Popliteal artery entrapment syndrome is a condition whereby compression of the popliteal artery, popliteal vein, and/or tibial nerve in the popliteal fossa by surrounding musculoskeletal structures results in vascular and neurogenic symptoms.1–5 This diagnosis should be considered especially when assessing young, often well-conditioned and physically active patients presenting with symptoms of intermittent claudication. Popliteal artery entrapment syndrome mostly affects patients younger than 30 years and might explain symptoms in 40% to 60% of young patients with ischemic-type pain.6 Popliteal artery entrapment syndrome is often confused with chronic exertional compartment syndrome because of its similar symptom of increased pain with activity.4,5 Although popliteal artery entrapment syndrome is relatively uncommon, a missed diagnosis could result in severe morbidity for patients, including unnecessary compartment releases or progression of symptoms. In one study, misdiagnosis reportedly resulted in 14% of patients with popliteal artery entrapment syndrome undergoing unnecessary surgical exploration without relief of symptoms.4
The constellation of symptoms and the diagnosis of popliteal artery entrapment syndrome were first described by Stuart5 in 1879 and have become better defined with improved diagnostic techniques.7 Popliteal artery entrapment syndrome was first described as an abnormal course of the popliteal artery that may result in limited blood flow during muscle contractions, leading to intermittent claudication or pain in the lower leg that is relieved with rest. The term popliteal artery entrapment syndrome was coined by Love and Whelan in 1965, and their modified classification system describes progressively worsening compression of the popliteal artery caused by anatomic variation of the gastrocnemius muscle or an aberrant course of the artery as well as an entrapment of the artery or nerve with motion.8–11 Functional popliteal artery entrapment syndrome was subtyped as a form of overuse injury associated with hypertrophy of the medial gastrocnemius, plantaris, and soleus muscles, without clear anatomic variants of the vasculature. In functional popliteal artery entrapment syndrome, during active plantarflexion, the neurovascular bundle is compressed against the lateral femoral condyle by the plantaris and gastrocnemius muscles proximally and the soleus muscle distally.4,5,12,13Figure 1 shows the course of the popliteal artery at the popliteal fossa, where it may be compressed by the medial head of the gastrocnemius in an example of an anatomic variant or functionally compressed at the soleus distally. Functional entrapment has been reported to progress to popliteal artery occlusion.5 Distal emboli may also occur as a consequence of focal thrombus formation at the site of entrapment or from popliteal aneurysm formation.14 The repetitive trauma to the popliteal artery may lead to intimal damage, aneurysm formation, thromboembolism, poststenotic dilatation, irreversible ischemic damage, and limb loss.7,15 Functional popliteal artery entrapment syndrome will show typical symptoms of intermittent claudication preoperatively but no anatomic correlate to cause occlusion of the popliteal artery intraoperatively.5,12
Illustrations of 2 types of popliteal artery entrapment syndrome. The popliteal artery has an abnormal course due to the origin of the medial gastrocnemius (A). With the gastrocnemius retracted, the soleus sling or hypertrophy of the popliteus could compress the artery (B).
A 20-year-old female collegiate lacrosse player presented with diffuse bilateral posterolateral pain in her legs during exercise that had progressed to unbearable shooting pain. She reported burning sensations and muscle cramps after running. Symptoms were exacerbated by increased activity and especially by running up stairs and ankle plantarflexion. Occasionally, she noticed paresthesias in her plantar foot as well. The pain in the calf and the foot was also present at night. Symptoms progressed such that they prevented her from playing lacrosse or running short distances. Her physical examination yielded essentially normal results, with no contributory findings.
The patient had been seen by 2 other clinicians prior to presentation and had been diagnosed with medial tibial stress syndrome and chronic exertional compartment syndrome. Magnetic resonance imaging, performed to rule out stress fracture, did not reveal any unusual anatomy. Her condition did not improve with treatment, including rest from sport, stretching, and dedicated physical therapy, for these diagnoses. A trial of gabapentin did not relieve symptoms. Additional workup, including compartment pressure measurements at rest and after exercise, completed prior to her presentation to the authors' office had negative results for exertional compartment syndrome.
After sufficiently ruling out compartment syndrome and because of the nature of the pain, the authors performed dynamic ultrasound. This revealed bilateral popliteal artery entrapment, showing loss of popliteal arterial flow with plantarflexion against resistance bilaterally. The left popliteal artery in neutral and with plantarflexion showing decreased flow is shown in Figure 2A and Figure 2B, respectively. A magnetic resonance angiogram showed compression of the popliteal vessels during dynamic plantarflexion (Figure 3).
Dynamic ultrasound of the left popliteal artery in neutral (A) and with plantarflexion against resistance showing decreased flow (B).
Preoperative axial magnetic resonance angiogram just distal to the knee joint showing the popliteal artery (arrow) in neutral (A) and mild narrowing of the popliteal artery (arrow) in the anteroposterior dimension in plantarflexion (B). No anatomic abnormality of the musculature was identified.
