Popliteal Artery Occlusive Disease

Updated: Feb 03, 2022
Author: Cynthia K Shortell, MD; Chief Editor: Vincent Lopez Rowe, MD 


Practice Essentials

Popliteal artery occlusive disease is a common occurrence, especially in elderly patients, smokers, and those with diabetes mellitus and other cardiovascular diseases. Each year, more than 100,000 peripheral arterial reconstructive operations and 50,000 lower-limb amputations for lower-extremity ischemia are performed in the United States. Many of these are related to popliteal artery disease.

Popliteal artery occlusion and the disease processes leading up to it cause morbidity and mortality by decreasing or completely blocking blood supply through the popliteal artery and into the lower leg and foot. As a result of tissue ischemia, these patients have a significant reduction in ambulatory activity, daily functional capacity, and quality of life. Lower-extremity ischemia can manifest as claudication, rest pain, or tissue loss (gangrene) and can lead to limb loss.

Once a portion of a lower extremity becomes gangrenous, the patient is at risk for limb loss and death. Diagnosing popliteal artery occlusive disease is very important because of the risk of chronic limb-threatening ischemia[1]  (CLTI; also referred to as critical limb ischemia [CLI]), thrombosis, or distal embolization. In addition, patients with peripheral artery disease (PAD), in general, have a markedly increased prevalence of coronary artery disease (CAD) and cerebrovascular disease and mortality. Recognition of this relationship allows proper management of medical comorbidities and risk factor reduction.

In addition to atherosclerosis, popliteal artery occlusive disease can be caused by emboli, popliteal entrapment syndrome, cystic adventitial disease, and trauma.

Regardless of the reason for popliteal artery occlusion, intervention is indicated in patients with severe claudication that alters lifestyle and does not respond to medical treatment and in patients with CLI. (See Treatment.)


The popliteal artery is characterized by distinct embryologic and anatomic features as compared with the femoral vessels. Embryologically, unlike the superficial femoral artery, the popliteal artery originates from the sciatic system.[2]

The popliteal artery sits on the posterior aspect of the leg, in the popliteal fossa. The superficial femoral artery becomes the popliteal artery as it passes through the adductor hiatus, and it proceeds until it bifurcates into the anterior tibial artery and the tibioperoneal trunk.

The tibioperoneal trunk divides into the posterior tibial and peroneal arteries. The popliteal artery is located between the two heads of the gastrocnemius. It lies posterior to the distal femur and anterior to the popliteal vein. The anatomic proximity of the popliteal artery to the distal femur and gastrocnemius makes this artery susceptible to injury during femoral fracture or knee dislocation and entrapment syndrome, respectively.

Compared with the superficial femoral artery, the popliteal artery is not located within the muscular compartment and is subjected to significant biomechanical torsional forces related to the repetitive knee flexion and extension.[3, 4, 5] This anatomic region is characterized by a high biomechanical stress, which consequently negatively affects patency rates associated with the popliteal artery bypass procedures and imposes technical limitations on endovascular stenting, in that biomechanical stress may lead to stent fractures.

At the level of the knee, the popliteal artery gives off genicular and sural branches. Above the knee joint, it gives off the superior lateral and superior medial genicular arteries. Below the knee, it gives off the inferior lateral and the inferior medial genicular arteries. These branches provide a rich network between the superficial femoral artery, the deep femoral (profunda femoris) artery, and the tibial arteries. This collateral circulation is very important in the presence of chronic occlusive disease of the popliteal artery.


During exercise, muscles require two to 10 times more oxygenated blood than they do when at rest. Mild nonocclusive arterial obstruction minimally affects resting blood flow but severely curtails the body's response to exercise. The first symptom of a decrease in the body's ability to deliver blood is ischemic pain during exercise. As the stenosis worsens, pain at rest and tissue loss follow.

As the stenosis progresses and proceeds to occlusion, collateral vessels, via the descending genicular artery, propagate and flourish, providing the distal leg with much-needed arterial blood. However, collateral circulation does not provide the amount of blood needed in the exercising leg, and it does not guarantee leg viability.

The extent to which different tissues in the lower extremity can tolerate ischemia depends on their metabolic rates. In general, muscles and nerves are the least resistant to ischemia, with an estimated ischemic tolerance of 6 hours. In the absence of sufficient collateral blood flow in the extremity with an occluded popliteal artery, limb viability is jeopardized. If the occluded popliteal artery is not treated in case of tissue loss, significant morbidity and mortality can result.


Atherosclerotic disease isolated to the popliteal vessels is not common; however, popliteal artery occlusive disease as a result of systemic atherosclerosis associated with other lesions is extremely common. Popliteal artery occlusion is usually the end stage of a long-standing disease process of atheromatous plaque formation.

Once formed, the atherosclerotic core is a highly thrombogenic surface that promotes platelet aggregation, which results in disturbances of blood flow. As the atherosclerotic lesion enlarges, normal laminar flow in the artery is disrupted, causing eddy currents and thrombus formation. Endothelial damage activates the repair process that results in neointimal hyperplasia, which results in additional attraction of platelets. Additionally, ulcerated plaques promote local thrombus formation, and the result is a primary popliteal thrombus that occludes flow.

Popliteal artery aneurysm

The exact cause of popliteal artery aneurysm (PAA) is not known.[6] Molecular studies suggest that PAAs are caused by a combination of a genetic defect and inflammation. Infiltration of inflammatory cells has been documented by observing that the PAA wall is associated with increased apoptosis and degeneration of extracellular matrix. Historically, the common causes of PAA were mycotic, syphilitic, or traumatic in nature.

