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by the American Institute of Ultrasound in Medicine J Ultrasound Med 23:1667-1674 • 0278-4297
Popliteal Artery Entrapment Syndrome in an Elite RowerSonographic AppearancesDepartment of Radiology, Virgen de la Victoria University Hospital, Malaga, Spain (I.A.R.); Vimac Rehabilitation Center, Malaga, Spain (G.A.R.); School of Physical Education and Sports Medicine, Malaga University, Malaga, Spain (J.R.A.C.); Center for General and Sports Medicine, Toledo, Spain (J.F.J.D.); and Department of Radiology, "Carlos Haya" Hospital, Malaga, Spain (G.A.B.). Address correspondence and reprint requests to Ignacio Alvarez Rey, MD, C/Las Espuelas 3, Urbanization Delta 1, Bloque 7-2°-1, 29016 Málaga, Spain. E-mail: nachoalvarezr{at}telefonica.net.
Abbreviations: MRA, magnetic resonance angiography • MRI, magnetic resonance imaging • PAES, popliteal artery entrapment syndrome • T1, longitudinal relaxation time
Popliteal artery entrapment syndrome (PAES) occurs when an abnormal anatomic relationship between the popliteal artery and the surrounding musculotendinous structures causes repeated arterial compression with exercise. Popliteal artery entrapment syndrome often affects young sports participants or athletes who have no known cardiovascular risk factors. Symptoms include transient tingling or coldness in the foot, with later intermittent claudication. If diagnosis is delayed, there may be irreversible arterial damage, which can impair viability of the affected limb. We present a case of PAES in a young rower and comment on the diagnostic findings with duplex color Doppler sonography, magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), and arteriography as well as on the course of the syndrome after treatment with intra-arterial thrombolysis and corrective surgery. We present sonographic descriptions of the 3 different pathologic stages of this entity.
The patient, a 22-year-old Olympic rower, noticed a sharp pain in the right calf and a fleeting episode of paleness and paresthesia of the first toe while training. Later, he noticed pain in the right calf while walking, which lessened while running, accompanied by a pigeon-toed walking gait. The symptoms persisted for 1 month, a possible fibrillary tear of the gastrocnemius muscle was finally diagnosed. Physical examination was unremarkable except for the absence of palpable pedal and right posterior tibial pulses. No abnormal biochemical or hematologic data were detected. Duplex color Doppler sonography of the arterial system of the right lower leg showed a complete lack of a signal at the level of the pedal artery. A color Doppler study of the posterior tibial artery captured continuous color flow, and pulsed Doppler imaging showed monophasic curves with low systolic-diastolic (tardus-parvus) velocity, indicative of an obstructive or severe stenotic lesion in the most proximal segments.
B-scan examination of the popliteal fossa, with the patient prone, showed reduced echogenicity of the musculotendinous area of the gastrocnemius muscle in front of the anterior wall of the popliteal artery. In the anterior wall of the middle third of the popliteal artery was an interrupted intima and a solid hypoechoic 2-cm lesion growing toward the interior of the lumen. The diagnosis of this was a probable thrombus or intramural hematoma occupying 50% of the arterial lumen; the rest of the lumen showed normal flow (Figure 1
Twenty-four hours after beginning to receive heparin, the patient reported paresthesias in the same leg. Duplex color Doppler sonography showed slight enlargement of the thrombus in the proximal third of the popliteal artery (Figure 5  ), and a B-scan image of the thrombus in the distal third of the artery now showed a double lumen with a central wall. Color Doppler sonography showed bidirectional flow in both lumina, interpreted as arterial dissection (Figure 6). The following day, the patient noticed sudden intense paleness and reduced temperature in the same leg. Sonography showed the arterial dissection of the distal popliteal artery to be total thrombosis with absence of any flow at this level or in the rest of the leg (Figure 7). Arteriography confirmed the total obstruction (Figure 8), and intra-arterial thrombolysis was performed for 48 hours, after which control arteriography showed complete patency of the popliteal artery and its distal branches. Surgery consisted of deinsertion of a large tendon of the medial head of the gastrocnemius. This was located higher and more external than usual and compressed the popliteal artery, which was deviated inward. This segment was excised, and an autogenous vein graft from the internal saphenous vein was inserted. Postoperative MRA showed patency and permeability of the distal branches (Figure 9). Periodic control studies with Duplex color Doppler sonography showed permeability of the graft and distal branches (Figure 10).
