Infrainguinal Occlusive Disease

Updated: Jun 01, 2020
Author: Christian Ochoa, MD; Chief Editor: Vincent Lopez Rowe, MD, FACS 


Practice Essentials

This article reviews chronic infrainguinal atherosclerotic arterial occlusive disease caused by atherosclerosis involving the femoral, popliteal, or infrapopliteal arteries. Because chronic atherosclerotic disease may result in acute circulatory compromise, acute arterial occlusion is also covered. Less common etiologies of lower-extremity arterial insufficiency, such as atheroembolism, thromboangiitis obliterans (Buerger disease), popliteal artery entrapment syndrome, and cystic adventitial disease, are briefly discussed.

Decision-making in the management of vascular disease changes frequently as new information becomes available and as new technologies emerge. Furthermore, therapeutic recommendations for a given population may not be applicable to individual patients with even slightly differing risk factors, comorbidities, or vascular anatomy.[1]

Although most patients with infrainguinal disease are treated nonoperatively, more than 100,000 vascular reconstructive procedures are performed each year in the United States alone. Unfortunately, intervention fails in as many as 50% of cases within 5 years.[2]

Of the symptomatic patients under medical care, approximately 25% develop progressive symptoms within 5 years, with 5-10% requiring surgical intervention and 1-2% undergoing major amputation within this same period.[3, 4]  The vast majority of patients with intermittent claudication remain stable or improve with noninvasive management. Surgical or endovascular intervention is indicated for intractable and disabling claudication, for ischemic pain at rest, and for ischemic necrosis. Surgery also may be useful for nonhealing ischemic ulceration.

According to Baumgartner et al, 25% of patients with claudication will eventually require revascularization and only 5% will develop critical limb ischemia (CLI).[5]  (The term chronic limb-threatening ischemia [CLTI] is increasingly used in preference to CLI.[6] ) Within the first year after the initial diagnosis, 6-9% of patients require intervention.[5]  Subsequently, 2-3% of patients per year require intervention.[5]

Because lower-extremity atherosclerosis is a marker for systemic atherosclerotic disease, these patients have significant systemic morbidities. About 30% of patients with peripheral artery disease (PAD) die within 5 years, and 40% die within 10 years.[3, 7]

Feringa et al observed a cohort of 2642 patients having ankle-brachial indices (ABIs) less than or equal to 0.9.[7]  They discovered that the major factors associated with mortality in this group of patients included renal dysfunction, heart failure, ST-segment changes, age greater than 65 years, hypercholesterolemia, ABI lower than 0.60, Q-waves, diabetes, cerebrovascular disease, and pulmonary disease. They also found that the use of statins, aspirin, and beta blockers correlated with reduced 10-year mortality.


The inguinal (Poupart) ligament is a tough, fibrous band stretching from the anterior superior iliac spine to the pubic tubercle. The common femoral artery is a continuation of the external iliac artery, beginning just under the middle of the inguinal ligament. It is palpable as the femoral pulse and is well suited to both percutaneous and surgical access because of its relatively superficial position.

Approximately 2.5-5.0 cm distal to the inguinal ligament, the common femoral artery divides into the deep femoral (profunda femoris) artery, usually arising in the posterolateral position, and the superficial femoral artery.

The deep femoral artery gives rise to several very proximal branches that tend to maintain patency even in persons with extensive atherosclerotic disease, thus providing the major source of collateral circulation around an occluded superficial femoral artery.

The term superficial femoral artery is somewhat of a misnomer, in that it is superficial for only a few inches until it courses under the sartorius and into the aponeurotic covering of the adductor (Hunter) canal.

When the superficial femoral artery emerges anterior to the adductor magnus, it becomes the popliteal artery. Because the popliteal artery is bounded posteriorly by the popliteal vein, nerve, and fascia and the semimembranosus, gastrocnemius, plantaris, and soleus muscles, it is the most difficult of the lower-extremity pulses to assess accurately.

The popliteal artery passes posterior to the knee joint and into the upper leg where, just distal to the popliteus, it divides into the anterior tibial artery and the tibioperoneal trunk.

The anterior tibial artery passes laterally through the interosseous membrane and lies on the interosseous membrane throughout much of the leg. As it reaches the lower leg, it lies on the tibia and then becomes superficial at the ankle joint, at which point it is called the dorsalis pedis artery and, hence, is palpable as the dorsalis pedis pulse.

The tibioperoneal trunk divides within approximately 2.5 cm of its origin into the peroneal artery and the posterior tibial artery.

The peroneal artery lies on the medial surface of the fibula and ends in terminal branches near the os calcis. The peroneal artery, which is too deep to be palpable as a pulse, often remains patent despite atherosclerotic occlusion of the anterior and posterior tibial arteries and, thus, may be a usable site for the distal anastomosis of bypass grafts in patients with advanced infrapopliteal occlusive disease.

The posterior tibial artery runs along the medial side of the leg and posterior to the medial malleolus, where it is superficial and palpable as the posterior tibial pulse.

The great (long) saphenous vein (GSV) originates on the medial side of the dorsum of the foot and runs anterior to the medial malleolus. It then runs posteromedially to the tibia, posteriorly to the medial condyle of the femur, and along the medial thigh, coursing anteriorly until it enters the femoral vein through the foramen ovale, just below the inguinal ligament. The length and relatively superficial course of the GSV make it ideally suited for use in infrainguinal bypass surgery.


Atherosclerotic occlusive disease

With atherosclerotic occlusion of a major lower-extremity artery, the limb is perfused via collateral pathways. Although this alternate pathway may be adequate at rest, it becomes inadequate as the oxygen demands of the leg musculature increase with activity. This results in calf muscle pain or fatigue, a symptom known as intermittent claudication. As the degree of atherosclerotic occlusion worsens, blood flow, even at rest, may become impaired. This may cause ischemic pain at rest, ischemic ulceration, and gangrene.

Acute arterial occlusion

Acute occlusion of peripheral arteries commonly involves the infrainguinal segment. Underlying atherosclerotic disease may result in intraluminal strictures that impair blood flow and cause acute thrombosis. Emboli typically lodge at bifurcations and, hence, tend to occlude the distal common femoral artery (the most common site, accounting for 34% of all arterial emboli) or the distal popliteal artery (14%). Popliteal artery aneurysms may thrombose as a result of turbulent blood flow.

The clinical indications of acute occlusion of lower-extremity arteries are the classic six Ps, as follows:

  • Paresthesias
  • Pain
  • Poikilothermia (coolness)
  • Pallor
  • Pulselessness
  • Paralysis

The anatomic level at which pulse loss occurs helps identify the location of the occlusion.


Commonly accepted risk factors for both the occurrence and the progression of atherosclerotic vascular disease include the following[8] :

  • Abnormal glucose tolerance
  • Cigarette smoking
  • Advanced age
  • Hyperlipidemia
  • Hypertension

Certain biochemical factors have also been shown to be independent risk factors for atherosclerotic peripheral vascular disease, including the following:

  • Increased plasma fibrinogen levels [9]
  • Hyperhomocysteinemia [10, 11]
  • High-sensitivity C-reactive protein (CRP) [12]

These factors may also increase the risk of bypass graft stenosis and reocclusion.