As the population ages, arteriosclerosis seems to be the dominant associated factor. Turbulent flow distal to arteriosclerotic lesions is believed to result in distal dilation of the vessel at the adductor hiatus. Decreased wall strength, turbulent flow, and constant kinking and motion from normal movement of the knee joint are believed to result in aneurysm formation.


About 15% of emboli emanating from proximal sources result in popliteal disease. Common sources include mural thrombi in the heart, diseased heart valves, abdominal aortic aneurysms (AAAs), or iliac aneurysms.

Popliteal entrapment syndrome

Popliteal entrapment syndrome is a developmental anomaly characterized by an abnormal anatomic relation of the popliteal artery to the gastrocnemius. This anomalous anatomic relation causes popliteal artery compression and occlusion. In rare cases, the popliteal artery is compressed by a fibrous band or by the popliteus. In 1985, Mosimann postulated that increased use of the knee joint causes intimal fibrosis of the vessel lumen, thereby decreasing flow and causing claudication and eventual occlusion.[7]

Cystic adventitial disease

The mechanism of cystic adventitial disease was first thought to be a primary dysplasia of the blood vessel wall. In a 1984 report, Leu et al suggested that the cysts associated with this disease originate from ectopic tissue of the joint capsule or bursa.[8]

Following some type of trauma to the popliteal area, collagenous and muscular fibers in the joint and the myocytes around it undergo focal necrosis. Multiple loculated cysts result, the lumen of which are filled with mucinous material containing amino acids without carbohydrates, cholesterol, or calcium. The cysts in the adventitia compress the popliteal artery, either causing thrombus or directly impinging and occluding arterial blood flow.


Injuries to the popliteal arteries may cause intimal damage and subsequent thrombus formation. Injuries affecting the popliteal artery are most commonly caused by anterior and posterior knee dislocation, as well as bony fractures. Motor vehicle accidents and penetrating trauma are the most common causes of popliteal artery injury. Because of its anatomic proximity to the distal femur and knee joint, trauma of the popliteal artery can also be related to iatrogenic injuries during knee surgery or intervention.


Atherosclerosis is by far the most common cause of popliteal artery occlusive disease. More than 1 million patients experience symptomatic disability related to atherosclerotic PAD in the United States each year. Moreover, atherosclerotic PAD is increasing in prevalence as a result of increased life expectancy.

PAAs are the most common peripheral aneurysms, occurring in 0.01% of all hospitalized patients. Between 50% and 70% of aneurysms are bilateral.

About 15% of lower-extremity emboli affect the popliteal artery. Atrial fibrillation is currently associated with two thirds to three quarters of all peripheral arterial embolization. Myocardial infarction is the next most important cause of peripheral emboli.

Popliteal entrapment syndrome is a rare cause of popliteal artery occlusive disease, with an estimated prevalence of 0.16%. This syndrome occurs most commonly in young (60% < 30 years old), healthy men (15:1 male predilection) who present with symptoms of calf claudication.

Cystic adventitial disease is an extremely rare cause of popliteal artery occlusion, accounting for only a few hundred reported cases since the first description by Ejrup and Hiertonn in 1954.


In patients with native conduits, intimal hyperplasia leading to narrowing of the vein graft and valvular hyperplasia are the two leading causes of graft failure. Studies suggest that geometric remodeling of the vein graft and decreased graft adaptation to the arterial environment are caused by inflammatory mediators.[9] Diminished graft blood flow can be detected before graft thrombosis occurs. If the lesion is not corrected, graft thrombosis occurs in most cases. As a result of graft thrombosis, acute ischemic events in the lower extremity can lead to limb loss.

Thus, establishing continued ultrasonographic surveillance after bypass and vein graft revision is important. In the event of vein graft stenosis, open surgical and endovascular vein graft revision are options to maintain patency prior to occlusion. Most of the lesions underlying graft failure can be corrected by means of percutaneous transluminal angioplasty (PTA), though in certain cases vein patch angioplasty or short bypass of a graft lesion is needed. PTA should be restricted to short lesions (< 2 cm).

Failure of a polytetrafluoroethylene (PTFE) graft is attributed to the thrombogenicity of the graft material and kinking of the graft from crossing knee joint, as well as anastomotic intimal hyperplasia and progression of atherosclerotic disease proximal or distal to the graft.

Vein bypasses are relatively effective, with 4-year patency rates of 68-80% and limb salvage rates of 75-85%. Bypasses performed with PTFE grafts yield comparable patency and salvage rates above the knee but are significantly less successful below the knee. Therefore, PTFE or other synthetic grafts should not be used below the knee unless no vein is available and the procedure is for limb salvage.

Infrainguinal surgical bypass is associated with significant morbidity and 30-day mortality (5.2%). Approximately 50% of patients require at least one secondary procedure within 3 months, and 50% require hospital readmission within 6 months.

A small study (N = 22) examined outcomes of revascularization of nonatherosclerotic occlusive popliteal artery disease.[10] Of the 22 subjects, three (13.6%) had cystic adventitial disease, 16 (72.7%) had popliteal artery entrapment syndrome, and three (13.6%) had thromboangiitis obliterans. Five (22.7%) underwent thrombectomy with patch angioplasty, eight (36.3%) underwent bypass surgery, and nine (40.9%) underwent graft interposition of the popliteal artery. The overall primary patency rates at 1, 3, and 10 years were 100%, 86.9%, and 69.5%, respectively. The results of surgical treatment for nonatherosclerotic disease were better than those for atherosclerotic popliteal artery disease.



History and Physical Examination

With the exceptions of acute thrombosis, emboli, and trauma, the course of disease culminating in popliteal artery occlusion is insidious. Most commonly, patients present with intermittent claudication.[11] Patients experience cramping pain distal to the level of obstruction. Symptoms are highly reproducible and disappear with rest.

