Secondary Logo

Journal Logo

Popliteal Artery Entrapment Syndrome

Joy, Susan M. MD; Raudales, Raul MD

doi: 10.1249/JSR.0000000000000199
Extremity and Joint Conditions: Section Articles

Popliteal artery entrapment syndrome (PAES) may be implicated as a cause of lower leg pain in active individuals. Though a relatively rare syndrome, it is likely underdiagnosed. History often includes exertional lower leg pain, cramping, and/or paresthesias rather quickly relieved by rest, though examination may be benign. When suspected, imaging is recommended to assess anatomic variations versus functional entrapment of the artery in the calf. Because there are a number of diagnostic modalities available, it seems prudent to begin with noninvasive testing, such as ultrasound with Doppler and provocative maneuvers. Thereafter, advanced imaging (magnetic resonance imaging/magnetic resonance angiography) or arteriography may help identify a specific anatomic obstruction. Once confirmed, surgical exploration has historically been the treatment of choice, though less invasive interventions have been proposed. Though most patients reportedly return to high-level training, decision-making remains highly individualized. Further study of younger, active individuals with PAES will help to further define these criteria.

Cleveland Clinic, Independence, OH.

Address for correspondence: Susan M. Joy, MD, Cleveland Clinic, Independence, OH.

Back to Top | Article Outline


Popliteal artery entrapment syndrome (PAES) should be considered in any athlete presenting with lower leg complaints, even younger athletes and those without any apparent risk factors for atherosclerotic disease. Although the syndrome is reportedly rare, it is also often overlooked and/or misdiagnosed. Clinicians should be alert to the possibility of this diagnosis in athletes with symptoms such as exercise-induced calf claudication, nocturnal cramps, and/or paresthesias and recognize the potential for arterial injury or even acute limb ischemia.

Back to Top | Article Outline


Within the popliteal fossa are the popliteal vein, popliteal artery, tibial nerve, and common fibular nerve (7). The proximal portion of the fossa comprises the semitendinosus muscle and semimembranosus muscle medially and the bicep femoris muscle laterally. Distally, the lateral margin includes the plantaris muscle and the lateral head of the gastrocnemius muscle. The distal medial aspect is defined by the medial head of the gastrocnemius muscle. With the knee in a prone position, the floor of the fossa is composed of the femur, tibia, capsule of the knee joint, and the popliteus muscle, and the roof is composed of the deep fascia.

The popliteal artery enters the proximal popliteal fossa on the superior medial side under the margins of the semimembranosus muscle. It typically descends in an oblique manner through the fossa along with the tibial nerve where it then enters the posterior compartment of the leg lateral to the midline between the gastrocnemius and the popliteus muscles. There it passes under the tendinous arch of the soleus (between the fibular and the tibial heads) and divides into the anterior and posterior tibial arteries. The popliteal vein runs superficially to the popliteal artery and travels along with it for a course before exiting the popliteal fossa superiorly.

Back to Top | Article Outline


The term was originally coined by Love and Whelan in 1965, though a case report dates back to 1879 (23). At least six different classification systems have been described incorporating both anatomic and functional entrapments (8). The most frequently referenced is that adapted by Rich et al. (18) from the original Love and Whelan classification incorporating a functional type in addition to the originally described anatomic variations. More than 60% of the anatomic variants described involve the popliteal artery medial to the medial head of the gastrocnemius (4). The natural history and cause of functional entrapment remains unknown, though hypertrophy of the medial gastrocnemius in well-trained individuals has been suspected as a contributing factor.

The anatomic incidence in the general population has been cited at 3 per 86; however, it has been reported in clinical practice to have an incidence as low as 17 per 4 million (5). Mean age is estimated to be 30 years with a male to female ratio of 2/1 to 15/1. Symptoms are present bilaterally in 30% to 67%. It is estimated that 17% are found as incidental findings on imaging studies (4). It has been suggested that functional PAES and anatomic PAES represent rather different clinical entities. One series found that functional entrapment patients were typically young athletic women (mean age, 26 years) with no evidence of ischemia, whereas the anatomic entrapment patients were predominantly men (70%) with a mean age of 46 years (23).