When more than one risk factor is present, the cumulative risk is often greater than individual risk factors combined. This is especially true of cigarette smoking, which, when accompanied by another risk factor (eg, hypertension or hyperlipidemia) increases the disease risk to more than twice the sum of the individual risks.


Chronic atherosclerotic lower-extremity disease is present in 20% of the population older than 55 years.[13] Most affected persons are asymptomatic. In fact, it has been estimated that only about 20% of people with atherosclerotic lower-extremity disease present to a physician because of symptoms. Another 20% are symptomatic but do not seek medical attention.


Medical management

Infrainguinal arterial disease is associated with a risk of limb-threatening ischemia. However, most patients improve with medical treatment. Approximately 10% of patients with intermittent claudication develop findings necessitating vascular reconstructive procedures.

Endovascular management

Patency rates following endovascular treatment of infrainguinal occlusive disease vary significantly among published series. Overall, primary patency has been somewhat inferior to that of bypass surgery. Nonetheless, successful endovascular management improves quality of life and patient satisfaction.[14]  Furthermore, further endovascular or surgical management can often correct a failed endovascular intervention.[15, 16]

Surgical management

Graft patency rates vary widely among series. One study in which graft patency was assessed by means of magnetic resonance angiography (MRA) disclosed an 84% limb salvage rate and a 78% primary graft patency rate at 21 months' follow-up. Prosthetic grafts carry a primary 3-year patency rate of 39% and a 3-year secondary patency rate of 59%, with a 25% risk of amputation within 3 years.[17]

Limb salvage rates are lower among patients with insulin-dependent diabetes.[18]  Infrainguinal reconstructive surgery is associated with a mortality of somewhat less than 5% despite the high-risk nature of these patients.[19]  The likelihood of coexisting coronary artery disease is a major risk factor.

A British study reports that the major amputation rate after femorodistal bypass remains high, with adverse events occurring after approximately 38% of femoropopliteal procedures and nearly 50% of femorodistal bypasses. The main predictors of a poor outcome reportedly were diabetes and chronic renal failure.[20]

The overall survival rate for patients with lower-extremity arterial occlusive disease is approximately 50% over 10 years. For patients who require bypass surgery, the survival rate drops to approximately 50% over 5 years.

A study by Suckow et al explored associations between statin use and long-term mortality, graft occlusion, and amputation after infrainguinal bypass.[21]  The investigators found that such therapy yielded a significant benefit with respect to 5-year survival but did not offer a significant advantage with respect to 1-year amputation or 1-year graft occlusion rates.

Khoury et al studied trends in mortality, readmissions, and complications after endovascular and open infrainguinal revascularization for PAD.[22] They found that open infrainguinal revascularization, though associated with lower rates of adverse events in comparison with endovascular therapy, was independently associated with increased risks of short-term (30-day) readmission, complications, and mortality. 




Most people harboring atherosclerotic disease of the lower extremities are asymptomatic; others develop ischemic symptoms. Some patients attribute ambulatory difficulties to old age, unaware of the existence of a potentially correctible problem.

Symptomatic patients may present with intermittent claudication, ischemic pain at rest, nonhealing ulceration of the foot (see the image below), or frank ischemia of the foot.

Pressure ulcer of heel exacerbated by infrainguina Pressure ulcer of heel exacerbated by infrainguinal arterial occlusive disease.

Cramping or fatigue of major muscle groups in one or both lower extremities that is reproducible upon walking a specific distance suggests intermittent claudication. This symptom increases during ambulation until walking is no longer possible, and it is relieved by several minutes of rest. The onset of claudication may occur sooner with more rapid walking or when walking uphill or up stairs.

The claudication of infrainguinal occlusive disease typically involves the calf muscles, whereas symptoms that occur in the buttocks or thighs suggest aortoiliac occlusive disease.[23]

Physical Examination

Physical examination discloses absent or diminished peripheral pulses below a certain level. Although diminished common femoral artery pulsation is characteristic of aortoiliac disease, infrainguinal disease alone is characterized by normal femoral pulses at the level of the inguinal ligament and diminished or absent pulses distally.

Specifically, loss of the femoral pulse just below the inguinal ligament occurs with a proximal superficial femoral artery occlusion. Loss of the popliteal artery pulse suggests superficial femoral artery occlusion, typically in the adductor canal. Loss of pedal pulses is characteristic of disease involving the distal popliteal artery or its trifurcation.

It is important, however, to be aware that absence of the dorsalis pedis pulse may be a normal anatomic variant, noted in approximately 10% of the population. On the other hand, the posterior tibial pulse is present in 99.8% of persons aged 0-19 years. Hence, absence of both pedal pulses is a more specific indicator of peripheral arterial disease.

Other findings suggestive of atherosclerotic disease include a bruit heard overlying the iliac or femoral arteries, skin atrophy, loss of pedal hair growth, cyanosis of the toes, ulceration or ischemic necrosis, and, after 1-2 minutes of elevation above heart level, pallor of the involved foot followed by dependent rubor (see the image below).

Cyanosis of first toe and dependent rubor of foot, Cyanosis of first toe and dependent rubor of foot, characteristic of arterial insufficiency.


Diagnostic Considerations


Although ischemic findings in the face of absent pulses clearly pinpoint arterial insufficiency as the culprit, intermittent claudication, even when associated with absent pulses, is not always due to arterial insufficiency.

If symptoms are not always reproducible (ie, if the patient sometimes has "good days" when ambulation is not limited by claudication) or if the symptoms are associated with low back pain or radiculopathy, the clinician should consider the possibility of pseudoclaudication, which occurs as a result of spinal stenosis or cauda equina syndrome.

In that case, the pulse deficit may be an incidental finding of asymptomatic atherosclerosis. Noninvasive vascular laboratory testing (see Laboratory Studies), lumbosacral imaging, and neurologic evaluation all may contribute to distinguishing between these possibilities.

Two rather unusual conditions, venous claudication due to extensive iliofemoral venous thrombosis and chronic compartment syndrome due to calf muscle hypertrophy in athletes, result in a bursting type of pain in the calf with ambulation, which subsides slowly with elevation. In each case, the etiology is impaired venous outflow.


Patchy areas of ischemia involving the feet, especially in the presence of palpable pedal pulses, suggest the possibility of atheroembolism of plaque fragments from ulcerated, although nonocclusive, proximal atherosclerotic plaques or from thrombus lining the wall of an infrarenal aortic aneurysm (see Abdominal Aortic Aneurysm).[24]

Thromboangiitis obliterans (Buerger disease)

Severe ischemia of the toes with absent pedal pulses but normal proximal pulses in a man aged 35-50 years who smokes cigarettes may be the result of thromboangiitis obliterans (Buerger disease).[25]  Ischemia of the fingers may also be present. The digits are cool, moist, mottled, and sometimes have tender shallow ulcers. Migratory superficial phlebitis may occur.

Collagen-vascular disease must be excluded.[26]  Angiography reveals pathognomonic findings of "corkscrew" arteries. Treatment is discontinuation of smoking and good local wound care. Vascular surgery is rarely possible because of the poor quality of the distal arteries.

