pulse volume recording; toe pressure < 30 mm Hg
6 Major tissue loss extending above transmetatarsal level; functional foot unsalvageable Same as category 5

Treadmill test is 5 minutes at 2 mph on a 12-degree incline.

Not all ulcers represent CLI. Patients with severe diabetic neuropathy can develop ulceration over pressure points such as the metatarsal head. These are usually painless and associated with callous formation. Venous ulcers are distinguished from lesions due to arterial insufficiency by their typical medial location around the medial ankles in the lower leg, rich vascularity, and associated manifestations of chronic venous stasis (see Fig. 16-19 ).

The distribution of lower-extremity atherosclerosis is symmetric in almost 80% of patients, although the severity of the lesions may not match ( Box 15-4 ). Involvement of adjacent segments is common, with combined iliac artery and SFA disease in 46%, and femoropopliteal and tibial disease in 38%. The iliac arteries are diseased in 46% of patients with SFA and popliteal stenoses. There are several well-recognized patterns of distribution of disease, including normal inflow with severe infrapopliteal artery disease in patients with diabetes and renal failure; isolated distal aortic and bifurcation disease in middle-aged females; and iliofemoral disease in smokers ( Fig. 15-19 ).

Box 15-4
Typical Locations for Atherosclerotic Stenosis in the Lower Extremities

  • Superficial femoral artery in Hunter canal

  • Common iliac artery

  • Popliteal artery at joint line

  • Tibioperoneal trunk

  • Origins of tibial arteries

Figure 15-19, Gadolinium-enhanced three-dimensional magnetic resonance angiogram runoff in a patient with diabetes and foot pain with nonpalpable pedal pulses. The arteries are widely patent to the level of the distal tibial arteries where occlusions are seen of all three tibial arteries at various levels in the calves.

Most patients (70%-80%) have stable symptoms over 5 years, whereas 10%-20% note an increase in severity, and 5%-10% progress to CLI. Limb loss is one of the most clearly defined measures of outcome in peripheral vascular disease. Only 12% of symptomatic patients require amputation within 10 years of diagnosis, or roughly 1% of claudicants per year. Diabetes and continued smoking result in higher rates of amputation.

Patients presenting with CLI (about 1%-3% of newly diagnosed patients per year) have a worse prognosis than claudicants. Up to 25% require amputation at the time of presentation, more than half undergo revascularization, and the remainder can be managed medically. Within a year, 25% of these patients will have died, the same percentage will have undergone below- or above-knee amputations, and similar proportions will be symptom free or still in a state of CLI.

Management is conservative for most patients with claudication. Lifestyle modification (cessation of smoking being the most important), exercise programs, lipid management, and control of comorbid diseases such as diabetes are frequently successful in stabilization or slight improvement of symptoms in patients able to comply. A 6-month trial of conservative therapy is usually indicated before considering more aggressive treatment. Supervised exercise programs reliably reduce reported claudication symptoms and increase walking time. Few medications, however, have been shown to conclusively improve claudication symptoms. One that is effective is cilostazol, a phosphodiesterase inhibitor that can increase walking distance by up to 50% in some patients. The typical dose is 100 mg by mouth twice daily. Cilostazol is contraindicated in patients with congestive heart failure. Aspirin and other antiplatelet drugs reduce overall risk of cardiovascular events, but have little impact on claudication symptoms.

Patients with progressive symptoms or who are severely limited by their claudication may be considered for revascularization procedures. Patients with critical ischemia (rest pain, tissue loss, and gangrene) often require aggressive intervention to preserve the limb. As a general rule, healing of an ischemic foot ulcer will not occur in the absence of a pulse in at least one pedal artery.

The workup of a patient with peripheral arterial disease begins with a history and physical examination. The nature and onset of the symptoms, comorbid conditions, and clinical evidence of cardiac or cerebrovascular disease should be determined. The physical examination is of paramount importance and includes a comprehensive pulse examination, careful inspection of the limb for evidence of ischemic disease, and detection of clues indicative of nonarterial causes of the presenting symptoms.

Physiologic testing is relatively inexpensive and has a major role in the diagnosis and follow-up of patients with symptomatic peripheral vascular disease. Patients with true claudication can be separated from patients with limb pain due to spinal stenosis and osteoarthritis. Progression of disease and effectiveness of interventions can be documented objectively. Exercise testing should be obtained in any patient with suspected claudication whose study results are normal or near-normal while at rest.