The type of entrapment may be quite different between anatomic PAES versus functional entrapment. Computed tomography angiography (CTA) has indicated that functional entrapment patterns manifest from side-to-side compression, which results in long-segment stenosis, whereas anteroposterior compression in anatomic entrapment leads to short-segment stenosis (3). There have not been studies to date specifically looking at clinical outcomes that might be related to these varying etiologies (Table 1).

Table 1

Table 1

Back to Top | Article Outline

Differential Diagnosis

The differential diagnosis of recurrent lower leg pain in an athlete is a lengthy one. More common potential causes include medial tibial stress syndrome, stress fracture, stress reaction, nerve entrapment, tendinopathy, and chronic exertional compartment syndrome (CECS). Other etiologies may include vascular problems such as arterial aneurysm, arterial dissection, embolism, adventitial cystic disease, and Buerger’s disease (thromboangiitis obliterans) as well as systemic or metabolic issues, neuromuscular disorders, and referred pain syndromes. There has been some suggestion that CECS may be present as a secondary diagnosis and warrant consideration of treatment at the time of surgery (10). In one series, nearly half of the functional entrapment patients reportedly had either coexistent CECS symptoms or had previously been surgically treated for the condition before entrapment release surgery (23). Although the precise relationship between these two conditions is not well understood, it seems that appropriate testing to differentiate the two should always be considered before undertaking any surgical intervention for either problem in isolation.

Back to Top | Article Outline

Clinical Evaluation

A thorough history often reveals recurrent deep upper calf muscle cramping worsened by running, particularly on inclines, or by repetitive jumping with or without complaints of plantar paresthesias (23). Symptoms may correlate more with intensity of exercise than overall volume and resolve quickly once activity ceases (15). Physical examination may reveal tenderness over the medial head of the gastrocnemius (10), a popliteal bruit accentuated by forceful active ankle plantarflexion (15), or the absence of distal pulses with plantarflexion (17) but is quite often normal.

Testing to rule out other causes of lower leg pain should be individualized based on a patient’s history and examination and may include plain radiographs, standard magnetic resonance imaging, exertional compartment pressure testing, running gait evaluation, or laboratory testing.

Noninvasive screening tests for PAES include pulse volume recording, plethysmography, and duplex Doppler imaging done in neutral and provocative positions (15). It is important to note that such testing may not adequately differentiate structural versus functional causes of entrapment and may have a high false-positive rate in athletes (8).

Plethysmography done with positional stress testing has been described as an inexpensive, noninvasive diagnostic tool. One such method uses a 10-cm cuff inflated to 60 mm Hg with the patient supine, knees extended, and foot in neutral, forced plantar, and dorsiflexed positions. A drop of greater than 30% in the ankle-brachial index (ABI) or flattening of the waveforms in plantar and/or dorsiflexion positions is considered abnormal (23). However, other authors have reported that ABI measurements are not reliable in determining the degree of popliteal artery compression (16), though one may still consider ABI as a noninvasive test to do before more invasive testing in those with possible PAES. One case series demonstrated that postoperative measurements can adequately assess for appropriate decompression of the entrapment and thus aid follow-up assessment (20).

Changes in popliteal artery blood flow on dynamic ultrasound imaging have been seen in more than 85% of normal healthy volunteers suggesting that compression during plantarflexion is a physiological phenomenon (1,2). The incidence of asymptomatic occlusion in the general population has been estimated to be 30% to 40% approaching 50% in highly trained athletes (20). Confirmative findings described on ultrasound imaging include an immediate complete disappearance of the velocity waveform coupled with the disappearance of the artery or a gradual increase in the velocity waveform with simultaneous narrowing of the artery on forceful plantarflexion (16). It is important to ensure that the probe remains stable during provocative testing so as to minimize false-positive results with sudden calf movement (2). A peak systolic velocity ratio exceeding 200% of the velocity of the proximal normal vessel segment is suggestive of significant stenosis and confirmative of the diagnosis (2). In athletes with exercise-associated, deep, cramping posterior lower leg pain, duplex ultrasound (with or without ABI testing) is increasingly becoming the initial test of choice before undertaking more expensive or invasive testing.