Complex regional pain syndromes

Complex regional pain syndromes (CRPSs; eg, posttraumatic pain syndromes, causalgia, mimocausalgia, Sudeck atrophy, reflex sympathetic dystrophy) have been classified by the World Health Organization into the following two variants:

  • CRPS II (ie, causalgia), which is associated with a demonstrable nerve injury
  • CRPS I (ie, mimocausalgia, reflex sympathetic dystrophy, Sudeck atrophy), which includes the remainder

Causalgia (from the Greek words kausos ["heat"] and algos ["pain"]) was first described in patients with arterial and nerve injuries sustained during the American Civil War. Both variants of CRPS remain poorly understood and often misdiagnosed.

Although the exact pathophysiology is elusive, the sympathetic nervous system clearly plays a focal role. Therefore, surgical sympathectomy—perfected decades ago by vascular surgeons to manage nonreconstructible arterial disease (a common situation at the time)—was once the mainstay for treatment of the CRPSs.

Although surgical sympathectomy is now mostly notable only for historic purposes, sympathetic blockade is quite effective and is commonly performed for the CRPSs. Hence, currently the treatment of CRPSs is performed mainly by pain management specialists. Nonetheless, because the vascular surgeon has always been primarily responsible for the diagnosis of extremity symptoms, it is not uncommon for patients with CRPS to report to a vascular surgeon because of extremity pain.

Such pain may occur after extremity trauma but may seem disproportionate to the degree of injury.[27]  Pain may also manifest after delayed revascularization of an acutely ischemic extremity. The diagnosis is often one of exclusion and thus requires a high index of clinical suspicion.

The diagnosis should be considered more strongly if severe superficial burning pain and agonizing hypersensitivity are present and are associated with vasomotor abnormalities such as edema, erythema, and hyperhidrosis. Radiographic studies may demonstrate relative and patchy osteopenia in the involved extremity.

In addition to symptomatic relief, management of the CRPSs requires sympathetic blockade. This is best performed during the early (acute) stage when the clinical course may be reversible. As the disease progresses, the erythema gives way to cyanotic mottling, the acute edema transforms to brawny edema, and the pain becomes unrelenting and disabling. These findings occur at approximately the third month and represent the second (dystrophic) stage. At this point, both plain radiographs and bone scans tend to demonstrate indicative findings.

Over time, disuse leads to atrophy, soft-tissue fibrosis, and joint contractures. Radiographs confirm ankylosis and severe osteoporosis. This signals the third (atrophic) stage. Note that atrophy can also occur because of intentional disuse for anticipated secondary gain. Such patients reportedly do not respond to treatment until litigation has concluded.

Typically, the clinician does not even consider the diagnosis of a CRPS until the second stage. At that point, a dramatic clinical response to sympathetic blockade may confirm the diagnosis. Unfortunately, too much damage may have already occurred for sympathetic ablation to be effective and to break the vicious cycle of pain, sympathetic overactivity, and pain; the progression of the CRPS may be inexorable and irreversible.

One other caveat is that in the face of coexisting arterial disease, the vascular surgeon who may attribute the symptoms to ischemia and thereby may consider bypass should be aware that a surgical incision tends to exacerbate the pain in an extremity afflicted with a CRPS.

For more information, see Complex Regional Pain Syndrome in Emergency Medicine.

Popliteal artery entrapment syndrome

Intermittent claudication occurring in younger persons (from the teens to approximately age 45 years), particularly males, raises the possibility of popliteal artery entrapment syndrome.[28]

In this unusual condition, the artery follows an aberrant course around the gastrocnemius, usually medial to the medial head instead of between the two heads of this muscle. Ambulation causes the muscle to compress the artery and results in transient loss of distal blood flow. Over time, the artery may thrombose or become aneurysmal.

Before complete thrombosis, this condition can sometimes be confirmed clinically by noting loss of the pedal pulse upon active plantarflexion or passive dorsiflexion of the foot. Computed tomography (CT) or magnetic resonance imaging (MRI) can reveal the muscular abnormality, and angiography with stress views can confirm the diagnosis.

Treatment entails sectioning the aberrant muscle fibers. Bypass grafting is needed if the occlusion is chronic in nature. Assessing the contralateral side is important because one third of cases are bilateral.

Cystic adventitial disease of popliteal artery

Intermittent claudication of abrupt onset occurring in a relatively young male also may be the result of cystic adventitial disease of the popliteal artery.[29]

This rare congenital anomaly is the result of ganglionlike cysts, perhaps from an adjacent synovium, compressing the artery. This compression may eventually lead to thrombosis of the artery.

Prior to occlusion, pedal pulses may be found to disappear with flexion of the knee joint. Ultrasonography (US), CT, or MRI may demonstrate the cyst, whereas angiography may demonstrate a characteristic hourglass deformity, which has been termed the scimitar sign.

Cystic adventitial disease of the popliteal artery is treated surgically by removing the cyst. Vascular bypass is required if occlusion has occurred.[30]



Laboratory Studies

Screening laboratory studies

Several screening laboratory studies are useful to evaluate the possibility of associated systemic risk factors and contributing problems.

Perform a complete blood count (CBC) to screen for hematologic diseases such as thrombocytopenia, thrombocytosis, polycythemia, and leukemia. Obtain a fasting blood glucose level to screen for diabetes. Creatinine and blood urea nitrogen (BUN) determinations help screen for renal insufficiency. A fasting and lipid profile helps screen for hyperlipidemia. Perform a urinalysis to screen for glycosuria or proteinuria.

Perform a coagulation workup to assess the prothrombin (PT) and activated partial thromboplastin (aPTT) times. In some cases (eg, patients with a personal or family history of thrombotic problems, particularly a history of failed vascular interventions), the workup should include a fibrinogen level, a euglobulin lysis time, a protein C assay, a protein S assay, antiphospholipid antibody titers, and an anticardiolipin antibody assay.

Consider obtaining a serum homocysteine level to screen for hyperhomocysteinemia in patients with an atypical history, early onset, or a family history. This problem, which is associated with both arterial and venous disease, can be treated by dietary supplementation with folate and vitamin B12. However, note that no conclusive data indicate that such treatment lowers long-term vascular risks.

Consider determining the erythrocyte sedimentation rate (ESR). Although elevation of the ESR is a nonspecific finding, the test screens patients with vascular disease for two potential risk factors that are somewhat difficult to measure directly—namely, hyperfibrinogenemia and hyperviscosity syndromes.

Noninvasive vascular laboratory evaluation

Pulse-volume recording (PVR), or plethysmography, uses pneumatic cuffs encircling the thighs, calves, ankles, feet, and sometimes toes to sense segmental volume changes with each pulse beat. The resulting tracings provide useful information about the hemodynamic effects of the arterial disease at each level.

In patients with severe disease, tracings at the transmetatarsal level may become nearly flat. In patients with mild disease, particularly disease involving the aortoiliac segment, PVR tracings may appear normal at rest and may become abnormal only after the patient walks until symptoms occur. PVR is noninvasive and rapid; therefore, it may be repeated frequently to help assess the overall hemodynamic response to medical or surgical treatment.

A handheld Doppler scanner may be used to assess arterial signals, to localize arteries to facilitate palpation of pulses, or to determine loss of the Doppler signal as a proximal blood pressure cuff is inflated. The latter pressure divided by the upper-extremity systolic pressure is called the ankle-brachial index (ABI) and can help indicate the severity of arterial compromise.[31]

A normal ABI averages 1. An ABI less than 0.9 suggests atherosclerotic disease with a sensitivity of approximately 95% and a specificity of 99%.[5] In general, an ABI below 0.3 suggests a poor chance for healing of distal ischemic ulcerations. Unfortunately, the ABI is often falsely elevated if the underlying arteries are heavily calcified, a finding common in patients with diabetes.