The decision to pursue imaging in a patient with peripheral vascular disease is dependent upon the management plan. Owing to the expense and potentially invasive nature of the imaging studies, these examinations should not be obtained unless a patient requires revascularization. The history, physical examination, and results of physiologic testing are sufficient to diagnose peripheral vascular disease in almost all patients.

Noninvasive imaging with ultrasound, MRA, and CTA has reported sensitivities and specificities for occlusive lesions exceeding 95% for all three modalities. MRA and CTA are particularly useful in imaging the lower-extremity runoff in patients with infrarenal aortic occlusions, in that both the arterial inflow and outflow can be visualized (see Fig. 10-26 ). Ultrasound does not reliably image aortic and iliac inflow, but can quantify flow through abnormal areas. The degree of a focal arterial stenosis is often overestimated on MRA and CTA, and metal in vascular clips or joint prostheses can create signal loss on MRA. Streak artifacts from joint prostheses seen on CTA can obscure adjacent blood vessels. In patients with mild renal insufficiency, allergy to iodinated contrast, and severe multilevel disease, MRA and ultrasound are excellent imaging choices.

Conventional angiography remains crucially important in the management of patients with symptomatic chronic peripheral vascular disease. Angiography is indicated when a percutaneous intervention is highly probable based on examination or noninvasive testing, or when discrepant results are obtained. Surgical bypass can be performed on the basis of high-quality ultrasound, MRA, or CTA.

Percutaneous access for angiography in patients with severe occlusive disease or prior surgery can be challenging. Posterior plaque in the CFA is common and can impede insertion of a guidewire. Patients with prior surgery or angiograms may have scarring of the soft tissues that prevents advancement of a catheter. In this situation, overdilation of the tract by 1 French size over a stout guidewire (e.g., Amplatz) is necessary before placement of the catheter. The presence of an aortobifemoral bypass graft can also complicate the initial access (see Fig. 2-33 ). When femoral access cannot be obtained, axillary, radial, or translumbar puncture may be required. Patients having undergone prior distal surgical bypass procedures may require additional views in opposing obliquities for a complete study. Surgical anastomoses frequently have a flared appearance (“the hood” of the graft) related to the manner in which the graft is attached to the native vessel ( Fig. 15-20 ). Distal bypasses may arise from the CFA, PFA, SFA, or even the popliteal artery. The proximal anastomosis is usually on the anterior wall of the vessel when the origin is the CFA, PFA, or SFA; filming in a steep anterior oblique projection may be necessary for adequate visualization. Distal anastomoses vary in orientation depending upon the target vessel. The course of the bypass graft may be similar to the native artery or may be extraanatomic (see Fig. 15-3 ). Careful attention to coning and positioning during the angiogram is necessary to avoid inadvertently excluding a portion of the graft. When there is a severe stenosis in the mid or distal portion of the graft, contrast injected proximal to the graft may not opacify the stagnant column of blood in the graft. This “pseudo occlusion” should be suspected when a definite meniscus is not seen at the origin of the graft or when a pulse is known to be present in the nonvisualized bypass. Selective injection into the graft is necessary to determine the status of the graft in these cases.

Figure 15-20, Digital subtraction angiogram of reversed great saphenous vein graft from the common femoral artery to the right anterior tibial artery. The course of the graft is posterior and lateral to the knee joint in an extraanatomic location to facilitate anastomosis to the anterior tibial artery. Proximally there is an area of stenosis (bent arrow) in the graft (which later underwent angioplasty); open arrow indicates the location of a venous valve; arrowhead identifies the stump of a ligated venous branch; arrow is pointing to the flared distal anastomosis of the vein end-to-side to the anterior tibial artery.

The most common surgical interventions in patients with chronic occlusive disease are various bypass procedures. A number of surgical conduits have been investigated, but autogenous vein and polytetrafluoroethylene (PTFE) have proven the most successful, with single segment great saphenous veins having the best results. In general, synthetic grafts are used only when autogenous vein is not available. Veins may be harvested from either leg (great and small saphenous vein), or constructed from available lengths of arm veins (cephalic, basilic, brachial veins). An in situ great saphenous vein graft is created by fashioning proximal and distal arteriovenous anastomoses without removing the vein from the leg. Intraluminal cutting devices are used to destroy the intervening vein valves, and all side branches are carefully obstructed by direct ligation/clipping or endovascular coil embolization. The size of the vein at the anastomosis site approximates that of the artery. Reversed saphenous vein grafts are first harvested from the leg, followed by ligation of branches. The vein is then tunneled through the soft tissues in reverse orientation, so that the smaller (formerly most peripheral) end is at the CFA, and the larger (formerly most central) end is at the distal anastomosis. Local endarterectomy procedures alone or in combination with distal bypass are sometimes used, especially for lesions of the CFA and PFA origin.