Other conditions involving the lower extremity should be differentiated from intermittent claudication. These include pseudoclaudication, lumbar disk disease, and spinal stenosis. In most cases, the differential diagnosis between true claudication and pseudoclaudication can be made on the basis of careful history taking. The mortality associated with patients who present with claudication is 50% at 5 years.

Rest pain represents the next clinical step in the progression of peripheral artery disease (PAD) and is a pathognomonic sign of critical limb ischemia (CLI; or chronic limb-threatening ischemia [CTLI]). Rest pain characteristically presents as a burning in the toes, forefoot, and instep. It is aggravated by elevation and frequently awakens the patient at night. The pain is relieved by dependency (dangling the feet or a brief walk). When taking the patient’s history, distinguishing true rest pain from other causes (eg, arthritis and neuropathy) is important.

Mortality for patients presenting with rest pain reaches 75% at 5 years and 85% at 10 years and is inversely proportional to the ankle-brachial index (ABI) at the time of presentation. Patients with the most severe manifestations of PAD present with ischemic ulcerations and gangrene. Lesions are typically located at the tips of toes and over pressure points. Patients with rest pain and gangrene should undergo revascularization for limb salvage and preservation of function if they are ambulatory and do not have prohibitive comorbidities.


These patients are older (sixth and seventh decades of life) and may be asymptomatic or have claudication, rest pain, or tissue ischemia or loss below the knee. Chronic decreased blood supply also manifests as loss of hair on the affected limb, thickened toenails, dependent rubor, and pallor upon elevation.

Popliteal artery aneurysm

At the time of presentation, approximately two thirds of patients with popliteal artery aneurysms (PAAs) are symptomatic. The most common presenting symptoms are lower-extremity ischemia and compression of adjacent anatomic structures, notably nerves (causing paresthesias) and veins (leading to deep vein thrombosis and edema). Patients typically present in their sixth or seventh decade of life, with a pulsatile mass in the subsartorial or popliteal area, as observed upon physical examination.

The major complications of PAA result from thrombosis and embolism. Thrombosis occurs in as many as 55% of patients, and 6-25% of patients have evidence of distal emboli. Many patients with acute PAA thrombosis present on an emergency basis with limb-threatening ischemia. Rarely, these aneurysms can rupture, causing a threat to leg viability. Limb-threatening ischemia associated with PAA rupture results in a 50-70% amputation rate.

Rupture of a PAA is uncommon, occurring in approximately 2-7% of cases. This occurs much less frequently than thrombosis of the aneurysm. By contrast, an AAA is more likely to rupture than to thrombose.

Emphasizing that 33-43% of PAAs are associated with a coexisting AAA is important. A high index of suspicion in these patients should result in a careful evaluation of the aorta and the iliac, femoral, and contralateral popliteal arteries. Patients with bilateral PAA extrapopliteal aneurysm are even more common, with a reported incidence as high as 78%.

Popliteal entrapment syndrome

These patients are young, otherwise healthy, athletic males who present with symptoms of calf claudication. In rare cases, paresthesia, rest pain, or ulcer might be present. The symptoms most commonly described include aching and cramping in the calf or foot and coldness, blanching, and numbness in the foot associated with walking and relived by rest. The resting ABI is normal. Findings from Doppler examinations at rest are normal; abnormal findings with dorsiflexion of the foot are diagnostic of popliteal entrapment syndrome.

Cystic adventitial disease

Patients are usually healthy, nonsmoking, middle-aged men with a sudden onset and rapid progression of intermittent claudication. The important physical examination sign is a loss of foot pulses with knee flexion (Ishizawa sign). This demonstrates that cystic disease has resulted in stenosis of the popliteal artery with preservation of patency.

With progressive narrowing of the arterial lumen, blood flow may possibly occur only during the peak of a systole. The altered blood flow can be auscultated as a bruit in the popliteal fossa. Symptoms are predominately unilateral. In time, enlargement of the cyst can cause total occlusion of the popliteal artery. Given the slow progressive nature of the occlusion caused by cystic adventitial disease and healthy proximal and distal arteries, acute limb threat is unlikely to occur.


The Rutherford and Fontaine classifications were developed in an effort to categorize the extent of PAD on the basis of presenting clinical symptoms and thus to facilitate standardization of treatment outcomes reporting. (See Table 2 below.)

Table 1. Rutherford and Fontaine Classifications for Evaluating Extent of Peripheral Artery Disease (Open Table in a new window)

Rutherford Classification

Fontaine Classification













Mild claudication


Mild claudication



Moderate claudication


Moderate to severe claudication



Severe claudication


Ischemic rest pain



Ischemic rest pain


Ischemic rest pain



Minor tissue loss


Ulceration or gangrene



Major tissue loss





Laboratory Studies

In addition to clinical evaluation of patients with suspected popliteal artery occlusive disease, laboratory tests should be performed, including a complete blood count (CBC) and blood chemistries. If a hypercoagulable state is suspected to be the underlying cause of thrombosis, a hypercoagulability profile should be ordered as well. In addition, chest radiographs should be ordered and electrocardiography (ECG) performed. Laboratory studies are used to assess intraoperative and postoperative morbidity and mortality risk.


Conventional angiography

Conventional angiography is the criterion standard evaluation for identifying popliteal occlusion. It also allows visualization of possible targets for distal bypass. It is invasive and uses ionizing radiation and contrast material. It is two-dimensional (2D).

Magnetic resonance angiography

Magnetic resonance angiography (MRA) is a modality that does not require conventional contrast agents and often yields good arterial images. It is more sensitive than conventional angiography in imaging distal runoff vessels. Combined with arterial duplex scanning, MRA has the potential to replace contrast arteriography in the assessment of patients with distal arterial occlusive disease. MRA images can be reformatted into three-dimensional (3D) angiographic images; however, MRA has lower spatial resolution than computed tomography (CT) angiography (CTA) does.

