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Popliteal artery occlusive disease :

Popliteal Artery Thrombosis India offers information on Popliteal Artery Thrombosis in India, Popliteal Artery Thrombosis cost India, Popliteal Artery Thrombosis hospital in India, Delhi, Mumbai, Chennai, Hyderabad & Bangalore, Popliteal Artery Thrombosis Surgeon in India

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 limb ischemia are performed in the United States. Many of these are related to popliteal artery disease.

What is it?

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 markedly increased prevalence of coronary artery disease (CAD) and cerebrovascular disease and mortality. Recognition of this relationship allows for 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 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 (PAA) are the most common peripheral aneurysms. They occur in 0.01% of all hospitalized patients. From 50-70% 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 2-10 times more oxygenated blood than 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. Recent 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 (AAA), or iliac aneurysms.

Popliteal entrapment syndrome

Popliteal entrapment syndrome is a developmental anomaly characterized by an abnormal anatomic relationship of the popliteal artery to the gastrocnemius muscle. This anomalous anatomic relationship causes popliteal artery compression and occlusion. In rare cases, the popliteal artery is compressed by a fibrous band or by the popliteus muscle. 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 and associates suggest 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. Due to 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.

Signs and Symptoms

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 patientís history, distinguishing true rest pain from other causes (eg, arthritis and neuropathy) is important.

Mortality rates for patients presenting with rest pain reaches 75% at 5 years and 85 % at 10 years and are 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 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 emergently 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% PAA 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, 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. ABI at rest is normal. Findings from Doppler examinations at rest are normal. Abnormal findings after Doppler examination 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.

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.


Laboratory Studies

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

Imaging Studies

Other Tests

  • Ankle-brachial index is used to assess the amount of blood going to the distal leg relative to that in the brachial vessels.


Medical Therapy

The advent and subsequent FDA approval of cilostazol was a significant advance in the pharmacologic therapy for patients with intermittent claudication. Cilostazol is phosphodiesterase III inhibitor with several mechanisms of action. The most important of these are inhibition of platelet aggregation (via inhibition of ADP pathway) and vasodilatation. Clinical data, based on several randomized studies, have emerged demonstrating a significant improvement in overall walking distances and quality of life in patients taking cilostazol.

The main adverse effects include headache, diarrhea, and palpitations. Approximately 15% of patients can not continue with this therapy due to side effects. Starting with low doses and then gradually increasing to the recommended dose (100 mg twice a day) 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, the 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 traditional risk factors for atherosclerosis, cigarette smoking is most strongly correlated with PAD.

Popliteal artery aneurysm

Because of the high rate of complications from aneurysms, 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 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.

Surgical Therapy

Popliteal artery occlusion

Surgical therapy for popliteal artery occlusion is 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, nonreversed or 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, the superficial femoral vein, the popliteal vein, or cryopreserved veins.

The popliteal artery is accessible from medial thigh and calf incisions. The anastomosis can be performed either end-to-end or side-to-side. 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 that stents could increase long term results of PTA has not been 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 indications in patients with prohibitive surgical risks.

Popliteal artery aneurysm

Elective surgical repair is indicated in all patients with PAA regardless of size. Even a small PAA can produce limb-threatening ischemia secondary to thrombus or distal embolization. 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.

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


Emboli may be evacuated from distal vessels by 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.

Recent evidence emerged that suggests that when a popliteal artery has undergone fibrotic changes and occlusion, resection and vein graft (preferably GSV) 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 has had a 94% initial success rate in 68 operations performed. Evacuation with a vein patch has had a 66% initial success rate in 9 operations performed. Evacuation with a synthetic patch has had a 75% initial success rate in 4 operations performed.

Aspiration has had a 66% initial success rate in 3 operations performed. Simple aspiration of the cyst under US or CT guidance 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 has had a 95% initial success rate in 54 operations performed. Resection with synthetic graft placement has had a 90% initial success rate in 10 operations performed. Resection with end-to-end anastomosis of primary vessel has had a 100% initial success rate in 3 operations performed. Resection with homograft placement has a 100% initial success rate in 2 operations performed. Three cases resolved spontaneously. Angioplasty has not been successful.


  • 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)

Outcome and Prognosis

In patients with native conduits intimal hyperplasia, leading to the narrowing of the vein graft and valvular hyperplasia are the 2 leading causes of graft failure. The most recent studies suggest that geometric remodeling of the vein graft and decreased vein graft adaptation to the arterial environment are caused by mediators of inflammation. 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 US surveillance after bypass procedure 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 PTA, although in certain cases vein patch angioplasty or short bypass of a graft lesion is needed. PTA should be restricted to short lesions (less than 2 cm). Prosthetic (PTFE) graft failure 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 ranging from 68-80% and limb salvage rates ranging from 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 has 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.

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