Perioperative mortality for peripheral vascular bypass is 2%-5%, largely due to cardiac events. Early graft thrombosis (within 30 days) due to technical errors, such as kinking or a retained valve, or a hypercoagulable state occurs in 2%-7%. Intimal hyperplasia is the cause of most graft failures between 3 months and 2 years. In synthetic grafts this occurs at the anastomoses or at sites of clamp placement on native vessels. In addition to these locations, intimal hyperplasia can occur anywhere within a vein graft, but usually occurs at the sites of valves, branch vessels, or vein-to-vein anastomoses. Graft failure after 2 years is usually the result of progression of disease in the inflow or outflow vessels. However, vein bypass grafts can remain patent despite occlusion of the native inflow. Graft infection and anastomotic pseudoaneurysms are additional complications. The overall results of surgical bypass grafts are listed in Table 15-7 . Long-term rates of limb salvage and patient survival are best when the indication for surgery is severe claudication rather than critical ischemia.

Table 15-7
Results of Lower-Extremity Surgical Bypass
Procedure 5-Year Primary Patency (%)
Femoral to Popliteal Artery Bypass
Synthetic above-knee 60
Synthetic below-knee 35
Saphenous vein above-knee 75
Saphenous vein below-knee 75
Femoral to Tibial Artery Bypass
Synthetic 14
Saphenous vein 75
Femoral to Pedal Artery Bypass
Saphenous vein 45

Graft surveillance with ultrasound is important to prevent thrombosis and extend the life of the bypass. A decrease in the ABI of 0.15-0.2, or identification of a new hemodynamically significant stenosis at any point in the graft, should prompt further imaging. Focal stenoses are usually treated first with percutaneous angioplasty (see Fig. 15-20 and Fig. 15-21 ). These are fibrotic lesions and may require a cutting or scoring balloon. Long-segment lesions are best managed with graft revision or insertion of a jump graft around the stenotic area. Thrombolysis of an acutely thrombosed graft may unmask an underlying stenosis, although no lesion is found in up to one third of cases. When the graft crosses the knee joint and no stenosis is found after thrombolysis, flexion and stress views should be obtained to exclude kinking or external compression ( Fig. 15-22 ).

Figure 15-21, Angioplasty of a vein graft stenosis. A, Digital subtraction angiogram (DSA) showing focal stenosis (arrow) of a reversed saphenous vein bypass from the common femoral artery to the anterior tibial artery. The deviation in the popliteal artery (arrowhead) with an associated bulge is the site of the distal anastomosis of an old occluded graft to the popliteal artery. B, DSA after angioplasty of the stenosis showing an excellent result (arrow) that remained widely patent for several years.

Figure 15-22, Graft entrapment in the popliteal fossa. A, Digital subtraction angiogram (DSA) in neutral position of a left femoral to below-knee popliteal artery saphenous vein bypass graft after successful thrombolysis of a graft thrombosis. Other views of the graft showed no evidence of stenosis. B, DSA with slight flexion of the knee shows compression of the graft (arrow) at the level of the knee joint consistent with graft entrapment. This was released surgically, and the graft has remained patent since.

Percutaneous Superficial Femoral Artery and Popliteal Interventions

Percutaneous intervention for occlusive disease of the infrainguinal arteries has a long history; the first percutaneous angioplasty ever was performed in the leg (see Fig. 4-1 ). A wide variety of technologies have since been applied to this vascular bed, including angioplasty, stents, drug-eluting stents, stent-grafts, mechanical atherectomy, drills, freezing or drug-eluting balloons, and lasers. Devices for treatment of occlusive disease in this vascular segment are a focus of intense commercial activity.

Catheter-based interventions for SFA and popliteal artery occlusive disease have undergone numerous clinical trials, but until recently few were prospective and even fewer randomized. One challenge has been the rapid evolution in technology and clinical practice, such that multiyear trials may not produce results relevant to current practice. Nevertheless, these are the preferred interventions (over surgical bypass) in many situations ( Box 15-5 ). Stenoses and occlusions of almost any length can be treated, but the initial technical success and long-term results are proportional to lesion length and multiplicity, with shorter and fewer being better.

Box 15-5
Trans-Atlantic Inter-Society Consensus (TASC) II Recommendations for Femoropopliteal Interventions (2007)

These recommendations are likely to change as stent-grafts, drug-eluting stents, drug-eluting balloons, and pharmacologic adjuncts become scientifically evaluated.