Computed tomography angiography

CTA has become increasingly used and has evolved into a very effective imaging modality for patients with peripheral artery disease (PAD).[12] Besides being used for treatment decision and planning of the procedure, it is very useful for identifying graft failure and related complications. CTA is similar to MRA with respect to ease of use and clinical outcomes for initial imaging of PAD.

CTA makes use of ionizing radiation, and contrast material is used. The images it yields can be reformatted into 3D angiographic images. Total diagnostic cost is lower than that of MRA.[13] CTA uses the largest volume of contrast agent of all modalities and is relatively contraindicated in patients with renal insufficiency.

Duplex Ultrasonography

Examination of the popliteal region with duplex ultrasonography (US) is helpful for establishing the diagnosis of popliteal artery aneurysm (PAA), popliteal artery entrapment syndrome, and cystic degeneration of the popliteal artery. In comparison with angiography, the main benefit of duplex US is the noninvasive nature of the study. Duplex US shows less anatomic detail than angiography does.

A study by Martinelli et al found that duplex US had good diagnostic concordance with CTA in the femoropopliteal region and suggested that it could be a reliable alternative to CTA in patients undergoing endovascular revascularization.[14]

Ankle-Brachial Index

The ankle-brachial index (ABI) is used to assess the amount of blood going to the distal leg relative to that in the brachial vessels. It is capable of identifying the presence and severity of occlusive disease. 

Normally, the ABI is greater than 1.0 because ankle pressures are slightly higher than arm pressures. A correlation is found between the severity of signs and symptoms of arterial insufficiency and the ABI. Generally, the ABI is decreased to 0.4-0.8 in patients with claudication. An ABI lower than 0.4 is seen in patients with critical limb ischemia (CLI), or chronic limb-threatening ischemia [CTLI]; signaled by rest pain or tissue necrosis). (See Table 1 below.)

Table 2. Clinical Category and Ankle-Brachial Index (Open Table in a new window)

Clinical Category



>0.97 (usually 1.10)



Rest pain


Tissue loss


Acute ischemia

< 0.10

A normal ABI does not absolutely rule out the possibility of occlusion. A falsely elevated ABI can be recorded in diabetic patients and patients with renal failure because of incompressible calcified lower leg arteries. In these patients, inspection of flow velocity waveform recording from the pedal arteries in conjunction with toe pressure measurement can be used to determine the degree of ischemia. In addition, patients with mild PAD may have normal ABIs at rest and may require provocative testing with exercise to diagnose their PAD.



Approach Considerations

Regardless of the reason for popliteal artery occlusion, intervention is indicated in patients with severe claudication that alters lifestyle and does not respond to medical treatment and in patients with critical limb ischemia (CLI; also referred to as chronic limb-threatening ischemia [CTLI][1] ).[15]  (See Table 3 below.)

Table 3. Indications for Diagnostic and Therapeutic Interventions in Popliteal Artery Occlusive Disease [15] (Open Table in a new window)



Diagnostic/Therapeutic Interventions


No signs or symptoms

Never justified


Intermittent claudication (1 block) without physical changes

Usually unjustified


Severe claudication (< 50% blocked), dependent rubor, decreased temperature

Sometimes justified, not always necessary; patient may remain stable


Rest pain, atrophy, dependent cyanosis, decreased temperature

Usually indicated, but patient may do well for long periods without revascularization


Nonhealing ischemic ulcer or gangrene


Patients with infection or gangrene in deeper tissues require amputation. Amputation is also indicated for those patients who are unable to ambulate because of reasons other than popliteal artery occlusive disease. However, special consideration should be given to those patients in whom the effect of amputation would have deleterious effects on the ability to transfer to or balance in a wheelchair.

The vast majority of patients with atherosclerotic disease that is severe enough to cause popliteal artery occlusion have atherosclerotic disease elsewhere (including the coronary circulation). These patients require a workup to determine their operative morbidity and mortality risks. Those with coronary artery disease (CAD) or any other disease significant enough to increase morbidity and mortality substantially should be managed by means of either conservative medical therapies or limb amputation.

Percutaneous endovascular procedures are increasingly being used to treat peripheral artery disease (PAD). Bare-metal, drug-eluting, biodegradable, and covered stents (stent-grafts) are intended to provide enhanced treatment with a reduced risk of the perioperative complications associated with open surgical treatment. Endovascular management is a reasonable alternative to open surgery in patients for whom standard surgery poses a considerable risk because of coexisting medical conditions.

Short-term results for infrainguinal percutaneous interventions have been favorable and have been associated with reduced periprocedural morbidity and 30-day mortality. However, the favorable results associated with endovascular treatment options have come at the cost of diminished durability and a potentially increased need for reintervention.

Medical Therapy

The advent of cilostazol and its subsequent approval by the US Food and Drug Administration (FDA) represented a significant advance in pharmacologic treatment of patients with intermittent claudication.

Cilostazol is a phosphodiesterase III inhibitor with several mechanisms of action. The most important of these are inhibition of platelet aggregation (via inhibition of the adenosine diphosphate [ADP] pathway) and vasodilatation. Clinical data from randomized studies demonstrated a significant improvements in overall walking distances and quality of life in patients taking cilostazol.[16]

The main adverse effects include headache, diarrhea, and palpitations. Approximately 15% of patients cannot continue with this therapy, because of side effects. Starting with low doses and then gradually increasing to the recommended dose (100 mg q12hr) may alleviate some of these side effects. Cilostazol is absolutely contraindicated in patients with chronic heart failure of any severity.