Skin perfusion pressure (SPP) is defined as the pressure at which skin perfusion returns as an inflated blood pressure cuff is slowly deflated. This point can be measured using washout of a radioisotope, the reappearance of pulsatile flux on photoplethysmography, or the motion of erythrocytes on laser Doppler. An SPP higher than 40 mm Hg correlates with the likelihood of the healing of ischemic wounds.[32]

Duplex scanning can provide images of arterial segments that help localize the extent of disease, and simultaneous Doppler measurement of flow velocity can help estimate the degree of stenosis. Duplex scanning is quite useful in visualizing aneurysms, particularly of the aorta or popliteal segments. Unfortunately, Doppler techniques are not accurate for assessing the hemodynamic consequences of atherosclerotic peripheral arterial disease involving the extremities.

Imaging Studies

Conventional angiography

If surgical treatment is contemplated, angiography is needed to delineate the extent and significance of atherosclerotic disease. (See the image below.) Major risks associated with conventional contrast-injection angiography are related to the puncture and to the use of contrast agents.

Contrast angiogram showing severe atherosclerotic Contrast angiogram showing severe atherosclerotic disease in distal superficial femoral artery.


Typically, a catheter is inserted retrograde via a femoral puncture, and contrast is power-injected into the infrarenal aorta. Films are taken as the contrast is followed down to both feet. In certain cases, as with aortic occlusion, a femoral approach to the aorta may not be possible. In this case, the radiologist may use an alternate entry such as via an axillary artery or even directly into the infrarenal aorta via a translumbar approach.

Puncture-related complications

The arterial catheter is usually passed through a 5-French sheath that is 1.6 mm in diameter. This is a sizable hole in the femoral artery, which may be only 6-10 mm in diameter. After the catheter is removed, gentle pressure must be applied to the puncture site for approximately 30 minutes, and the radiologist must balance the need for hemostasis against the possibility of arterial occlusion.

Risks include hemorrhage, pseudoaneurysm formation, and clotting or dislodgment of an intimal flap, which may acutely occlude the artery at or near the entry site. Current methods of percutaneous closure of the puncture sites have significantly reduced the site complication rates.

Contrast-related risks

Angiographic contrast material is nephrotoxic. The risk of precipitating acute renal failure is highest in patients with underlying renal insufficiency and those with diabetes; patients with both of these risk factors have a 30% rate of acute renal failure following contrast angiography. Hence, an acceptable serum creatinine level must be confirmed prior to elective angiography.

Avoid contrast angiography (if possible) for patients with any significant degree of renal impairment. If contrast angiography is absolutely required despite renal impairment, use a minimal volume of contrast material. In addition, providing adequate hydration prior to, during, and after the procedure is essential. Oral administration of the antioxidant acetylcysteine the night prior to and then just before angiography may be protective of renal function for patients at risk for contrast-induced nephropathy.[33]

Metformin warning

To prevent the possibility of fatal lactic acidosis, patients with diabetes who are taking metformin must not take this medication immediately following contrast angiography. Patients may resume taking the medication when normal renal function is confirmed 1-2 days after contrast exposure.

Alternatives to conventional angiography

Magnetic resonance angiography

Magnetic resonance angiography (MRA) is an alternative for patients who are allergic to iodinated contrast material. However, MRA is not innocuous. Gadolinium chelates, the contrast agents used in MRA, have been linked to three potentially serious side effects in patients with renal insufficiency: acute renal injury, pseudohypocalcemia, and nephrogenic systemic fibrosis.[34]

MRA is contraindicated in patients with implanted hardware, such as a hip prosthesis or pacemaker. The resolution may be inadequate for the vascular surgeon in planning reconstructive procedures, particularly in the smaller infrapopliteal arteries, though MRA technology and contrast agents continue to improve.[35]

Multidetector computed tomographic angiography

Multidetector CT (MDCT) angiography avoids arterial puncture. By using precisely timed intravenous contrast injection, 16- or 64-channel MDCT scanners can generate angiographic images of excellent resolution and at a relatively high acquisition speed. MDCT carries the contrast-related risks described above.[36]

Carbon dioxide angiography

Carbon dioxide angiography is an alternative for patients with renal insufficiency; however, it is not widely available and requires some iodinated contrast material in addition to the carbon dioxide gas in order to provide useful images.

Plain radiography

Plain radiographs are not routinely obtained in the workup of peripheral arterial occlusive disease. This is because arterial calcification seen on plain radiography is not a specific indicator of severe atherosclerotic disease. Calcification of the arterial media is not diagnostic of atherosclerosis, and even calcification of the arterial intima, which is diagnostic of atherosclerotic disease, does not necessarily imply hemodynamically significant stenosis.

Histologic Findings

Atherosclerotic vessels demonstrate proliferation of smooth-muscle cells in the intima and invasion of the damaged intima by atherosclerotic plaque consisting of necrotic cells, lipids, cholesterol crystals, and connective tissue. These lesions typically occur in an eccentric location with respect to the arterial lumen. Soft thrombus may deposit on ulcerated atherosclerotic plaques.


Rutherford et al described a classification scheme for lower-extremity chronic limb ischemia (see Table 1 below).[37]  The term chronic limb-threatening ischemia (CLTI) is increasingly preferred to CLI.[6]

Table 1. Staging for Chronic Limb Ischemia (Open Table in a new window)

Rutherford Category

Fontaine Grade

Clinical Description

Objective Criteria



Asymptomatic – No hemodynamically significant disease

Normal treadmill or reactive hyperemia test



Mild claudication

Completes treadmill exercise (5 min at 2 mph on 12% incline)

AP* after exercise >50 mm Hg but at least 20 mm Hg lower than resting value



Moderate claudication

Between Rutherford categories 1 and 3



Severe claudication

Cannot complete treadmill exercise and AP after exercise < 50 mm Hg



Ischemic rest pain

Resting AP < 40 mm Hg, flat or barely pulsatile ankle or metatarsal PVR**; TP † < 30 mm Hg



Minor tissue loss (nonhealing ulcer, focal gangrene with diffuse pedal ischemia)

Resting AP < 60 mm Hg, ankle or metatarsal PVR flat or barely pulsatile; TP < 40 mm Hg



Major tissue loss (extending above transmetatarsal level, functional foot no longer salvageable)

Same as Rutherford category 5

*AP = Ankle pressure.

**PVR = Pulse-volume recording.

† TP = Toe pressure.

The Society for Vascular Surgery (SVS) subsequently proposed a lower-extremity threatened limb classification system based on grading three major factors—wound, ischemia, and foot infection [WIfI])—on a scale of 0 to 3, where 0 represents none, 1 mild, 2 moderate, and 3 severe.[38] The wound component evaluates ulceration and gangrene. The ischemia component addresses hemodynamics and perfusion by measuring ABI, ankle systolic pressure, toe pressure, or transcustaneous oxygen tension. The foot infection component assesses clinical manifestations of infection, including extent, depth, and systemic inflammatory response.