Intravascular ultrasound accessing the popliteal artery via the femoral artery has been used to confirm the length of compression as well as assess luminal narrowing with provocative testing and evaluation of intimal change or vessel wall damage (5).

CTA has been shown to be a useful tool for assessing the anatomy of the popliteal fossa as well as defining the location and extent of stenosis, occlusions, and collateral circulation of the popliteal artery under conditions of both rest and stress (3). Because of the high degree of soft tissue contrast with CTA, this imaging modality can discriminate vessel, muscle, fascia, fat, and bone in the popliteal fossa, and using axial plane imaging and reconstructive techniques, the relationship of the vessel to the surrounding muscles and tissue can be defined (25).

Magnetic resonance imaging (MRI) has been utilized in the evaluation of PAES. A retrospective analysis found no discrepancy between CT and MRI in defining anatomic abnormalities in confirmed cases of PAES with the proposed benefit of MRI being a noninvasive test without ionizing radiation (13). A combination of stress positional T2-weighted MRI and magnetic resonance angiography (MRA) has been utilized for identifying abnormal musculotendinous structures about the popliteal fossa and providing accurate arterial imaging in younger healthier individuals (23). There has been work attempting to utilize dynamic MRI imaging; however, it was reportedly difficult for the subjects to maintain contraction during the imaging sequences and images were inadequate because of motion artifact (16). There also have been some concerns about limitations of MRA in this setting. Decreased spatial resolution of MRA and related volume-averaging effects may lead to false-negative studies, particularly with stenosis of 50% or less (13). Nonetheless, MRI can be very useful for the structural assessment of the gastrocnemius musculature and embryological remnants or abnormal fascial bands associated with arterial entrapment, and future work on methods of dynamic assessment with MRI seems to hold promise.

Though invasive, angiography has historically been the gold standard for diagnosis (15,22). With future study, it is certainly possible that newer methods emerge or that technological advancements of those modalities discussed may obviate the need for such invasive testing.

At this time, there is no consensus as to the single, optimal means of evaluating symptomatic individuals for PAES (22). Although improving, there remains limited understanding of how best to surmise if the compression is functional and/or clinically significant as changes can be found incidentally and in asymptomatic individuals. A suggested approach is to first obtain ultrasound with color Doppler and provocative testing (with or without ABI testing). If peak flow velocity changes are suggestive of compression, MRI (with or with MRA) may be utilized to evaluate for structural causes of PAES and assist in surgical planning. In consultation with vascular surgery, arteriography may be utilized if additional confirmation is needed or if possible intravascular damage warrants further assessment (Table 2).

Table 2

Table 2

Back to Top | Article Outline


Treatment of PAES depends upon the etiology. Once the diagnosis is confirmed, it is important to alleviate the entrapment to avoid repeated microtrauma and the sequelae of progressive fibrosis, intimal damage, thrombus, occlusion, and possible ischemia.

Surgical techniques that have been described are varied, reflecting the numerous ways in which the popliteal artery may be structurally or functionally compressed. Operative intervention may include decompression, division, or resection of the compressing portion of the medial gastrocnemius muscle or tendon, excision of anomalous fascial bands, thrombectomy, venous interposition grafting, percutaneous transluminal angioplasty, arterial bypass, and prophylactic four-compartment fasciotomy (4,10,17,21,24). Reconstruction of the medial head of the gastrocnemius has not been described (2). However, there is a suggestion that in the presence of functional entrapment, resecting the soleal fascia band distally at the exit of the popliteal fossa versus myectomy of the medial head of the gastrocnemius muscle may provide adequate relief without compromise of muscle function, particularly in higher level athletes (23). Patients have been reported to experience anywhere from 70% to 100% symptom relief after surgical intervention (22).

