Popliteal Artery Occlusive Disease

Updated: Apr 15, 2015
  • Author: Cynthia K Shortell, MD; Chief Editor: Vincent Lopez Rowe, MD  more...
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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 limb-threatening ischemia, 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.




Atherosclerosis is by far the most common cause of popliteal artery occlusive disease. More than 1 a 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.

Popliteal artery aneurysms (PAAs) are the most common peripheral aneurysms. They occur in 0.01% of all hospitalized patients. Between 50% and 70% of aneurysms are bilateral.

Fifteen percent 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 254 reported cases since the first description by Ejrup and Hiertonn in 1954.



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 PAA is not known. 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.


Fifteen percent 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. [1]

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. [2]

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.



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. 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 disc disease, and spinal stenosis. In most cases, the differential diagnosis between true claudication and pseudoclaudication can be made based on careful history taking. The mortality rate associated with patients who present with claudication is 50% at 5 years.

Rest pain represents the next clinical step in the progression of PAD and is a pathognomonic sign of critical limb ischemia. 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 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 PAA is uncommon, occurring in approximately 2-7% of cases. This occurs much less frequently than thrombosis of the aneurysm. By contrast, AAA is more likely to rupture than 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 adventitial cystic disease and healthy proximal and distal arteries, acute limb threat is unlikely to occur.



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. [3] (See Table 1 below.)

Table 1. Indications for Diagnostic and Therapeutic Interventions [3] (Open Table in a new window)

Stage Presentation Diagnostic and Therapeutic Indications
0 No signs or symptoms Never justified
I Intermittent claudication (1 block) without physical changes Usually unjustified
II Severe claudication (less than half blocked), dependent rubor, decreased temperature Sometimes justified, not always necessary, may remain stable
III Rest pain, atrophy, dependent cyanosis, decreased temperature Usually indicated but patient may do well for long periods of time without revascularization
IV Nonhealing ischemic ulcer or gangrene Indicated


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.


Relevant Anatomy

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. [4]

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. [5, 6, 7] 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 the 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.



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 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.