Approach Considerations

Guidelines for management of infrainguinal occlusive disease have been formulated by the Society for Vascular Surgery (SVS),[39]  as well as by the European Society for Cardiology (ESC) in collaboration with the European Society for Vascular Surgery (ESVS).[40]  (See Guidelines.) Guidelines for management of chronic limb-threatening ischemia (CLTI; a term increasingly favored over chronic limb ischemia [CLI]) have been formulated by the SVS, the ESVS, and the World Federation of Vascular Societies (WFVS).[6]

Indications for lower-extremity revascularization include the following:

  • Gangrene
  • Pain at rest
  • Nonhealing arterial ulcer
  • Disabling claudication

In nonambulatory patients with ischemic pain at rest, gangrene, or extensive nonhealing wounds, primary lower-extremity amputation may be a better choice than vascular bypass surgery.

Technological enhancements and wider availability of existing technology should continue to improve the safety and efficacy of endovascular and vascular surgical techniques.[41, 42]

Imaging technology continues to be refined.[43]  Three-dimensional (3D) ultrasonographic (US) visualization can help better detect early plaque formation to allow for even more timely correction of vein graft stenoses. Gadolinium-enhanced 3D magnetic resonance angiography (MRA) images can provide highly detailed views of the arterial system. The applications of MRA, including guidance of endovascular interventions,[44]  will expand with continuing improvements in hardware, software, and nonnephrotoxic contrast agents.

Endovascular procedures continue to benefit from improved technology both in imaging modalities and instrumentation.[45]  In the performance of an in-situ bypass, endovascular technology allows valvulotomy and coil occlusion of side branches by direct angioscopic visualization.

As in other surgical fields, endoscopy may have a greater role in infrainguinal vascular surgery. For example, endoscopic harvesting of the saphenous vein limits the extent of the dissection required for bypass procedures.[46]

Studies have suggested that in patients with limb-threatening ischemia but inoperably diseased distal arteries, arterialization of the distal venous bed may be of benefit.[15, 47]

Gene therapy holds promise for inhibiting vascular restenosis after endovascular procedures or bypass surgery. Rat and rabbit models suggest that neointimal hyperplasia after arterial injury is inhibited by overexpression of the GAX gene and that adenovirus-mediated delivery of the GAX gene diminishes proliferation of intimal cells in animal models. Gene therapy may be suitable for vein grafts prior to implantation.

Some research is underway on inhibitors of smooth-muscle proliferation, such as drugs that block E2F transcription factors.[2, 48]  A multicenter, randomized, double-blinded study of 1404 patients revealed no benefit from the use of edifoligide, an E2F inhibitor.[49, 50]

Low-dose intravascular beta-irradiation may inhibit restenosis by blocking early medial and adventitial cell proliferation.[51]

Various endovascular devices have been developed for lower-extremity revascularization, including the following[52, 53] :

  • Catheters to cross chronic total occlusions [54]
  • Reentry device
  • Stent graft
  • Debulking devices (excisional atherectomy, rotational atherectomy, laser)
  • Cryoplasty
  • Embolic protection device
  • Cutting balloon

Development of new technologies and refinement of existing devices will improve the armamentarium of endovascular therapy. The long-term outcome of endovascular treatment compared with open surgical bypass has not yet been sufficiently well studied, and further research is warranted.[55, 56]

Medical Therapy

Most patients with atherosclerotic lower-extremity disease do not undergo surgical treatment. In fact, only 25% of patients presenting with intermittent claudication eventually require invasive treatment of limb-threatening ischemia or intractable symptoms, and only 5-10% do so within 5 years of the onset of claudication.

The cornerstones of medical management of intermittent claudication are walking and elimination or control of medical risk factors.[57, 58] (See also Noncoronary Atherosclerosis and Coronary Artery Atherosclerosis.)


Encourage walking.[59] Regular walking of approximately 1 hour per day usually results in a significant increase in walking distance over time. This increase in walking distance has been noted to range from 80% to more than 200%. Improvement results from improved flow in collateral pathways.

Risk factor management

A major factor contributing to progressive and intractable atherosclerotic disease is cigarette smoking. One study noted an 85% chance of improvement if smoking is stopped versus only a 20% chance of improvement if the patient continues smoking.

Other medical risk factors that must be assessed and controlled are obesity, hypertension, hyperlipidemia, and diabetes.[60]

Because an ischemic foot is at risk for developing limb-threatening ulceration from even minor trauma, good foot hygiene and appropriately fitting shoes are important. This is even more vital for patients with diabetes, who are also at risk for neuropathic foot ulcers.


Currently available drugs that may benefit patients with mild or moderate claudication include pentoxifylline and cilostazol.[61, 62] Controlled studies suggest that each of these drugs improves walking distance by approximately 20% more than placebo, cilostazol perhaps slightly more than pentoxifylline.

Cilostazol, administered at 100 mg orally twice daily, has demonstrated some benefit for claudication symptoms.[63] Cilostazol is contraindicated in patients with congestive heart failure,[64] as noted in the product's black box warning.

Pentoxifylline, 400 mg orally three times per day taken with meals, has been available for many years. After 2-3 months of use, 25-60% of patients demonstrate some improvement in walking distance. However, much of this improvement may be attributable to exercise and to modification of the risk factors mentioned above. The major adverse effects of this medication are gastrointestinal in nature.

Antiplatelet agents (eg, aspirin, clopidogrel), angiotensin-converting enzyme (ACE) inhibitors, and statins should also be considered.

Caveats regarding pharmacotherapy are that vasodilators and chelation therapy have no demonstrated benefit in the treatment of claudication. Beta-blocking agents may worsen claudication and must be discontinued, if medically feasible.

Indications for Nonmedical Intervention

Surgical or endovascular intervention is indicated for intractable and disabling claudication, for ischemic pain at rest, and for ischemic necrosis. Surgery also may be useful for nonhealing ischemic ulceration.

Before considering surgical intervention, the clinician must address the possibility of coexisting atherosclerotic heart and cerebrovascular disease, which are extremely common in patients with atherosclerotic peripheral arterial disease (PAD). One study found that only 14% of patients with PAD had normal coronary arteries, whereas 15% had severe coronary artery disease (CAD) that required surgical correction. (See Atherosclerosis for the cardiologic workup.)

Patients with a prior ipsilateral peripheral endovascular intervention have been found to have a higher likelihood of a poor outcome when undergoing lower-extremity bypass for CLTI.[65] Reported 1-year amputation and graft occlusion rates have been higher in these patients than those who have not undergone prior revascularization procedures (eg, prior ipsilateral bypass). These factors can help determine revascularization options in patients with CLTI.[65]

However, Uhl et al carried out a retrospective analysis comparing patients who had undergone tibial or peroneal bypass surgery for CLTI after prior endovascular interventions with patients who had received a tibial or peroneal bypass as a primary revascularization procedure because primary endovascular therapy had been considered unfeasible.[66] They found that prior endovascular intervention in femorotibial vessels did not negatively affect the outcome of subsequent tibial or peroneal bypass surgery.

A British study reports that the major amputation rate after femorodistal bypass remains high, with adverse events occurring after approximately 38% of femoropopliteal procedures and nearly 50% of femorodistal bypasses. The main predictors of a poor outcome reportedly were diabetes and chronic renal failure.[20]

Obtain appropriate imaging studies. Before surgical intervention, the exact extent of the atherosclerotic disease is mapped by using high-quality contrast angiography (see Imaging Studies).