More recently, botulinum toxin has been proposed as a treatment option for PAES. If there is functional popliteal artery compression by a hypertrophied or thick region of muscle, theoretically, treatment aimed at reducing the volume and/or tone of the muscle could reduce the stress on the artery. It is proposed that such treatment may reduce the volume of the muscle without the same degree of potential functional consequences resulting from surgical myotomy (12). More investigation is clearly warranted.

Back to Top | Article Outline

Return to Play

There has yet to be a large series of high or moderate level athletes with PAES reported in the literature. Thus, it is difficult to make a truly evidence-based recommendation on return to play in this population after treatment. It is recommended that treatment be undertaken to alleviate the entrapment so as to avoid long-term arterial injury; however, even the timing of intervention as it relates to a competitive season also has not been well defined. Whether different types of entrapment and subsequent treatment affect ultimate return to activities also is not clearly elucidated. Thus, there currently exists no consensus on timing of return to play after surgical treatment for PAES, though it has been documented that many patients do return to their prior level of activity after surgery (19). Symptoms should be closely monitored with progression of activities after treatment as, theoretically, athletes may in fact be able to progress beyond where their training was previously hampered by the entrapment.

Certainly, sports medicine providers should work in close collaboration with the treating vascular surgeon and help assess activity progression. A graded physical therapy rehabilitation protocol with an accompanying exercise test at 6 wk has been proposed, though to this point, the specific progression has neither been described in detail in the literature nor have associated observer- or patient-reported outcomes been widely published (22). There may even evolve differing thoughts on rehabilitation and return to play in functional versus more historically described anatomic entrapment, and future study is needed. Until then, typically gradual activity progression can commence after the immediate postoperative period in conjunction with any rehabilitation that may favorably affect overall healing and the individual’s particular biomechanics.

Back to Top | Article Outline


Popliteal artery entrapment should be considered in the differential diagnosis of exertional lower leg pain in athletes and active individuals. Although physical examination may be normal, appropriate interpretation of imaging studies can help to define areas of functional or anatomic compression and allow correlation with clinical findings. Initial testing should ideally be noninvasive and bilateral testing is recommended. It is important to intervene surgically in diagnosed cases before arterial wall injury or other vascular complications develop. Thankfully, case reports and series in the athletic population thus far report very good outcomes with return to activities and no significant vascular sequelae. Additional longitudinal outcome studies in the athletic population with symptomatic popliteal artery entrapment will continue to refine recommendations in an evidence-based manner.