Atherosclerotic popliteal thrombosis in which the limb is not imminently threatened is best treated medically. Cardiovascular disease is the major cause of death in patients with PAD. Thus, treatment should be directed not only at improving walking distance and alleviating presenting symptoms but also at reducing cardiovascular risk factors.

Conservative treatment can begin with simple modification of life-style and risk factors, such as smoking, hyperlipidemia, diabetes mellitus, hypertension, and obesity. Institution of various exercise programs has also been proven to be beneficial. Among the traditional risk factors for atherosclerosis, cigarette smoking is most strongly correlated with PAD.

Popliteal artery aneurysm

Because of the high rate of complications from popliteal artery aneurysms (PAAs), medical therapies such as clot lysis are not routinely initiated except to identify an artery for distal anastomosis or when the patient is critically ill and cannot withstand an operation.


Treatment with lysis, such as with urokinase and alteplase (TPA), can be efficacious. However, emboli are likely to recur if definitive therapy is not undertaken for the underlying problem.

Popliteal entrapment syndrome

Aside from surgical intervention, rest is the only other treatment shown to decrease symptoms.

Cystic adventitial disease

No effective medical treatments are available for cystic adventitial disease.

Preoperative and Intraoperative Considerations

Given that most patients with occlusion of the popliteal artery have some component of CAD or another comorbid condition, it is essential to take patients' current functional status into consideration.

Preoperative electrocardiography (ECG), chest radiography, and coagulation studies are recommended. In nonemergency cases, performing lower-extremity angiography is important for identifying the site of occlusion, any collateral circulation, and possible target vessels for bypass, as well as for visualizing runoff vessels. If the use of a vein is anticipated, duplex ultrasonography (US) should be performed to assess the caliber and patency of the veins.

Those patients with gangrene of the affected leg require a course of antibiotics and wound care prior to the bypass operation. Although leg infections do not constitute an absolute contraindication, they increase the incidence of graft infections and subsequent failure.

Careful cardiac monitoring must be used in operative intervention for popliteal artery thrombosis. These patients usually have significant comorbid conditions (eg, CAD or chronic obstructive pulmonary disease [COPD]) that increase the risk of stroke, myocardial infarction, or bleeding episodes. Upon completion of the bypass, some form of confirmation of technical competency must be performed (eg, completion angiography, intraoperative duplex US, or continuous-wave Doppler US).

Surgical and Endovascular Therapy for Popliteal Artery Occlusion

Surgical therapy for popliteal artery occlusion involves bypass of the occlusion, which can be achieved with grafts, including great saphenous vein (GSV) or prosthetic (eg, polytetrafluoroethylene [PTFE]) grafts.

GSV bypass can be used in a reversed or a nonreversed in-situ orientation. The reverse vein bypass graft, first described by Kunlin in 1949, has become the favored operation for bypass of an occluded popliteal artery. The ipsilateral GSV is the conduit of first choice. If that is unavailable, alternative autogenous conduit options that can be used include the contralateral GSV, arm veins (basilic and cephalic), the small saphenous vein (SSV),[17] the superficial femoral vein, the popliteal vein, or cryopreserved veins.

The popliteal artery is accessible via medial thigh and calf incisions. The anastomosis can be performed in either an end-to-end or a side-to-side fashion. If the latter is chosen in the case of an aneurysm, the aneurysm must be excluded from the circulation by ligature.

Percutaneous transluminal angioplasty (PTA) is a less invasive intervention in the treatment of popliteal artery occlusive disease. PTA is indicated for short (< 2 cm) lesions in patients who have claudication and good runoff. Initial enthusiasm for the possibility that stents could improve long-term results of PTA was not supported by subsequent studies. The primary patency rate at 1 year is 65%. However, PTA may be a reasonable alternative to open surgery for limb salvage in patients with prohibitive surgical risks.

Although open repair has traditionally been recommended for TransAtlantic Inter-Society Consensus (TASC) II class D femoropopliteal lesions, there is evidence to suggest that in some cases, endovascular repair is a reasonable alternative for these lesions.[18]

Some studies have suggested that the use of drug-coated balloons (DCBs) is safe and effective for femoropopliteal disease, especially for preventing restenosis.[19, 20]  However, controversy has surrounded the use of paclitaxel-coated devices in this setting.[21]

The relative lack of long-term success rates with PTA and stenting led to the development of other endovascular procedures, such as atherectomy, laser angioplasty, cutting balloon angioplasty, cryoplasty, and brachytherapy. Although initial results using directional atherectomy were disappointing,[22] subsequent developmental and technical modifications of newer-generation atherectomy systems led to promising mid- and long-term patency rates.[23]

On the basis of the clinical data, PTA has been the initial preferred option for endovascular treatment of symptomatic PAD caused by femoropopliteal lesions, followed by stent placement in patients with suboptimal or failed balloon dilation. This strategy was featured in the 2005 American College of Cardiology (ACC)/American Heart Association (AHA) practice guidelines for the management of PAD,[24] , as well as the updated 2007 inter-society consensus for the management of PAD (TASC II).[25]  Updated ACC/AHA guidelines were published in 2010 and 2016.[26]  (See Guidelines.)

Iida et al reported 2-year results of the MDT-2113 SFA Japan randomized trial (N = 100), which assessed the longer-term safety and efficacy of the IN.PACT Admiral DCB (n = 68) for  treatment of de-novo and nonstented restenotic lesions in the superficial femoral or proximal popliteal artery vs uncoated PTA (n = 32).[27]  End points included primary patency and a composite safety endpoint of freedom from device- and procedure-related death through 30 days, freedom from target-limb major amputation, and freedom from clinically driven target lesion revascularization (CD-TLR) at 24 months. The DCB was associated with persistently superior patency and low CD-TLR rates through 2 years.