Symptoms and Diagnosis
Patients with popliteal artery entrapment syndrome typically present as described above, with calf or lower leg pain that is sometimes accompanied by paresthesias of the posterior lower leg or foot. Clinical evaluation should entail detailed observation and palpation of the lower extremities for pain, swelling, ecchymosis pulses, and deformity. Pulses are normal at rest if occlusion, which is a late, severe finding, has not occurred. Symptoms have sudden onset, are usually precipitated by episodes of intense physical activity, and may last well after activity has stopped. Additional reported symptoms include cramps in the calf and the foot, coldness, blanching, and numbness. The sudden onset of severe, disabling claudication in a young adult without atherosclerotic risk factors is highly suggestive of popliteal artery occlusion due to entrapment.
The differential diagnosis includes tibial stress fracture, medial tibial stress syndrome, exertional compartment syndrome, and metabolic disorder of muscle. It may be most difficult to distinguish popliteal artery entrapment syndrome from exertional compartment syndrome. Key characteristics of both are listed in the Table.
Key Characteristics of Exertional Compartment Syndrome Versus Popliteal Artery Entrapment Syndrome
Surgical management requires release of extrinsic compression to preserve or restore arterial flow. For more severe cases involving arterial damage, bypass may be necessary. Some authors have described posterior approaches2; however, the current authors prefer a medial surgical approach to release, which was used in the current case. An incision, approximately 8 cm long, was made 4 fingerbreadths below the medial joint line in a longitudinal fashion. Dissection was carried through the skin and subcutaneous tissue until the fascia overlying the gastrocnemius and soleus in the posterior compartment of the leg was visualized and then incised. The pes anserine tendons were left intact, and the gastrocnemius muscle was retracted posteriorly to visualize the soleus muscle. The crescent-shaped sling of the soleus muscle that surrounds the popliteal artery, popliteal vein, and tibial nerves was released. The plantaris tendon was also visualized and released. Palpation was performed to assess adequate release around the gastroc–soleus sling and the plantaris tendon and to ensure that the popliteal artery, popliteal vein, and tibial nerve were extensively freed.
Postoperatively, the patient was instructed to elevate the bilateral lower extremities as much as possible and to keep compression on the area to decrease swelling and allow for wound healing. She followed gradual return to exercise, with progression to a stationary bike between 2 and 4 weeks postoperatively. Eleven months postoperatively, she had returned to full activity and collegiate lacrosse and was symptom free. Physical examination showed full, pain-free range of motion at the knee and the ankle and soft, compressible leg compartments. The patient had normal dorsalis pedis and posterior tibial pulses with both ankle plantarflexion and dorsiflexion. Four years postoperatively, the patient continues to do well and has unrestricted full activity.
Various diagnostic modalities, including the following, are available for evaluating suspected popliteal artery entrapment syndrome: (1) post-exercise treadmill test, in which vigorous activity identifies and reproduces symptoms; (2) Doppler ultrasound imaging/ankle–brachial pressure index, which assesses for the disappearance of pedal pulses when the patient plantarflexes against resistance4,5,11,12; (3) dynamic ultrasound, which visualizes occlusive disease, abnormal course, or aneurysmatic changes with ankle motion5,8,12; (4) arteriography (provocative and static), which is considered the gold standard4,5,11,14; (5) cross-sectional magnetic resonance imaging/magnetic resonance angiogram, which provides a detailed evaluation of musculotendinous and arteriovenous anatomy in the popliteal fossa5–7; (6) computed tomography/computed tomography angiography, which analyzes the anatomy of the popliteal artery4,5,14; and (7) intravascular ultrasound, which assesses the extent of popliteal artery compression, confirms the length of compression and luminal narrowing with provocation, and assesses the arterial lumen for intimal change and potential irreparable vessel wall damage.
It has been reported that, after surgical release of the popliteal artery, symptoms of arterial insufficiency resolve and dynamic ultrasound shows restoration of popliteal flow.7 A systematic review showed that many patients required reconstructive procedures in addition to release, with a median failure rate of 23.5% for this treatment.1 In those studies reporting on symptoms after surgery, a median of 77% of patients were symptom free.1 Given that most of the studies they reviewed did not have enough data, likely due to the relative rarity of this condition, the current authors do not have an accurate report of the success rates of surgery. Treatment should be patient specific. For athletes, resecting the soleal fascia band distally at the exit of the popliteal fossa—such as was done in the current case—is recommended to improve symptoms without risking muscle function, which may occur if gastrocnemius muscle is released instead.3
Because progressive fibrosis of the entrapped vessel may lead to aneurysm formation and thrombosis, early operative intervention is supported. It is possible that once a popliteal artery has undergone occlusion, it may be beyond repair, requiring bypass grafting.14
This report has described a case of bilateral functional popliteal artery entrapment syndrome and its successful surgical management, which allowed for a pain-free return to full, high-level sport in a young patient. Popliteal artery entrapment syndrome is a rare but important cause of peripheral arterial insufficiency. Young patients with intermittent claudication should be carefully evaluated for this disease because early diagnosis and surgical intervention are important for good outcomes. A delay in surgical treatment may result in worse outcomes, including aneurysm or thrombosis.
