Popliteal Artery Occlusive Disease

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