Data from various studies indicated that primary stenting of the popliteal lesion is associated with relatively high patency rates[28] and suggested that primary stenting can be preferred over balloon dilatation and provisional stenting of the lesion.[29, 30, 31]

In 2013, Scheinert et al documented that primary patency rates were 94.6 ± 2.3% at 6 months and 87.7 ± 3.7% at 1 year and that respective secondary patency rates were 97.9 ± 1.5% and 96.5 ± 2% in 101 consecutive patients with PAD due to atherosclerotic lesions located in the popliteal artery.[32]  

In this study, all patients were treated with primary placement of the self-expanding interwoven nitinol stents (n = 125) in the popliteal artery.[32] In addition, the authors documented statistically significant improvement in mean ankle-brachial index (ABI; from 0.58 ± 0.15 at baseline to 0.97 ± 0.18 at 1-year follow-up) and reduction in the mean Rutherford-Becker class of the lesion (from 3.1 ± 9 at baseline to 1.4 ± 0.8 at 1-year follow-up).

Owing to its anatomic location and the fact that the popliteal artery is not contained within the muscular compartment, this vascular territory is exposed to the significant mechanical forces caused by the knee flexion/extension, which raises concerns regarding the suitability of popliteal artery stenting and the high incidence of stent fracture.[33] However, radiographic evaluation of 51 patients in the study by Scheinert et al showed an absence of stent fractures in 100% of cases, at a mean of 15.2 months after the initial procedure.[32]

In a study that evaluated woven nitinol stents in 34 patients with isolated severe popliteal artery occlusive disease that progressed to tissue necrosis in 38.2% of patients and rest pain in 35.3%, Kaplan-Meier analysis of patency and limb loss demonstrated primary, primary assisted, and secondary patency rates of 79.2%, 88.1%, and 93%, respectively (mean follow-up, 8.4 months; range, 0-26.8 months).[34]

Three patients (8.8%) sustained limb loss in the study.[34] No stent fractures were identified during radiologic follow-up (mean, 17.3 ± 6.2 months). Stent occlusion was observed in six (17.6%) cases. The relatively high number of patients who required reintervention emphasizes that frequent and short-term surveillance after stenting is critical for the identification and management of stent occlusion.

Although initial results with stenting across the lesions exposed to significant biomechanical forces (eg, lesions of the popliteal artery) using novel nitinol stents were promising and suggested that the interwoven stent design may better serve areas under extreme mechanical stress, level 1 data from better-designed randomized clinical trials are needed for accurate evaluation of the efficacy and safety, as well as the feasibility, of nitinol stents for the treatment of the popliteal artery occlusive disease.

Initial data on directional atherectomy from one of the largest multicenter, nonrandomized, observational studies (Treating Peripherals With SilverHawk: Outcomes Collection; TALON), which involved 19 medical centers in the United States, demonstrated excellent procedural success rates of 97.6% and less than 50% residual stenosis achieved in 94.7% of treated lesions.[35]

Of 1258 symptomatic atherosclerotic lower-extremity lesions in 601 patients enrolled in the TALON registry, 182 (14.5%) affected the popliteal artery.[35] In the same study, the overall 6- and 12-month freedom-of-target-lesion revascularization rates were 90% and 80%, respectively.

In a single-center study assessing DCB angioplasty against directional atherectomy with antirestenotic therapy (DAART) for isolated lesions of the popliteal artery, Stavroulakis et al found that DAART yielded a higher primary patency rate (82%) than DCB angioplasty (65%) for these lesions, though both modalities were associated with excellent 12-month secondary patency.[36]  Aneurysmal degeneration of the popliteal artery was more common after DAART, and bailout stenting was more common after DCB angioplasty, but neither difference was statistically significant.

It has been suggested that distal embolic protection may be helpful for patients undergoing directional atherectomy for femoropopliteal lesions; however, there has not been a consensus on this issue. A study by Krishnan et al concluded that distal embolic protection is warranted for cases of chronic total occlusion; in-stent restenosis; thrombotic, calcific lesions larger than 40 mm; and atherosclerotic lesions larger than 140 mm.[37]  

A subgroup of PAD patients with calcified popliteal stenotic lesions represents a special therapeutic challenge. Stenting of calcified lesions is frequently complicated by stent underexpansion, which is associated with an increased risk of in-stent restenosis and thrombosis.[38, 39]

Data from a European study that included 38 patients with calcified lesions, treated with directional atherectomy, demonstrated primary and assisted primary (defined as freedom of restenosis after repeated intervention) patency rates of 68% and 79%, respectively, in the cohort of patients (n = 29) with a lesion located in the proximal or distal 3 cm of the superficial femoral artery or in the popliteal artery.[40]

In the same cohort of patients, the ABI increased from 0.7 ± 0.4 to 1.1 ± 0.4 at 6 months and to 1.0 ± 0.3 at 12 months after the atherectomy. Additionally, the mean Rutherford score decreased from 4.3 ± 1 to 1.1 ± 1.3 at 6 months and to 0.9 ± 1.3 at 12 months.[40]

Although results from clinical trials that evaluate the above-mentioned evolving endovascular treatment modalities have been promising, the efficacy and safety of endovascular modalities have not been extensively investigated, and the role of these modalities remains controversial owing to the lack of abundant randomized data supporting any improved long-term patency rates in comparison with a surgical approach.

Surgical and Endovascular Therapy for Popliteal Artery Aneurysm

Elective surgical repair is indicated in all patients with PAA, regardless of the size of the aneurysm. Even a small PAA can produce limb-threatening ischemia secondary to thrombus or distal embolization. Recommendations regarding treatment of PAA have been published by the Society for Vascular Surgery (SVS).[41] (See Guidelines.)