In recognition of the importance of the pathologic anatomy in decision making, the Trans-Atlantic Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC) published a set of guidelines for treatment of lower-extremity PAD (see Table 2 below).[67]

Table 2. TASC Classification for Femoral Popliteal Lesions (Open Table in a new window)



Type A lesions

  • Single lesions ≤10 cm in length

  • Single occlusions ≤5 cm in length

Type B lesions

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

  • Single stenosis or occlusion ≤15 cm not involving the infrageniculate popliteal artery

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

  • Heavily calcified occlusion ≤5 cm in length

  • Single popliteal stenosis

Type C lesions

  • Multiple stenoses or occlusions totaling >15 cm with or without heavy calcification

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

Type D lesions

  • Chronic total occlusions of common femoral artery or superficial femoral artery (>20 cm, involving the popliteal artery)

  • Chronic total occlusion of popliteal artery and proximal trifurcation vessels

The general recommendations are endovascular intervention for TASC type A lesions and open surgery for TASC type D lesions. Insufficient data are available on type B and C lesions; however, type B lesions are probably best treated endovascularly and type C lesions best treated with open surgery.

Surgical and Endovascular Therapy

Preparation for surgery

Prior to vascular surgery, a routine laboratory workup is performed, including complete blood count, biochemical profile, clotting studies, urinalysis, chest radiography, and electrocardiography (ECG). Abnormalities are addressed.

Although some suggest discontinuing clopidogrel preoperatively to minimize intraoperative bleeding risks, one analysis suggests that this is not necessary and that clopidogrel therapy can be safely continued.[68]

Radiographic contrast

If an endovascular procedure is to be performed, iodinated contrast material is required, and hence, one must check for renal insufficiency, a history of contrast allergy, and the use of metformin (see Imaging Studies).

Infection prevention

Take appropriate measures to prevent vascular graft infection. For routine prophylaxis in bypass surgery, a broad-spectrum antibiotic (eg, a broad-spectrum cephalosporin, a penicillin/beta-lactamase inhibitor, or an aminoglycoside) is administered just before surgery and postoperatively for one to three doses. If there is known colonization with or local prevalence of methicillin-resistant Staphylococcus aureus (MRSA), consider vancomycin or teicoplanin.[69]

Consider a preoperative antiseptic shower or scrub.

Patients harboring a potential infection (eg, foot ulcer or gangrene) may fare better having the infected tissue excised, even with limited amputations, prior to vascular intervention in order to avoid graft or wound infections.

Urgent intervention

If urgent intervention is required, the workup may have to be truncated. In the case of acute arterial occlusion, the workup may have to be minimal because prompt thrombectomy is often required for limb salvage. Preoperative angiography may still be warranted, especially if evidence of underlying atherosclerotic disease is present.

Operative details

Although PAD is a diffuse process, the preponderance of findings can often be attributed to a particular segment of the arterial tree. Angiographic findings combined with knowledge of the patient's symptoms, physical findings, and noninvasive laboratory results leads the vascular specialist to determine which artery or arteries are best treated by invasive means.[70]

This determination is not an exact science, and it is not unusual for the vascular specialist to correct a single lesion and then discover that the recurring symptoms dictate another procedure at a later date. Nonetheless, attempting to correct all diseased segments at once usually confers too high an operative risk.

Disease of iliac artery

Hemodynamically significant disease involving the iliac arteries, particularly short-segment stenotic and even occlusive disease, can usually be successfully treated with percutaneous angioplasty, percutaneous insertion of an arterial stent, or both.[71, 72]

If endovascular reconstruction is not possible, femorofemoral crossover bypass is usually the best choice for unilateral iliac artery occlusion, and aortobifemoral bypass is usually the best choice for bilateral or diffuse aortoiliac disease.[73]

Axillofemoral bypass is an alternative in high-risk patients who cannot tolerate an intra-abdominal or retroperitoneal operation (see Aortoiliac Occlusive Disease).

Disease involving femoral artery

Hemodynamically significant disease involving the femoral artery is usually the result of relatively long-segment occlusion of the distal superficial femoral artery in the adductor canal.

Endovascular approaches to infrainguinal disease have become increasingly successful. Secondary interventions are often required, but assisted patency rates are reported as over 90% in appropriately selected patients.

Correction of this type of disease often requires bypass from a pulsatile distal common femoral artery to the pulseless popliteal artery. Such a bypass is best performed by using the ipsilateral great (long) saphenous vein (GSV). If this vein is not suitable or has been used previously, alternative conduits for above-the-knee bypasses include expanded polytetrafluoroethylene (ePTFE) prosthetic graft, Dacron graft, tanned bovine umbilical vein graft, and glutaraldehyde-tanned human umbilical vein.[74]

Because of inferior patency rates with prosthetic grafts extending below the knee, the vascular surgeon usually tries to locate a usable autologous vein from the contralateral lower extremity by combining available short segments from both sides, upper-extremity veins, or even composite grafts (in which a prosthetic graft extends to the knee and a piece of autologous vein is attached distally or when a vein patch is used to attach the prosthetic graft to the distal artery).

In a study of diabetic patients with CLTI, autologous saphenous vein operations for below-the-knee bypasses were superior to ePTFE grafts in terms of primary patency. However, secondary patency rates were not statistically different between the two procedures, and limb salvage rates were comparable.[75]

Angioplasty with or without stenting may be appropriate for short-segment superficial femoral artery occlusive disease.

Disease involving infrapopliteal arterial tree

Extensive disease involving the infrapopliteal segments is best managed by means of autologous vein grafting. Arguably, the best technique is the use of the ipsilateral saphenous vein in situ.

This is a somewhat tedious procedure in which the saphenous vein is first disconnected from the femoral vein in the groin and anastomosed to the common femoral artery. The vein is then transected distally, and a valvulotome is inserted retrograde and withdrawn so as to destroy the valves that would have prevented arterial flow from the groin to the leg in the vein.

Next, an anastomosis is created between the distal end of the vein and a usable small artery, even as far distally as the dorsalis pedis at the ankle or foot. Finally, the vein branches are ligated to stop arteriovenous flow.

Patients must be selected carefully for this technique. The vein must be patent and of adequate length and caliber, and a usable, soft distal artery must be available. Preoperative vein mapping using duplex scanning is sometimes helpful.

Endovascular procedures

Percutaneous transluminal angioplasty is often appropriate for strictures or short-segment occlusions of the superficial femoral, popliteal, and, occasionally, infrapopliteal arteries.[76, 3, 77]  Angioplasty is performed by passing a guide wire through the lumen of the strictured artery and then advancing a balloon angioplasty catheter over the guide wire. The balloon is inflated to several atmospheres of pressure under angiographic visualization. This effectively disrupts the plaque and provides a wider, patent lumen.

