Popliteal Entrapment Syndrome

Article Author:
Heitham Wady
Article Editor:
Palma Shaw
10/27/2018 12:31:48 PM
PubMed Link:
Popliteal Entrapment Syndrome


Popliteal artery entrapment is an anatomic anomaly that was first discovered in 1879 by a medical student in Edinburgh. The rare clinical manifestation of Popliteal Artery Entrapment Syndrome (PAES) was defined approximately 40 years ago. It has a predilection for young to middle-aged patients.The hallmark of this disease is a vascular compromise within the popliteal fossa resulting in an insidious, progressive course of exercise intolerance and calf pain with exertion relieved by rest (claudication). While the incidence of this disease has risen slightly in recent years, the true prevalence is unknown as the number of cases is likely underreported.


The anatomic variability of this pathology is related to the embryonic development of the structures making up the popliteal fossa. The popliteal artery and medial head of the gastrocnemius muscle develop about the same time. The popliteal artery develops from the extension of the femoral artery proximally and the sciatic artery distally. The sciatic artery contributes to the development of the popliteal artery and tibial arteries. Ultimately the femoral artery dominates, and the sciatic artery regresses. Various anomalies relating to the relative position of the popliteal artery, medial head of the gastrocnemius (MHG) and popliteus muscles make up the different types of Popliteal Artery Entrapment syndrome. Aberrant migration of the medial head during embryological development can result in malpositioning of the muscle in relation to the nearby vessels. A functional type of Popliteal Artery Entrapment syndrome also has been described. Interestingly, many people born with the congenital form are often asymptomatic, suggesting a likely multifactorial process contributing to disease progression. Although this pathology is present from birth, it appears later, likely due to changes related to use of the gastrocnemius muscle in activities such as running or marching causing muscle hypertrophy with external compression and impingement of the popliteal artery by the medial head.


Among other causes of popliteal artery luminal narrowing, such as adventitial cystic disease, Popliteal Artery Entrapment syndrome should be considered when a young person, usually younger than the age of 40, presents with claudication. Although Popliteal Artery Entrapment syndrome remains a rare cause of vascular compromise, the incidence of the disease has risen over recent years. Recent reports estimate the overall incidence in the general population to be in the range of 0.17% to 3.5%. Almost 85% of patients diagnosed are males, with almost 60% of cases occurring in male athletes younger than age 30. Up to 30% of cases can be bilaterally symptomatic.


Anatomical Popliteal Artery Entrapment Syndrome is classified into one of five different subtypes based on anatomical abnormalities: 

  1. An aberrant medial course of the artery around a normally positioned MHG
  2. MHG attaches abnormally more laterally on the femur causing the artery to pass medially and inferiorly
  3. Abnormal fibrous band or accessory muscle arising from the medial or lateral condyle encircling the artery
  4. Popliteal artery lying in its primitive deep or axial position within the fossa, becoming compromised by the popliteus muscle or fibrous bands
  5. Entrapment of both the popliteal artery and vein due to any of the causes mentioned above.

Functional Popliteal Artery Entrapment Syndrome (Type VI or F) describes another subtype of disease that is not due to inherited anatomic abnormalities. It has been postulated that repeated microtrauma results in the growth of connective tissue, destruction of the internal elastic lamina, and damage to the smooth muscles resulting in fibrosis and scar formation. Thrombosis, embolization, or aneurysmal degeneration can ensue. Tibial nerve involvement can occur with all five anatomical Popliteal Artery Entrapment syndrome subtypes.

History and Physical

Symptoms typically present in the second to third decade of life and are insidious in onset. Classically, patients are young athletes without cardiovascular risk factors who present with complaints of leg claudication that can be quite severe and disabling. Additionally, the patient may also note paresthesia, discoloration, pallor, or coolness of the distal extremities. The calf muscles may appear hypertrophied. On exam, comparison of distal pulses at baseline and with dorsiflexion/plantar flexion may elicit diminished, unequal, or even absent pulses. Sudden onset of more severe pain in a young adult after an episode of robust exercise should increase suspicion of this process. An ankle-brachial index will be low with profound disease progression.


Duplex Arterial Ultrasonography using provocative maneuvers (leg/foot positioned first in neutral position and then in resisted plantar flexion) provides a quick, inexpensive, and non-invasive initial screening test. Findings of arterial compromise or prominent collaterals in the fossa suggest the diagnosis. Angiography can be performed with provocative maneuvers and would typically demonstrate a medially deviated proximal popliteal artery, focal occlusion or narrowing of the mid-popliteal artery, post-stenotic dilatation or aneurysm of the distal popliteal artery. Testing with CT angiography or Magnetic Resonance Angiography can confirm the diagnosis when the artery is occluded but do not allow for provocative testing. MRI is the gold standard for defining popliteal fossa anatomy as it can define anomalous muscle positioning.

Treatment / Management

For asymptomatic patients with incidental findings of popliteal artery entrapment, management is typically expectant, as the majority of these patients never experience symptoms or disease progression. For symptomatic patients, surgery with popliteal artery release allows for the definitive reestablishment of normal anatomy and often portends excellent results. Through either a posterior or medial approach, the MHG or musculotendinous band can be divided. The artery can then be palpated to determine its patency and determine if the bypass is required. Reconstruction of the adjacent muscles is not necessary as this is well tolerated without functional limitation. Open surgical procedures offer the best results to address the entrapment and assess the artery for repair or bypass. In cases where there is extensive arterial wall damage, occlusion, or aneurysm development interposition bypass grafting, using autogenous vein via a posterior approach or medial bypass to extend farther down the below-knee popliteal artery have been advocated. The medial approach may be better for the management of Type I and II while a posterior approach may be better for type III and IV.  Management of functional Popliteal Artery Entrapment syndrome is controversial although some have had success with gastrocnemius debulking. Postoperatively, surveillance is performed using arterial duplex imaging at 1, 3, 6, and 12 months, and annually after that. Endovascular therapy with balloon angioplasty, thrombolysis, and delayed release of the entrapment has been reported, but long-term efficacy remains unclear.


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