Elective repair assures that procedure is not performed in the setting of limb-threatening ischemia. Elective repair is associated with little risk to the patient, better overall results and lower incidence of amputation. Surgical PAA repair consists of either resecting the aneurysm sac and interposing a bypass graft or proximal and distal ligation of the popliteal artery combined with bypass grafting.

Endovascular repair with a percutaneously delivered covered stents (stent-grafts) has become an alternative to open repair, but long-term results are unknown.

Improvements in stent grafts and endovascular techniques in general have extended the treatment options for lesions in different vascular territories, including patients with PAA. Endovascular repair of PAA has emerged as a reasonable treatment option in patients with favorable anatomy.[42, 43]

However, currently available data on the endovascular management of acute complications of the PAA are limited. This is very important in that thrombosis and distal embolization resulting in acute limb ischemia are the most common complications of the PAA and are associated with a high risk for amputations. Although rupture of the PAA is rare, approximately 50-75% of patients with ruptured PAA present with limb ischemia.[23]

A Mayo study evaluated 25 patients (31 limbs) who underwent elective (61%) and emergency (39%) endovascular PAA repair.[24]  The patients with ruptured PAA (n = 11) underwent thrombolysis before endovascular repair. The 30-day primary and secondary patency rates were 100% in the elective group and 83.3% and 91.6%, respectively, in the emergency group.[24]  At 1-year follow-up, authors documented primary patency of 86% (95% in the elective group, 69% in the emergency group) and secondary patency of 91% (100% in the elective group, 91% in the emergency group). The cumulative 1-year limb salvage rate was 97%.

Five stent occlusions were identified at 1-month follow-up.[24]  Four occlusions (80%) occurred in the elective group. One stent fracture was noted in an asymptomatic patient. Type I endoleak and type II endoleak were documented in 1 (3.2%) and 3 (10%) cases, respectively. All type II endoleaks occurred in the elective group. Most of the major adverse events, leading to death, occlusion, or reoperation, were documented it the emergency group. The 2-year survival was 93% for the elective group and 73% for the emergency group.

The results of this study showed that elective endovascular PAA repair is technically feasible in elective and emergency settings and suggested that elective endovascular PAA repair is reasonable in anatomically suitable patients with increased risk for open repair.[24] Although it did not reach statistical significance, emergency endovascular PAA repair was associated with a higher rate of major adverse events and higher mortality rates.

In a study that included 231 legs in 212 patients treated for PAA, Cervin et al compared the results of open surgical repair (154 legs) with those of endovascular repair (77 legs).[44]  They found that the legs treated with endovascular repair had a 2.7-fold increased risk of occlusion and 2.4-fold increased risk of permanent occlusion. Risk factors for occlusion in this group included poor outflow, smaller stent graft diameter, acute ischemia, and angulation/elongation. The authors identified an association between indication, acute ischemia, and small stent graft diameter.

As with popliteal artery stenting, data from prospective randomized clinical trials with higher numbers of patients are needed before endovascular PAA repair can be accurately evaluated, especially in emergency settings.

Surgical and Endovascular Therapy for Emboli, Popliteal Entrapment Syndrome, and Cystic Adventitial Disease


Emboli may be evacuated from distal vessels by means of either the use of a balloon catheter or intraoperative thrombolysis.

Popliteal entrapment syndrome

Surgical treatment is advised in all types of popliteal entrapment syndrome. Recognition of progressive fibrosis with subsequent thrombosis in untreated entrapped artery supports early surgical intervention. Individual anatomic considerations play an important role in determining the best surgical approach.

Although the posterior approach has been most commonly advised because it most clearly delineates the anatomy of the lesion, the medial calf approach is more appropriate when the occlusion extends distally to the popliteal artery bifurcation. Myotomy of the compressing muscle or transection of fascial band leads to decompression of the artery and prevention of secondary fibrotic changes. If the artery is not occluded and fibrotic change has not occurred, no further intervention is necessary.

There is evidence to suggest that when a popliteal artery has undergone fibrotic changes and occlusion, resection and vein (preferably GSV) graft interposition are required to ensure optimal long-term patency in these often young, physically active individuals.

Cystic adventitial disease

Cystic adventitial disease has been treated in numerous ways. Evacuation with removal of the cyst wall had a 94% initial success rate in 68 operations performed. Evacuation with a vein patch had a 66% initial success rate in nine operations performed. Evacuation with a synthetic patch had a 75% initial success rate in four operations performed.

Aspiration had a 66% initial success rate in three operations performed. Simple aspiration of the cyst under the guidance of US or computed tomography (CT) may decompress the cyst initially and improve arterial caliber but is associated with higher rate of recurrence, presumably because of ongoing secretion by the cyst lining.

Resection with a vein graft had a 95% initial success rate in 54 operations performed. Resection with synthetic graft placement had a 90% initial success rate in 10 operations performed. Resection with end-to-end anastomosis of primary vessel had a 100% initial success rate in three operations performed. Resection with homograft placement had a 100% initial success rate in two operations performed. Three cases resolved spontaneously. Angioplasty has not been successful.

Postoperative Care

On postoperative day 1, patients should begin aspirin therapy and, if indicated, beta blockers. A postoperative ABI should be obtained before the patient is discharged from the hospital. This serves as a baseline value to which subsequent ABIs can be compared in the event of restenosis. Postoperative visits for duplex US scanning of the graft are undertaken every 3 months for a year and every 6 months thereafter.


Potential complications include the following:

  • Intraoperative bleeding
  • Perioperative myocardial ischemia or infarct
  • Stroke
  • Death
  • Limb loss
  • Graft infection
  • Graft thrombosis
  • Wound infection
  • Reocclusion
  • Numbness at operative site or vein harvest site
  • Arteriovenous fistula (in-situ GSV graft)

Long-Term Monitoring

Follow-up should be performed at regular intervals to assess for restenosis, which usually results from technical failures, intimal hyperplasia, or disease progression at other sites, at 1 month, 18 months, and 2 years or more, respectively.