Popliteal artery entrapment refers to compression of the popliteal artery due to an abnormal anatomic relationship between the vessel and the neighboring musculotendinous structures or to muscle hypertrophy of the popliteal region, especially the gastrocnemius muscle. This may lead to functional impairment1,2 or arterial compression, which may cause chronic vascular microtrauma of the arterial wall with intramural hematoma or thrombus, episodes of distal embolization, aneurysm, dissection, and later thrombosis with acute distal ischemia.3,4 We detected this sequence of events with duplex color Doppler sonography. Popliteal artery impingement was first described in 1879 by Stuart,5 with the first clinical case reported in 1959 by Hamming.1 Love and Welham6 coined the term PAES in 1965. In 1971, Ezzet and Yettra7 reported a case of bilateral compression of the popliteal artery caused by a fibrous band. Popliteal artery impingement generally affects young men, often athletes or soldiers, both groups habitually undertaking vigorous exercise producing a high degree of muscular development, which unmasks the occult disorder. The most common sporting activities associated with PAES include basketball, football, rugby, and the martial arts; to our knowledge, there has been no reference to PAES in an Olympic rower to date. It has also been reported in drivers of heavy military vehicles.8 Popliteal artery entrapment syndrome is uncommon, and until 1994, only 300 cases had been reported. Autopsy series suggest that the prevalence of anatomic abnormalities of the popliteal artery may be 3.5%, although the clinical prevalence of major impingement is about 1.7%, with a male-female ratio of 9:1.9–11 The condition can be found bilaterally in 25%4 to 36% of patients.12 New diagnostic imaging techniques, mainly MRI, enable detection of bilateral abnormality, albeit asymptomatic, in 67% of cases.13 Various types of popliteal entrapment exist, depending on the musculoligamentous abnormalities or the arterial path. In 1970, Insua et al14 proposed the first classification, modified by Delaney and Gonzalez15 in 1971. Type 1 is when the popliteal artery is markedly deviated medially around the proximal insertion of the gastrocnemius muscle and passes inside and below the normal insertion. Type 2 involves minimal medial deviation of the popliteal artery, passing inside and below the gastrocnemius muscle, whose aberrant insertion is more external at the intercondylar region. In type 3 entrapment, the artery follows its normal course but becomes compressed by an additional bundle or accessory insertion of the gastrocnemius muscle. Type 4 consists of an abnormal path of the artery, deep to the gastrocnemius and popliteal muscles or trapped by a fibrous band. Finally, type 5, added by Rich et al12 in 1979, is any form of entrapment also affecting the popliteal vein. There also exists functional entrapment of the popliteal artery with complete absence of any muscle or tendon anomalies. This is caused by vigorous repetitive exercise with active plantar flexion16 or by excessive gastrocnemius muscle hypertrophy, sometimes coinciding with the use of anabolic steroids.17 The frequency of presentation is as follows: type 1, 20%; type 2, 38%; and type 3, 26%.13 Our patient had type 2 entrapment. The clinical signs vary and are related to the degree of involvement of the popliteal artery. Initially, when the artery remains unharmed and is still permeable, symptoms are limited to transitory cramping or coldness coinciding with contraction of the gastrocnemius muscle. When the lesion is established (eg, stenosis or intramural hematoma), the main symptom is atypical gastrocnemius and plantar claudication with paresthesia, hypoesthesia, and occasionally coldness of the foot. Symptoms may worsen suddenly because of distal embolisms or complete thrombosis of the popliteal artery. Strangely, claudication can be more prominent when walking than running,1,18 possibly because gastrocnemius contraction is more sustained during walking. Physical examination requires careful palpation of the popliteal and pedal pulses with the ankle in both passive dorsiflexion and forced plantar flexion. Pulse loss during these maneuvers has been considered pathognomonic,19 although pulse reduction can occur in individuals without abnormalities.20 The first diagnostic technique of choice in patients with possible PAES should be duplex color Doppler sonography with high-frequency transducers. This noninvasive technique enables correct vision of the 3 anatomic segments of the popliteal artery. It shows the presence or absence of flow at this level and enables study of the more distal pedal and posterior tibial arteries, both at rest and during stress exercise (forced dorsiflexion of the foot and active plantar flexion or forced extension of the knee). These studies may reveal functional compression of the popliteal artery or other more distal areas. Doppler color sonography, however, provides little information about possible muscle or tendon anomalies, and other diagnostic techniques are necessary. Arteriography, the traditional reference standard, is an invasive test; furthermore, it fails to provide information about musculotendinous structures. Computed tomography, with or without 3-dimensional reconstruction, is good for diagnosing popliteal entrapment, but it too uses contrast material and ionizing radiation.21,22 Magnetic resonance imaging and MRA, with or without gadolinium, show the popliteal arteries and veins together with the surrounding tissues. They can be undertaken at rest and during provocative maneuvers, thus showing functional entrapment even in persons with no symptoms of PAES. Magnetic resonance imaging is therefore the diagnostic method of choice when there is clinical evidence or a duplex Doppler imaging suggestion of PAES.2,23 The differential clinical diagnosis of unilateral intermittent claudication in an active sports participant younger than 30 years should include muscle rupture, tendinopathies, acute and chronic compartment syndrome, popliteal artery adventitial cystic disease, stress fractures, medial tibial periostitis, effort-induced venous thrombosis, nerve impingement, and fascial defects.24 Treatment of PAES depends on the severity of the symptoms and the imaging findings. If diagnosis is made during the dynamic or functional entrapment stage, before the artery shows evidence of parietal or intraluminal damage, ceasing those exercises that cause muscle hypertrophy will sometimes suffice; otherwise, resection of the causative anomalous muscle or fibrous tissue is required. In cases of local damage to the popliteal artery, with retained permeability of the leg, resection of the affected segment is advised, with reconstruction of the arterial axis by placement of an autologous venous bypass graft. In cases of obstruction of the popliteal artery due to acute thrombosis, intra-arterial fibrinolysis is indicated. After permeability of the affected vessel, corrective surgery of the musculotendinous lesion and a vein graft are indicated.
Received June 16, 2004, from the Department of Radiology, Virgen de la Victoria University Hospital, Malaga, Spain (I.A.R.); Vimac Rehabilitation Center, Malaga, Spain (G.A.R.); School of Physical Education and Sports Medicine, Malaga University, Malaga, Spain (J.R.A.C.); Center for General and Sports Medicine, Toledo, Spain (J.F.J.D.); and Department of Radiology, "Carlos Haya" Hospital, Malaga, Spain (G.A.B.). Revision requested July 13, 2004. Revised manuscript accepted for publication August 5, 2004. We thank Ian Johnstone for help with the English version of the manuscript.
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