  • Lesion type A: Endovascular is treatment of choice

    • Single stenosis ≤ 10 cm (unilateral/ bilateral)

    • Single occlusion ≤ 5 cm length

  • Lesion type B: Endovascular frequently used but insufficient scientific evidence

    • Multiple lesions, each ≤ 5 cm in length (stenoses or occlusions)

    • Single stenosis or occlusion ≤ 15 cm in length, not involving the distal popliteal artery

    • Heavily calcified occlusion ≤ 5 cm in length

    • Single popliteal stenosis

    • Single or multiple lesions in the absence of continuous tibial vessels to improve inflow for distal bypass

  • Lesion type C: Surgical treatment used more often but insufficient scientific evidence

    • Recurrent stenoses or occlusions that need treatment after two prior endovascular interventions

    • Multiple stenoses or occlusions totaling > 15 cm, ± heavy calcification

  • Lesion type D: Surgery is treatment of choice

    • Chronic total occlusion of CFA or SFA (>20 cm), involving the popliteal artery.

    • Chronic total occlusion of the popliteal artery proximal trifurcation vessels

CFA, Common femoral artery; POP, popliteal artery; SFA, superficial femoral artery.

Long occlusions can be treated either through the native lumen, or with subintimal angioplasty (see Fig. 4-5 ). Drug-eluting stents hold promise for use in long-segment recanalization of the SFA and popliteal artery, and for below-knee interventions. When fresh-appearing thrombus is present in an occlusion, a short trial of catheter-directed thrombolysis may convert it to a stenosis and decrease the risk of distal embolization (see Fig. 4-28 ).

The most direct approach to infrainguinal interventions is from an antegrade puncture in the ipsilateral CFA, which provides the greatest mechanical advantage and permits use of standard length delivery systems. Antegrade puncture is frequently not possible, however, because of a large abdominal pannus. From the contralateral approach, a 30- to 45-cm flexible sheath placed over the aortic bifurcation provides a stable platform for most interventions. Longer guidewires are often necessary with this access, especially when working in the distal SFA. Typical balloon diameters for the SFA are 5-7 mm, and for the popliteal artery 4-6 mm, on 5-French or smaller catheters. Balloon lengths of 20 cm or more are available for treatment of long-segment disease. Rapid-exchange balloon catheters are an advantage when working in the distal SFA or popliteal artery. Cutting and scoring balloons and debulking devices are useful for recalcitrant stenoses (see Figure 4-15, Figure 4-26, Figure 4-27 ). Most operators judge the results of angioplasty visually, with rapid flow and decreased filling of collaterals, and by improvement of distal pulses if present. An irregular lumen with visible fissures in the plaque are common after adequate angioplasty and should not be interpreted as dissections requiring additional treatment when flow is brisk and distal perfusion improved (see Figure 4-9, Figure 4-10 ). Intravascular ultrasound, transcutaneous ultrasound, and pressure measurements using special guidewires can provide more objective assessment of technical results.

When the results of angioplasty are unsatisfactory or when extensive disease is present, self-expanding bare metal stents or stent-grafts improve the lumen ( Fig. 15-23 ). In many practices, stent placement is the norm. Balloon-expandable stents should not be used in the SFA or popliteal artery, because they can be crushed by external forces. The choice between bare metal stent and stent-graft is also often subjective. Stent-grafts usually require larger diameter delivery systems and exclude potential collateral branches, whereas bare metal stents are subject to restenosis over their entire length. ( Fig. 15-24 and see Fig. 4-24 ) When placing either of these devices it is believed important to limit balloon inflations beyond the ends of the stent or stent-graft to decrease the occurrence of intimal hyperplasia in these locations. Intravascular brachytherapy and drug-eluting stents may decrease intimal hyperplasia.

Figure 15-23, Recanalization of a distal superficial femoral artery (SFA) occlusion with a stent. A, Digital subtraction angiogram (DSA) before the intervention showing the well-collateralized occlusion of the distal SFA with reconstitution at the adductor canal. B, DSA after successfully crossing the lesion and angioplasty showing an unsatisfactory result with a narrow, irregular arterial lumen and continued filling of collaterals. C, DSA following self-expanding bare metal stent placement and repeat angioplasty. There is now excellent flow through the stented region without visualization of collaterals.