Although angioplasty has been used increasingly for claudication, whether the risks justify the benefits for many patients in this group is a serious question.[78]  In a randomized controlled trial, Bradbury et al found that angioplasty has a high failure rate (~25%) in patients with severe limb ischemia from infrainguinal occlusive disease and that patients who underwent bypass after failed angioplasty fared significantly worse than those who underwent surgery as their first procedure.[79]

Nevertheless, Bradbury et al suggested that in patients with severe limb ischemia whose life expectancy is less than 2 years, balloon angioplasty should usually be offered before bypass surgery, in that it is associated with less morbidity and cost, and such patients are unlikely to enjoy the longer-term benefits of surgery.[79]

In patients who are expected to live beyond 2 years, bypass surgery should usually be offered first, especially where a vein is available as a conduit. However, patients who cannot undergo a vein bypass may often be better served by a first attempt at balloon angioplasty than prosthetic bypass.

Somewhat surprisingly, even if the guide wire cannot negotiate the lumen of a stricture and instead passes through the subintimal plane, subintimal (extraluminal) angioplasty may succeed.[80]  This method seems to create a new channel in a virgin plane. Low echogenicity at the distal end of the plaque, as measured by duplex ultrasound–derived gray-scale median, seems to increase the chance of successful subintimal angoplasy.[81]

Chronic total occlusions of infrainguinal vessels may be resistant to conventional guide-wire techniques. In the PATRIOT trial, which included 85 patients with a previous or concurrent failed attempt to cross such an occlusion with a standard guide-wire approach, Laird et al found that the Crosser chronic total occlusion recanalization system facilitated the crossing of chronic infrainguinal occlusions that were resistant to guide-wire crossing, while posing only a minimal risk of clinically significant vessel perforation.[54]

Angioplasty approaches making use of drug-coated balloons (DCBs) have been described. A systematic review and meta-analysis of industry-sponsored trials by Caradu et al found that DCB angioplasty was associated with high procedural success in the treatment of femoropopliteal disease and that it consistently reduced late lumen loss, binary restenosis, and target lesion revascularization as compared with plain balloon angioplasty.[82]  The authors noted the need for further independent, non-industry-sponsored RCTs to better delineate the role of DCBs in this setting.

Angioplasty may be combined with percutaneous stenting. Self-expanding nickel-titanium alloy (nitinol) stents have demonstrated a 2-year primary patency rate of 47% and a limb salvage rate of 66% when used to treat limb ischemia.[83]

Despite the success of drug-eluting stents in the coronary circulation, initial reports using drug-eluting stents in the peripheral circulation were disappointing. However, European investigators documented success with a slow-release everolimus stent to prevent restenosis following peripheral arterial intervention.

The first-in-human Superficial Femoral Artery Treatment with Drug-Eluting Stents (STRIDES) trial showed primary patency (freedom from ≥50% in-stent restenosis) rates of 94 ± 2.3% and 68 ± 4.6% at 6 and 12 months, respectively, for the treatment of symptomatic superficial femoral and proximal popliteal arterial occlusive disease.[84]

In addition to intra-procedure anticoagulation, patients are typically treated with an antiplatelet agent, such as clopidogrel, both before and for a month or more postprocedure.[83]

Percutaneous endovascular removal of atherosclerotic plaque (ie, atherectomy) seemed promising in the early 1990s, but it was abandoned because of very poor long-term success rates. Subsequently, however, it garnered some renewed interest in research settings.[85, 86, 87, 88, 89, 90]


Removal of atherosclerotic plaque and underlying diseased arterial intima (endarterectomy) at anastomotic sites is sometimes necessary as an adjunct to bypass surgery but is indicated only rarely as the sole management for lower-extremity arterial occlusive disease.

One exception is endarterectomy of the deep femoral (profunda femoris) artery (profundoplasty), which may be useful in the rare case of severe limb-threatening stenosis of the origin of the deep femoral artery associated with a superficial femoral artery occlusion that cannot be bypassed for technical reasons.

Another indication for endarterectomy is to remove localized embolizing ulcerated plaque.

Management of acute arterial occlusion

The usual immediate management of acute arterial occlusion consists of immediate heparin anticoagulation and rapid surgical thromboembolectomy. If time allows, especially if atherosclerotic thrombosis is suggested, preoperative angiography is often wise. It may provide information vital to performing bypass surgery should thrombectomy disclose severe underlying atherosclerotic disease.

In some cases, particularly very high-risk patients, thrombolytic therapy by selective intra-arterial infusion (if available) is a reasonable alternative to emergency surgery. For infrainguinal acute occlusions, a medial approach to the distal popliteal artery trifurcation is usually the best method to allow complete evaluation and clearance of all outflow vessels.

After relief of an acute arterial occlusion, one must be alert to the possibility of reperfusion complications such as compartment syndrome or myopathic-metabolic-nephrotic syndrome. Compartment syndrome is characterized by tense edema of the leg, which raises interstitial tissue pressures and impedes arterial inflow. Emergency four-compartment fasciotomy can save limbs.

Myopathic-metabolic-nephrotic syndrome is the result of reperfusion of essentially irreversibly ischemic muscle. It is characterized by metabolic acidosis, dark urine, and renal failure. Emergency limb amputation may be required to save the patient's life.

After emergency treatment to salvage the ischemic limb, the clinician must determine the etiology of the acute occlusion. If it was thrombotic, the underlying atherosclerotic disease may require correction. If it was embolic, the source must be sought.

Ninety percent of arterial emboli originate in the heart. The remaining emboli originate in the aorta (see DDx) or from venous thrombi that pass into the arterial circulation via a right-to-left intracardiac shunt (paradoxic embolism). Sometimes, the source can be treated, but usually, long-term anticoagulation is required.

Aneurysm resection is indicated for symptomatic, expanding, or sizable popliteal artery aneurysms. A vein graft is usually used to replace the resected or excluded popliteal artery segment. (See Thoracic Aortic Aneurysm.)

Postoperative Care

Postoperative care after vascular surgery requires in-hospital observation in order to expeditiously detect and treat complications.[91]


The most frequent complication of endovascular and vascular surgical procedures is occlusion. Some authorities recommend the use of antiplatelet therapy (eg, aspirin or clopidogrel) starting before angioplasty or bypass surgery and continuing indefinitely. For grafts considered to be at high risk for thrombosis, such as those with poor runoff, with a previous occlusion, with a prosthetic graft, or in a hypercoagulable state, heparin may be given perioperatively, and warfarin may be administered for long-term prophylaxis.

Acute postoperative thrombosis

Any change in circulatory status beyond the bypass graft warrants a rapid evaluation. If thrombosis has occurred, rapid return to the operating room for thrombectomy and repair is required. In such cases, a technical problem (eg, intimal flap) must be sought.

Normal postoperative recovery

Ambulation with the assistance of a physical therapist usually starts gradually on postoperative day 1 or 2. The timing of hospital discharge varies with the extent of the procedure and the patient's general condition. If bypass surgery has been performed in conjunction with significant distal amputations, recovery in a skilled nursing facility or rehabilitation center may be beneficial.

Management following percutaneous procedures

After percutaneous procedures, the patient is observed from 4 hours to overnight to ensure absolute bed rest and detect possible complications of the puncture and intervention. Antiplatelet therapy is usually prescribed. For patients with renal compromise and those on metformin, check serum creatinine values 1-2 days after the procedure.


Important complications of vascular surgery include early postoperative occlusion, hemorrhagic problems, graft infection, cardiac morbidity, and restenosis.