SVS Guidelines for Popliteal Artery Aneurysms

Guidelines on popliteal artery aneurysms (PAAs) were published in January 2022 by the Society for Vascular Surgery (SVS).[41]  The recommendations are summarized below.

Grade 1 (strong) recommendations

Screen patients who present with a PAA for both a contralateral PAA and an abdominal aortic aneurysm (AAA).

Patients with an asymptomatic PAA at least 20 mm in diameter should undergo repair to reduce their risk of thromboembolic complications and limb loss.

Stratify intervention for PAA thrombotic and/or embolic complications based on the severity of acute limb ischemia (ALI) at presentation:

  • Patients with mild to moderate ALI (Rutherford grade I and IIa) and severely obstructed tibiopedal arteries - Thrombolysis or pharmacomechanical intervention to improve runoff status, with prompt transition to definitive PAA repair
  • Patients with severe ALI (Rutherford grade IIb) - Prompt surgical or endovascular PAA repair, with the use of adjunctive surgical thromboembolectomy or pharmacomechanical intervention to maximize tibiopedal outflow
  • Patients with nonviable limbs (Rutherford grade III) - Amputation

Follow up patients who undergo open PAA repair (OPAR) or endovascular PAA repair (EPAR) with the use of clinical examination, ankle brachial index (ABI), and duplex ultrasonography (DUS) at 3, 6, and 12 months during the first postoperative year and, if stable, every year thereafter.

In addition to DUS evaluation of the repair, evaluate the aneurysm sac for evidence of enlargement. If there are anomalies on clinical examination, ABI, or DUS, administer appropriate clinical management according to the lower-extremity endovascular or open bypass guidelines. In the setting of compressive symptoms or symptomatic aneurysm sac expansion, surgical decompression of the aneurysm sac is suggested.

Grade 2 (weak) recommendations

For selected patients with an asymptomatic PAA of at least 20 mm in diameter who are at higher clinical risk of thromboembolic complications and limb loss, repair can be deferred until the PAA has become at least 30 mm, especially in the absence of thrombus.

Consider repair for patients with a PAA smaller than 20 mm, in the presence of thrombus and a clinical suspicion of embolism or imaging evidence of poor distal runoff, to prevent thromboembolic complications and possible limb loss.

For asymptomatic patients, with a life expectancy of at least 5 years, the SVS suggests open PAA repair, as long as there is an adequate saphenous vein present. For those whose life expectancy is diminished, if intervention is indicated, consider endovascular repair.

Yearly monitoring for changes in symptoms, pulse examination, extent of thrombus, patency of the outflow arteries, and aneurysm diameter is suggested for patients with an asymptomatic PAA who are not offered repair.

ACC/AHA Guidelines for Lower-Extremity Peripheral Arterial Disease

In November 2016, the American College of Cardiology (ACC) and the American Heart Association (AHA) issued updated recommendations regarding lower-extremity peripheral artery disease (PAD), including the following[26] :

  • The vascular examination for PAD includes pulse palpation, auscultation for femoral bruits, and inspection of the legs and feet; lower-extremity pulses are assessed and rated as follows: 0, absent; 1, diminished; 2, normal; or 3, bounding
  • To confirm the diagnosis of PAD, abnormal physical examination findings must be confirmed with diagnostic testing, generally with the ankle-brachial index (ABI) as the initial test
  • Patients with confirmed diagnosis of PAD are at increased risk for subclavian artery stenosis; an interarm blood pressure difference of >15 to 20 mm Hg is abnormal and suggestive of subclavian (or innominate) artery stenosis; measuring blood pressure in both arms identifies the arm with the highest systolic pressure, a requirement for accurate measurement of the ABI
  • Resting ABI results should be reported as abnormal (ABI ≤0.90), borderline (ABI 0.91-0.99), normal (1.00-1.40), or noncompressible (ABI >1.40)
  • ABI is not recommended in patients who are not at increased risk of PAD and who do not have a  history or physical examination findings suggestive of PAD
  • Toe-brachial index (TBI) should be measured to diagnose patients with suspected PAD when the ABI is >1.40
  • Patients with exertional non–joint-related leg symptoms and normal or borderline resting ABI (>0.90 and ≤1.40) should undergo exercise treadmill ABI testing to evaluate for PAD
  • Patients with PAD should receive a comprehensive program of guideline-directed medical therapy, including structured exercise and lifestyle modification, to reduce cardiovascular ischemic events and improve functional status
  • Antiplatelet therapy with aspirin alone (range, 75-325 mg/day) or clopidogrel alone (75 mg/day) is recommended to reduce myocardial infarction (MI), stroke, and vascular death in patients with symptomatic PAD
  • Treatment with a statin medication is indicated for all patients with PAD
  • Patients with PAD who smoke cigarettes or use other forms of tobacco should be advised at every visit to quit
  • Cilostazol is an effective therapy to improve symptoms and increase walking distance in patients with claudication
  • Endovascular procedures are effective as a revascularization option for patients with lifestyle-limiting claudication and hemodynamically significant aortoiliac or femoropopliteal occlusive disease; it is unknown whether they are effective for isolated infrapopliteal disease
  • Endovascular procedures for PAD should not be performed solely to prevent progression to critical limb ischemia (CLI)
  • When surgical revascularization is performed, bypass to the popliteal artery with autogenous vein is recommended in preference to prosthetic graft material
  • Surgical procedures for PAD should not be performed solely to prevent progression to CLI