Figure 15-24, Long-segment superfi cial femoral artery (SFA) stenoses treated with ePTFE-covered stent graft. A, Digital subtraction angiogram (DSA) showing multiple stenoses in the distal SFA. Note the small muscular branches arising from the SFA. B, DSA following angioplasty and placement of a stent-graft (W. L. Gore & Associates, Inc.). The multiple small branches seen in the previous image are no longer present (arrows) .

The environment of the SFA is demanding, in that different forces act on different locations. The portion of the artery at the adductor canal is subject to compression, flexion, and rotation during normal bending and straightening of the knee. Stent fracture is a well-recognized event in this location, presumably related to these forces. The risk of fracture is linked to stent design and the number of stents placed (areas of overlap create rigid zones).

Crossing long-segment occlusions can be a particular challenge with SFA interventions, particularly with heavily calcified lesions. A number of tools have been developed to improve success rates. These can be used to get through or around occlusions (see Figure 4-4, Figure 4-6 ). When a subintimal approach is used intentionally (or unintentionally), some of these devices can be used to facilitate reentry into the true lumen below the lesion.

Careful monitoring of guidewire tip position during SFA interventions reduces the risk of spasm in distal vessels. Intraprocedural heparin (3000-5000 U), nitroglycerin, and antiplatelet drugs should be used. Larger doses of heparin should be used for longer segments of disease and longer interventions. Anticoagulation may be continued overnight when long-segment disease is treated or runoff is poor. As a minimum, patients should be discharged on aspirin 80-360 mg/day for life unless contraindicated. In addition, an oral platelet inhibitor such a clopidogrel 75 mg/day for 3 months may be beneficial.

The most common complications of SFA and popliteal interventions are intraprocedural thrombosis, occlusive dissection, and distal embolization. The overall rate of complications is less than 5% in most centers, but increases with the extent of preexisting disease, complexity of the procedure, and duration. The use of distal protection devices (see Fig. 4-19 ) should be considered when feasible in patients at risk for distal embolization, such as long segment interventions, irregular plaque with mobile components, or symptoms of distal embolization before the procedure. Intraprocedural thrombosis or embolization can be managed with thrombolysis, mechanical thrombectomy, or suction thrombectomy (see Fig. 4-33 ). Flow-limiting dissections are effectively treated with stent placement. Anticoagulation, gentle catheter and guidewire manipulation, and careful attention to guidewire and device positions minimize injury to the SFA or distal vessels.

The technical success rate for percutaneous SFA and popliteal interventions is greater than 95% for stenoses and 85%-90% for occlusions. The lower rate in occlusions is due to occasional failures to cross the lesion. Pressure gradients as a definition of technical success are usually not used in SFA and popliteal artery angioplasty. The degree of residual stenosis (<30%), qualitative assessment of flow, return of palpable distal pulses, or an ABI measured on the procedure table is used to determine the procedural endpoints.

The outcomes of SFA and popliteal artery interventions continue to be an area of intense investigation and redefinition. The easiest outcome to measure is freedom from amputation, but this may not be adequate for patients treated for severe claudication rather than critical ischemia. The Society of Vascular Surgery has recommended a composite endpoint for CLI of above-ankle amputation of the index limb or major reintervention (new bypass graft, jump/interposition graft revision, or thrombectomy/thrombolysis). This endpoint is termed a major adverse limb event (MALE). In patients treated for claudication, duration of symptomatic improvement and freedom from reintervention are important endpoints.

The BASIL (Bypass versus Angioplasty in Severe Ischemia of the Leg), a seminal multicenter trial comparing angioplasty to vein or synthetic conduit bypass demonstrated no difference in survival or amputation rates at 2 years (despite a 20% procedural failure rate for angioplasty). The vessels treated included the SFA and more distal arteries. However, after 2 years, patients randomized to bypass who had venous conduits had superior results with fewer reinterventions. The application of these results to current practice should be tempered, in that few interventionalists restrict SFA interventions to angioplasty alone.

Certain observations are consistent: interventions on short stenoses have the best outcome, with results deteriorating as lesions become longer and include occlusions; surgical bypass with good-quality single-segment saphenous vein has the best long term primary and secondary patency but is associated with longer recovery and more morbidity than percutaneous interventions; bare metal stents and stent-grafts improve long-term patency but restenosis remains a major issue ( Table 15-8 and Fig. 15-25 ). Drug-eluting stents and drug-coated balloons show promise in reducing the incidence of restenosis by as much as 50%. The long-term data on these devices has yet to be developed. In summary, percutaneous intervention has become the preferred treatment option for many patients with femoropopliteal artery disease, but much work is needed to understand outcomes in different populations.