Early postoperative occlusion

Early postoperative arterial or graft occlusion usually occurs as a result of technical factors such as an intimal flap or the use of a suboptimal conduit.[92] Early reocclusion warrants a quick return to the operating room for thrombectomy and repair of any potential technical defect. Unfortunately, the long-term prognosis after a take-back procedure for early graft occlusion is poor, with only approximately one quarter of such grafts still functional 5 years later.

Hemorrhagic problems

Hemorrhage and pseudoaneurysm formation may occur at the arterial puncture site or, less commonly, at a graft suture line. Management of the latter usually requires a return to the operating room for surgical repair; however, endovascular puncture site pseudoaneurysms can sometimes be treated with US-guided compression repair.[93]

In this technique, guided by continuous duplex scanning, the pseudoaneurysm is compressed just enough to stop flow outside the lumen of the involved artery but still preserve distal arterial flow. This compression continues for approximately 45 minutes, until the pseudoaneurysm thromboses. Arteriovenous fistulas have also been treated using this technique.

US-guided percutaneous thrombin injection has also been shown to be quite effective and more expeditious.[94]

Graft infection

Prosthetic graft infections are rare but serious and may require removal of the bypass graft and even amputation of the limb. They occur in approximately 1% of prosthetic graft bypasses. Currently, methicillin-resistant S aureus is the preponderant pathogen.

Treatment usually requires complete removal of the graft and, if possible, reconstruction using a new graft via an extra-anatomic pathway, such as an iliopopliteal bypass from the iliac artery via the obturator foramen to the popliteal artery beyond the infected graft's distal anastomosis.[95, 96]

Cardiac morbidity

Plaque in the superficial femoral artery tends to be a late development in patients with generalized atherosclerotic disease. Therefore, the presence of superficial femoral artery plaque conveys a very high likelihood of coexisting cardiac or carotid atherosclerosis.[97]

Because of this association of atherosclerotic CAD with PAD, postoperative myocardial events such as cardiac death, nonfatal myocardial infarction, unstable angina, ventricular tachycardia, and congestive heart failure may occur following infrainguinal bypass operations.

Although most studies suggest an overall cardiac complication rate of approximately 5%, one study found that such myocardial events occurred at an alarming rate of 24% in 87 patients undergoing infrainguinal reconstruction.


The most common late complication of both endovascular and vascular reconstructive procedures is restenosis resulting from a proliferation of smooth-muscle cells causing an excessively thickened neointima, which can lead to late arterial or graft reocclusion. This is best prevented by routine postoperative graft surveillance and managed by endovascular repair, patch grafting, of bypass revision before occlusion occurs (see Long-Term Monitoring). Postoperative statin use may decrease restenosis rates.[98]

Long-Term Monitoring

A routine postoperative follow-up assessment is essential, for two reasons.

First, medical management of the underlying atherosclerotic disease must continue.

Second, bypass graft surveillance using noninvasive vascular laboratory testing may help detect problems that can threaten graft patency, such as progressive atherosclerotic disease of inflow or outflow vessels or buildup of scar tissue (neointimal fibrous hyperplasia) at the anastomotic sites. If these problems can be detected before they lead to graft thrombosis, they may be corrected by endovascular means (ie, angioplasty or stenting). Open surgical revision for restenosis of vein grafts, however, carries a higher long-term success rate than percutaneous intervention.[99, 100]

A typical schedule for outpatient follow-up after peripheral arterial intervention is at 2 weeks, 1 month, 3 months, 6 months, and every 6 months thereafter.



SVS Guidelines for Femoropoliteal Occlusive Disease

In 2015, the Society for Vascular Surgery (SVS) issued practice guidelines for management of atherosclerotic disease of the lower extremities.[39]  Recommendations for interventions for femoropopliteal occlusive disease (FPOD) in intermittent claudication (IC) include the following:

  • Endovascular therapy (EVT) is preferred to open surgery for focal occlusive disease of the superficial femoral artery (SFA) that does not involve the origin at the femoral bifurcation (grade 1 recommendation; evidence level C).
  • Selective stenting is suggested for focal lesions (< 5 cm) in the SFA that have unsatisfactory technical results with balloon angioplasty (grade 2 recommendation; evidence level C).
  • Adjunctive use of self-expanding nitinol stents (with or without paclitaxel) is recommended for intermediate-length (5-15 cm) SFA lesions to improve the midterm patency of angioplasty (grade 1 recommendation; evidence level B).
  • Preoperative ultrasonographic vein mapping is suggested to establish the availability and quality of autogenous vein conduit in patients being considered for infrainguinal bypass to treat IC (grade 2 recommendation; evidence level C).
  • EVT is not recommended for isolated infrapopliteal disease in IC, because it is of unproven benefit and may be harmful (grade 1 recommendation; evidence level C).
  • Surgical bypass is recommended as an initial revascularization strategy for patients with diffuse FPOD, small vessel caliber (< 5 mm), or extensive SFA calcification if their anatomy is favorable for bypass (popliteal artery target, good runoff) and their operative risk is average or low (grade 1 recommendation; evidence level B).
  • The saphenous vein is the preferred conduit for infrainguinal bypass grafts (grade 1 recommendation; evidence level A).
  • In the absence of suitable vein, a prosthetic conduit is suggested for femoropopliteal bypass in claudicant patients if the above-knee popliteal artery is the target vessel and good runoff is present (grade 2 recommendation; evidence level C).

ESC/ESVS Guidelines for Infrainguinal Occlusive Disease

In August 2017, the European Society for Cardiology (ESC), in collaboration with the European Society for Vascular Surgery (ESVS), issued updated guidelines on the diagnosis and treatment of peripheral arterial disease (PAD)[40] ; these guidelines were also endorsed by the European Stroke Organisation (ESO).

Recommendations for revascularization of femoropopliteal occlusive lesions in patients with IC and severe chronic limb ischemia are as follows:

  • Endovascular-first strategy is recommended in short (< 25 cm) lesions (class I recommendation; evidence level C)
  • Primary stent implantation should be considered in short (< 25 cm) lesions (class IIa recommendation; evidence level A)
  • Drug-eluting balloons may be considered in short (< 25 cm) lesions (class IIb recommendation; evidence level A)Drug-eluting stents may be considered for short (< 25 cm) lesions (class IIb recommendation; evidence level B)
  • Drug-eluting balloons may be considered for treatment of in-stent restenosis (class IIb recommendation; evidence level B)
  • In patients not at high risk for surgery, bypass surgery is indicated for long (≥25 cm) SFA lesions when an autologous vein is available and life expectancy is >2 years (class I recommendation; evidence level B)
  • The autologous saphenous vein is the conduit of choice for femoropopliteal bypass (class I recommendation; evidence level A)
  • When above-the-knee bypass is indicated, the use of a prosthetic conduit should be considered in the absence of any autologous saphenous vein (class IIa recommendation; evidence level A)
  • In patients unfit for surgery, endovascular therapy may be considered in long (≥25 cm) femoropopliteal lesions (class IIb recommendation; evidence level C)

Recommendations for revascularization of infrapopliteal occlusive lesions are as follows:

  • In the case of chronic limb-threatening ischemia, infrapopliteal revascularization is indicated for limb salvage (class I recommendation; evidence level C)
  • For revascularization of infrapopliteal arteries, bypass using the great saphenous vein is indicated (class I recommendation; evidence level A); endovascular therapy should be considered (class IIa recommendation; evidence level B)