Back to Top | Article Outline


1. Akkersdijk WL, Eikelboom BC. Colour Doppler ultrasonographic imaging in the diagnosis of popliteal artery entrapment syndrome. Br. J. Surg. 1995; 82: 134.
2. Altintas U, Helgstrand UV, Hansen MA, et al. Popliteal artery entrapment syndrome: ultrasound imaging, intraoperative findings, and clinical outcome. Vasc. Endovascular Surg. 2013; 47: 513–8.
3. Anil G, Tay KH, Howe TC, Tan BS. Dynamic computed tomography angiography: role in the evaluation of popliteal artery entrapment syndrome. Cardiovasc. Intervent. Radiol. 2011; 34: 259–70.
4. Apigian AK, Landry GJ. Basic data underlying decision making in nonatherosclerotic causes of intermittent claudication. Ann. Vasc. Surg. 2015; 29: 138–53.
5. Causey MW, Quan RW, Curry TK, Singh N. Ultrasound is a critical adjunct in the diagnosis and treatment of popliteal entrapment syndrome. J. Vasc. Surg. 2013; 57: 1695–7.
6. Di Marzo L, Cavallaro A. Popliteal vascular entrapment. World J. Surg. 2005; 29( Suppl. 1): S43–5.
    7. Drake RL, Vogl AW, Mitchell AWM. Lower Limb In: Gray’s Anatomy for Students. 3rd ed. Philadelphia (PA): Elsevier Churchill Livingstone; 2014, pp. 533–681.
    8. Ehsan O, Darwish A, Edmundson C, et al. Non-traumatic lower limb vascular complications in endurance athletes. Review of literature. Eur. J. Vasc. Endovasc. Surg. 2004; 28: 1–8.
    9. Eiberg JP, Grønvall Rasmussen JB, Hansen MA, Schroeder TV. Duplex ultrasound scanning of peripheral arterial disease of the lower limb. Eur. J. Vasc. Endovasc. Surg. 2010; 40: 507–12.
      10. Gokkus K, Sagtas E, Bakalim T, et al. Popliteal entrapment syndrome. A systematic review of the literature and case presentation. Muscles Ligaments Tendons J. 2014; 4: 141–8.
      11. Hoffmann U, Vetter J, Rainoni L, et al. Popliteal artery compression and force of active plantar flexion in young healthy volunteers. J. Vasc. Surg. 1997; 26: 281–7.
        12. Isner-Horobeti ME, Muff G, Masat J, et al. Botulinum toxin as a treatment for functional popliteal artery entrapment syndrome. Med. Sci. Sports Exerc. 2015; 47: 1124–7.
        13. Kim HK, Shin MJ, Kim SM, et al. Popliteal artery entrapment syndrome: morphological classification utilizing MR imaging. Skeletal Radiol. 2006; 35: 648–58.
        14. Hedeager Momsen AM, Bach Jensen M, Norager CB, et al. Quality of life and functional status after revascularization or conservative treatment in patients with intermittent claudication. Vasc. Endovascular Surg. 2011; 45: 122–9.
          15. Pham T, Kapur R, Harwood MI. Exertional leg pain: teasing out arterial entrapments. Curr. Sports Med. Rep. 2007; 6: 371–5.
          16. Pillai J, Levien LJ, Haagensen M, et al. Assessment of the medial head of the gastrocnemius muscle in functional compression of the popliteal artery. J. Vasc. Surg. 2008; 48: 1189–96.
          17. Politano AD, Bhamidipati CM, Tracci MC, et al. Anatomic popliteal entrapment syndrome is often a difficult diagnosis. Vasc. Endovascular Surg. 2012; 46: 542–5.
          18. Rich NM, Collins GJ Jr, McDonald PT, et al. Popliteal vascular entrapment. Its increasing interest. Arch. Surg. 1979; 114: 1377–84.
          19. Rosset E, Hartung O, Brunet C, et al. Popliteal artery entrapment syndrome: anatomic and embryologic bases, diagnostic and therapeutic considerations following a series of 15 cases with a review of the literature. Surg. Radiol. Anat. 1995; 17: 161–9.
          20. Ruppert V, Verrel F, Geppert SN, et al. Results of perioperative measurements of ankle-brachial index in popliteal artery entrapment syndrome. J. Vasc. Surg. 2004; 39: 758–62.
          21. Simsek E, Bugra O, Teber MA, Katircioglu SF. What should be the first treatment of popliteal artery entrapment syndrome. Ann. Thorac. Cardiovasc. Surg. 2014; 20: 169–72.
          22. Sinha S, Houghton J, Holt P, et al. Popliteal entrapment syndrome. J. Vasc. Surg. 2012; 55: 252–62.
          23. Turnipseed WD. Popliteal entrapment in runners. Clin. Sports Med. 2012; 31: 321–8.
          24. Yamamoto S, Hoshina K, Hosaka A, et al. Long-term outcomes of surgical treatment in patients with popliteal artery entrapment syndrome. Vascular. 2014;1–6.
          25. Zhong H, Gan J, Zhao Y, et al. Role of CT angiography in the diagnosis and treatment of popliteal vascular entrapment syndrome. AJR Am. J. Roentgenol. 2011; 197: W1147–54.
          Copyright © 2015 by the American College of Sports Medicine.