Table 15-8
Results of Superficial Femoral and Popliteal Artery Angioplasty and Stents
Procedure Indication Primary Patency at 3 Years (%)
Angioplasty (stenosis) Claudication 62
Angioplasty (stenosis) Limb salvage 43
Angioplasty (occlusion) All 48
Bare stent, SFA All 65
Stent-graft, SFA All 70

Results for Viabahn (W. L. Gore) in long segment stenoses or occlusions.

Figure 15-25, Intimal hyperplasia within a bare metal stent (arrows) in the superficial femoral artery. This is the same patient as in Figure 15-23 , imaged 1 year later.

Tibial Artery Angioplasty and Stents

Tibial artery interventions are considered separately from the SFA and popliteal arteries because both the clinical and technical challenges are different. The indications are usually limb salvage in the setting of CLI with impending or ongoing tissue loss, or preservation of runoff distal to a bypass graft. Tibial artery occlusive disease is rarely isolated, but frequently occurs in conjunction with SFA and popliteal artery disease. Almost three fourths of patients undergoing tibial artery angioplasty are diabetic.

The optimal approach to tibial artery intervention is antegrade from the ipsilateral CFA. When this is not possible, use of a long, flexible sheath or guiding catheter placed over the aortic bifurcation is necessary to provide stability and allow contrast injections. Positioning the sheath or guide catheter in the SFA improves delivery of contrast to the target area. When working in tibial arteries over the bifurcation, long guidewires and balloon catheters are required. Angioplasty in pedal arteries is possible with these extra-long shaft balloons. Rapid-exchange balloon catheters are especially useful in this environment (see Fig. 4-14 ). Combined retrograde access through the dorsalis pedis or posterior tibial artery and antegrade access from a femoral approach are useful advanced techniques, especially for subintimal recanalization of long-segment distal occlusions.

Typical balloon diameters for tibial arteries are 2-4 mm. These small vessel balloons often require 0.018-inch or smaller guidewires. Lesions at the origins of the tibial arteries can undergo angioplasty safely using “kissing balloons” in both arteries or a safety wire in one and the balloon in the other ( Fig. 15-26 ). Long balloons (≥20 cm) are specifically designed for angioplasty of diffusely diseased tibial arteries ( Fig. 15-27 ). Angioplasty through the pedal arch is feasible with these specialized balloons.

Figure 15-26, Spot film showing positioning of angioplasty balloons (arrows) for kissing balloon angioplasty of anterior tibial and tibioperoneal artery origin stenoses.

Figure 15-27, Tibial artery reconstruction in a patient with critical limb ischemia. A, Digital subtraction angiogram (DSA) showing diffuse occlusive disease of the tibial arteries. ( Arrow, posterior tibial artery; arrowhead, occluded peroneal artery.) B, DSA of the foot showing the diseased distal posterior tibial artery supplying the plantar artery. C, Spot image of a 2 mm × 20 cm angioplasty balloon (arrows) in the posterior tibial artery. Angioplasty was also performed of the tibioperoneal trunk, the peroneal artery after recanalization with a guidewire, and the distal posterior tibial artery and lateral plantar artery. D, Completion DSA showing patent posterior tibial (arrow) and peroneal arteries (arrowhead) as well as the tibioperoneal trunk. E, Completion DSA of the foot.

Stents are increasingly used in this vascular bed ( Fig. 15-28 ). Drug-eluting stents may have an important role in these small-diameter arteries. Long-segment recanalization with subintimal techniques, atherectomy, or laser atherectomy improves procedural success but long-term outcomes are not known. Focal recalcitrant lesions can undergo angioplasty with cutting or scoring balloons

Figure 15-28, Stent placement in the peroneal artery. A, Digital subtraction angiogram obtained before intervention showing short occlusion of the peroneal artery (arrow) . Not shown are the distal occlusion of the anterior tibial artery and the occluded posterior tibial artery. B, During angioplasty of the peroneal artery an occlusive intimal flap occurred that was treated with a 2.75-mm diameter coronary stent (arrows) . The anterior distal anterior tibial artery was successfully recanalized with balloon angioplasty alone.

Intraprocedural thrombosis is of greater concern with tibial artery intervention than SFA or popliteal artery. Patients should be aggressively anticoagulated with heparin (ACT > 250) during the procedure. Addition of intravenous antiplatelet drugs, similar to the approach used in coronary interventions, is advocated by some interventionalists. Liberal use of intraarterial nitroglycerin is important to prevent spasm in these small vessels.