- Sinha S, Houghton J, Holt PJ, Thompson MM, Loftus IM, Hinchliffe RJ. Popliteal entrapment syndrome. J Vasc Surg. 2012; 55(1):252–262. doi:10.1016/j.jvs.2011.08.050 [CrossRef]
- Altintas U, Helgstrand UV, Hansen MA, Stentzer KF, Schroeder TV, Eiberg JP. Popliteal artery entrapment syndrome: ultrasound imaging, intraoperative findings, and clinical outcome. Vasc Endovascular Surg. 2013; 47(7):513–518. doi:10.1177/1538574413495466 [CrossRef]
- Turnipseed WD. Functional popliteal artery entrapment syndrome: a poorly understood and often missed diagnosis that is frequently mistreated. J Vasc Surg. 2009; 49(5):1189–1195. doi:10.1016/j.jvs.2008.12.005 [CrossRef]
- Joy SM, Raudales R. Popliteal artery entrapment syndrome. Curr Sports Med Rep. 2015; 14(5):364–367. doi:10.1249/JSR.0000000000000199 [CrossRef]
- Stuart TP. Note on a variation in the course of the popliteal artery. J Anat Physiol. 1879; 13(pt 2):162.
- Levien LJ. Popliteal artery entrapment syndrome. Semin Vasc Surg. 2003; 16(3):223–231. doi:10.1016/S0895-7967(03)00028-0 [CrossRef]
- Igari K, Sugano N, Kudo T, et al. Surgical treatment for popliteal artery entrapment syndrome. Ann Vasc Dis. 2014; 7(1):28–33. doi:10.3400/avd.oa.13-00081 [CrossRef]
- Levien LJ, Veller MG. Popliteal artery entrapment syndrome: more common than previously recognized. J Vasc Surg. 1999; 30(4):587–598. doi:10.1016/S0741-5214(99)70098-4 [CrossRef]
- Love JW, Whelan TJ. Popliteal artery entrapment syndrome. Am J Surg. 1965; 109:620–624. doi:10.1016/S0002-9610(65)80016-2 [CrossRef]
- Brewer RB, Gregory AJ. Chronic lower leg pain in athletes: a guide for the differential diagnosis, evaluation, and treatment. Sports Health. 2012; 4(2):121–127. doi:10.1177/1941738111426115 [CrossRef]
- Iwai T, Konno S, Soga K, et al. Diagnostic and pathological considerations in the popliteal artery entrapment syndrome. J Cardiovasc Surg (Torino). 1983; 24(3):243–249.
- Deshpande A, Denton M. Functional popliteal entrapment syndrome. Aust N Z J Surg. 1998; 68(9):660–663. doi:10.1111/j.1445-2197.1998.tb04839.x [CrossRef]
- Turnipseed WD, Pozniak M. Popliteal entrapment as a result of neurovascular compression by the soleus and plantaris muscles. J Vasc Surg. 1992; 15(2):285–293. doi:10.1016/0741-5214(92)90250-C [CrossRef]
- Ruppert V, Verrel F, Geppert SN, Sadeghi-Azandaryani M, Burklein D, Steckmeier B. Results of perioperative measurements of ankle-brachial index in popliteal artery entrapment syndrome. J Vasc Surg. 2004; 39(4):758–762. doi:10.1016/j.jvs.2003.11.035 [CrossRef]
- Chang MD, Steer A, Perera W, Robinson DR. Bilateral popliteal artery entrapment syndrome secondary to anomalous lateral heads of gastrocnemius [published online ahead of print March 11, 2015]. ANZ J Surg. doi:10.1111/ans.13047 [CrossRef].
Key Characteristics of Exertional Compartment Syndrome Versus Popliteal Artery Entrapment Syndrome
|Characteristic||Exertional Compartment Syndrome||Popliteal Artery Entrapment Syndrome|
|Demographics||Young (15–29 y), active, typically healthy||Young (15–29 y), active, typically healthy|
|Location of pain||Lower leg||Lower leg|
|Quality of pain||Cramping leg pain relieved rapidly by period of rest||Burning, shooting pain, cramping, or plantar paresthesias with walking. Symptoms continue after rest.|
|Physical findings||Fullness of legs after activity, normal results on pulse examination||Foot coldness, absent pulses in later stages|
|Diagnostic studies||Abnormal compartment pressure measurements after exercise||Dynamic ultrasound and magnetic resonance angiogram|
|Pathophysiology||Muscle swelling disrupting venous outflow||Dynamic compression of popliteal artery (or aberrant course of artery)|