Intervention in these small, diseased arteries is more prone to complications than in other peripheral arteries. Vessel rupture is usually of little consequence although compartment syndrome can occur. Occlusive flaps, thrombosis, and distal embolization are seen on 5%-10% of patients.

The published literature on tibial artery intervention is scant in comparison to more proximal lesions. The technical success approaches 95%, particularly for focal disease in native vessels that have inline runoff to the foot ( Table 15-9 ). Occlusions, stenoses of bypass graft anastomoses, and lesions in vessels with poor runoff have a lower technical success rate. Limb salvage is a more accurate measure of outcome than lesion patency, in that most tibial interventions are performed for this indication.

Table 15-9
Results of Tibial Artery Interventions
Parameter Result (%)
Technical success 95
Primary patency angioplasty 1 year 40
Primary patency bare stent 1 year 50
Primary patency drug-eluting stent 1 year 85

Acute Limb Ischemia

Acute limb ischemia is the sudden onset (less than 2 weeks) of a symptomatic limb due to arterial occlusion. The estimated incidence is 1.5 cases per 10,000 persons per year. Approximately 45% of patients will present with a viable limb, 45% with a threatened limb, and 10% with a nonviable limb. The acute, profoundly ischemic limb is a surgical emergency. Cell death begins after 4 hours of total ischemia and is irreversible after 6 hours. The clinical presentation can be summarized as the “six Ps” ( Box 15-6 ). These symptoms reflect the greater sensitivity of nerves and muscle to ischemia than skin and subcutaneous tissues. The mortality of patients with acute limb ischemia within 1 year is almost 20% despite aggressive intervention; amputation is undertaken in 15% of those who survive.

Box 15-6
Six “P”s of Acute Limb Ischemia

  • Pulseless

  • Pain

  • Pallor

  • Paresthesia

  • Paralysis

  • Poikilothermia (cool limb)

There are numerous causes of acute limb ischemia ( Box 15-7 ). A major diagnostic goal is the distinction between primarily embolic versus thrombotic occlusion ( Table 15-10 ). Embolic occlusions tend to result in profound ischemia owing to the absence of developed collateral circulation (see Fig. 1-33 ). Thrombosis of a preexisting stenosis is generally better tolerated because the collateral circulation is already established.

Box 15-7
Etiologies of Acute Limb Ischemia

  • Embolic

  • Trauma

  • Thrombosis of atherosclerotic stenosis

  • Thrombosis of surgical bypass graft

  • Thrombosis of degenerative popliteal aneurysm

  • Popliteal artery entrapment or cyst with thrombosis

  • Iatrogenic

  • Dissection

  • Vasospasm

  • Venous thrombosis (phlegmasia cerulea dolens)

  • Low-output cardiac state

Table 15-10
Differentiating Features of Acute Arterial Occlusion
Embolic Thrombotic
Identifiable source of emboli Frequent Rare
Preexisting claudication Rare Frequent
Physical examination Normal proximal and contralateral pulses Evidence of peripheral vascular disease in ipsilateral and contralateral limb
Degree of ischemia Frequently profound Frequently threatened but viable
Imaging findings Normal vessels with abrupt occlusion (sometimes multiple), frequently at major bifurcation of vessel, no collaterals, meniscus sign Diffuse atherosclerotic disease, well developed collaterals, usually midvessel occlusion

A classification system has been devised for describing the degree of acute limb ischemia ( Table 15-11 ). This classification is different from the one for patients with chronic ischemia, in that the clinical presentation and outcomes are different. For example, tissue loss and gangrene are late findings of ischemia, but paralysis and sensory loss indicate acute hypoxia of nerves and muscle.

Table 15-11
Clinical Categories of Acute Limb Ischemia
Physical Examination Doppler Signals
Category Definition Prognosis Sensory Loss Muscle Weakness Arterial Venous
I Viable Not immediately threatened None None + +
II Threatened
a. Marginally Salvageable with prompt treatment Minimal (toes) None Occasional +, frequently − +
b. Immediately Salvageable with immediate treatment More than toes, rest pain Mild to moderate Rare +, usually − +
III Irreversible Major permanent tissue loss Anesthetic Paralysis

Patients presenting with acute limb ischemia should be heparinized immediately to prevent propagation of thrombus and provide a mild vasodilatory effect. The history of onset of symptoms frequently suggests the etiology of the occlusion. Examination of all of the peripheral pulses is important to gauge the presence of peripheral vascular disease or multiple emboli. The electrocardiogram may provide an important clue regarding the etiology of the occlusion (looking specifically for atrial arrhythmias or prior myocardial infarction).

The decision to obtain an imaging test is based upon the clinical status of the limb and the probable etiology of the occlusion. Patients with critically ischemic but viable limbs due to a presumed embolus or graft thrombosis should proceed directly to surgical exploration; the delay required to obtain imaging may jeopardize the ability to salvage the extremity. Intraoperative angiography can be performed in patients with profound ischemia when visualization of distal runoff is necessary. Patients with threatened but viable limbs and extensive underlying vascular disease or a complex vascular surgical history benefit from preoperative imaging. Patients with nonviable limbs are managed with amputation of the affected extremity.

Imaging with MRA and CTA can provide diagnostic information in cooperative patients. These modalities are not considered first in many patients because current therapeutic endovascular procedures are not routinely feasible with CT or MR guidance. Conventional diagnostic angiographic studies have the potential for becoming therapeutic interventions, such as thrombolysis or pharmacomechanical thrombectomy.

The angiographic evaluation of a patient with acute limb ischemia should be tailored to the clinical situation. Standard catheters, guidewires, and injection rates can be used. Percutaneous access should be planned to support a possible intervention. In patients with suspected embolic disease, an aortogram may reveal silent emboli to renal or visceral branches, or pathology such as an aneurysm or large ulcerated plaque. As a minimum, imaging should span from the aortic bifurcation to below the level of the occlusion. Oblique views of the pelvis may demonstrate emboli in the hypogastric arteries, thus confirming the nature of the more distal occlusion. A dedicated, but reasonable effort should be made to image the reconstituted vessels distal to the occlusion to facilitate planning of interventions. However, in patients with poor collaterals this may be difficult or impossible.

Revascularization of the viable acutely ischemic limb is almost always indicated. Thrombectomy with Fogarty balloon catheters through limited CFA or popliteal artery incisions is an effective method to relieve acute obstruction, especially embolic obstruction. This can be accomplished with the patient under local anesthesia. Balloon catheters can also be passed in a retrograde manner into the pelvic inflow arteries. When embolectomy is unsuccessful in restoring sufficient flow for limb viability, bypass surgery can be performed. Fasciotomy may be necessary in patients in whom compartment syndrome (especially anterior calf) develops following surgery. Surgical interventions result in limb salvage in 75%-90% of patients and a 30-day mortality of 10%-15%. However, embolectomy is frequently incomplete, particularly in the tibial and pedal arteries, and may result in intimal injury.

Percutaneous interventions in patients with acutely ischemic but viable limbs (categories I, IIA, and IIB) are indicated when urgent surgery is not necessary and embolic occlusion is unlikely. The objectives of treatment are to rapidly restore flow and identify underlying lesions that subsequently can be corrected percutaneously or with surgery. Pharmacologic thrombolysis, mechanical thrombolysis, and aspiration thrombectomy are useful techniques in both embolic and thrombotic occlusions (see Fig. 4-28 ). Occlusions less than 14 days old are amenable to pharmacologic and mechanical thrombolysis. Mechanical thrombectomy devices are very useful for rapid restoration of flow. Subsequent pharmacologic thrombolysis may be used to clean up residual thrombus for optimal results. Aspiration thrombectomy should be considered for acute (<48 hours) occlusions, especially those occurring as complication of a revascularization procedure (see Fig. 4-33 ).

Thrombolysis or mechanical thrombectomy successfully restores antegrade flow in more than 95% of patients as long as the occlusion can be crossed with an infusion catheter or thrombectomy device. Causes of procedural failure include severe coexistent inflow or outflow disease, organized thrombus, or large atheromatous emboli. The results measured in terms of limb salvage range from 75% to 92% depending on the extent of underlying disease and patient comorbid conditions. With thrombolysis, the majority of severe complications are hemorrhagic, occurring in 6%-9% of patients and more commonly with long infusions, in hypertensive patients, in patients older than age 80 years, and in patients with thrombocytopenia. Mechanical thrombectomy, pharmacomechanical thrombectomy, ultrasound-assisted thrombolysis, and aspiration thrombectomy can shorten overall procedure times and thus should reduce complication rates (see Figure 4-31, Figure 4-32, Figure 4-34 ). There are no recent randomized prospective trials of endovascular versus surgical treatment for acute limb ischemia. Based on older studies of catheter thrombolysis compared with surgery, long-term limb preservation with thrombolysis with or without surgery is identical to surgical therapy alone, but mortality may be lower owing to fewer cardiovascular complications.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here