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Popliteal artery entrapment syndrome
(Portuguese PDF version)

Marcelo José de Almeida1, Winston Bonetti Yoshida2, Nathanael Ribeiro de Melo3

1. Graduate student, School of Medicine of Botucatu, Universidade Estadual Paulista.
2. Associate Professor, Department of Surgery and Orthopedics, School of Medicine of Botucatu, Universidade Estadual Paulista.
3. Professor, School of Medicine of Marília. (In memoriam)

Correspondence:
Marcelo José de Almeida
Rua Professor Francisco Morato, 135
CEP 17.501-020 - Marília - SP
E-mail: mjalme@terra.com.br

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ABSTRACT

Objective: The popliteal artery entrapment syndrome is characterized by extrinsic compression of this artery as a result of anatomic deviation from its usual course, or by compression from musculotendinous structures in the popliteal fossa. Clinical symptoms appear when these affected individuals do strenuous exercises. There are two types of popliteal artery entrapment syndrome: the classical or congenital form, and the functional or acquired form. In the classical form, disturbances in the embryogenesis lead either directly to popliteal artery anomalies or to alterations of adjacent structures that cause compression of the popliteal artery. In the functional form, hypertrophy of the gastrocnemius muscle secondary to exercise has been postulated as a cause. In both types, diagnosis is made through the detection of total occlusion or important stenosis of the popliteal artery. This is identified by duplex scan, magnetic resonance or arteriography during active plantar flexion-extension. A positive test in non-symptomatic subjects presenting no anatomical anomalies led to discussions about its specificity. This study presents a review of anatomical and functional popliteal artery entrapment syndrome and discusses accuracy, sensitivity and specificity of the diagnostic tests.

Key-words: popliteal artery, pathological constriction, diagnostic tests.
Palavras-chave: artéria poplítea, estenose, testes diagnósticos.

J Vasc Br 2003;2(3):210-8

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The popliteal artery entrapment syndrome (PAES) is characterized by the extrinsic compression of the popliteal artery. There are two types of popliteal artery entrapment syndrome: the classical or congenital/anatomical form, and the functional or acquired form. The congenital form^1-3 is related to the embryogenesis of the popliteal artery or of the musculotendinous components of the popliteal fossa, which causes anatomic deviation from its course or development of anomalies that compress the artery. In the functional form⁴ only hypertrophy of the gastrocnemius muscles is observed as possible cause for the entrapment.

Today, the disease is admittedly more common than it initially seemed. It is the major cause of intermittent claudication in young adults that practice sports on a regular basis. The anatomical form, if untreated, may evolve into arterial thrombosis, and the functional form can make individuals physically unable to do sports activities. Therefore, it is important to know about this syndrome, and establish diagnosis and treatment as early as possible.

EPIDEMIOLOGY

Necropsies performed by Gibson et al. and Paulo^5,6 revealed anomalies of the popliteal fossa in 3.4% and 3.3%, respectively. Classical PAES predominantly occurs in male individuals (ratio 8:1), with an incidence rate between 0.17% and 3.5%.

There is some evidence that genetic factors play a vital role in the development of the classical form of the syndrome. Berg-Johnsen and Holter⁷ reported cases in which two siblings had classical PAES. Jikuya et al.⁸ found PAES in two homozygous twins, and Soyka and Dunant⁹ observed this syndrome in three individuals of the same family.

After the first description of the syndrome in 1985¹⁰ several other individuals with functional PAES were identified, suggesting that this form could be more common than the anatomic form of popliteal entrapment. However, its precise incidence has not been estimated yet. This type of entrapment was predominantly observed in young athletes. There was no difference as to the incidence between males and females.^11,12

CLASSIFICATION

A large number of classifications for PAES were suggested by different authors. The modifications proposed over time were influenced by the number of case reports, by the new types of anomalies observed and by the approach used by the authors when studying the syndrome.

The most widely used classification is that proposed by Delaney and Gonzales in 1971.¹³ Later on, two new types of entrapment were added: type V, reported by Rich et al. in 1979,¹⁴ and type VI, described by Levien and Veller¹¹ in 1999. The types of entrapment are described next (Figure 1):

Figure 1 - Classification of PAES (Adapted from Levien, 1999¹¹).

Type I - the anatomic position of the medial head of the gastrocnemius muscle is normal (superior and posterior face of the medial femoral condyle), the popliteal artery is medially deviated, passes under the anterior face of the medial gastrocnemius and passes it by medially and posteriorly before it goes back to its natural course.

Type II - the medial head of the gastrocnemius muscle originates at the femoral metaphysis, laterally to its normal position, the popliteal artery passes medially and anteriorly to the muscle, with a more vertical path than that of Type I.

Type III - the accessory bundle of the medial head of the gastrocnemius muscle (which can have a tendinous, muscular or mixed aspect and variable thickness and width) entraps the popliteal artery, deviating it slightly from its normal course and separating it from the popliteal vein.

Type IV - the course of the popliteal artery is anterior to the normal one, being positioned between the tibia and the popliteal muscle. It is compressed by this muscle and may be deviated or not.

Type V - any anatomic alteration in which concomitant compression of the popliteal vein exists.

Type VI - extrinsic compression of the popliteal artery without identification of anatomical alterations; this type is also called "functional."

There are a large number of descriptions of anatomic variations that do not fit into any of the types presented. Examples of this are the isolated compressions of the popliteal vein¹⁵ and the compressions of the popliteal artery by Hunter's canal, reported by Araújo in 2002.¹⁶

ETIOPATHOGENICITY

Gibson, Mills et al.⁵ and Biemans & Van Bockel,¹⁷ in 1977, described two critical moments of embryogenesis that could explain the anomalies observed in popliteal entrapment: the formation of the popliteal artery and the migration of the medial gastrocnemius muscle.

The formation of the arterial system of the lower extremity starts with only one axial artery, originated from the fifth segmental artery.¹⁸ With embryo development, the growth of the axial artery slows down and the simultaneous growth of the primitive iliac artery occurs. After the second week of embryo development, the primitive iliac artery gradually replaces the vascularization of the lower extremity, giving rise to the deep and superficial femoral arteries, in addition to the tibial arteries. When fetal development reaches the ninth week, only part of the popliteal artery, fibular artery and a small branch into the sciatic nerve remain as indicative signs of the axial artery (Figure 2).

Figure 2 - Embryo development of the arterial system in the lower extremity. The fifth segmental artery forms the axial artery (in black). After the second week of embryo development, the primitive iliac artery gradually replaces the vascularization of the lower extremity (in red).

In the popliteal fossa, the proximal popliteal artery is in continuity with the superficial femoral plexus. The embryonic popliteal artery, derived from the axial artery and located in front of the popliteal muscle, deteriorates and is replaced with the definitive popliteal artery, originated from the new arterial development axis formed by the external iliac artery and by the superficial femoral artery. Around the seventh week of embryo development, the definitive popliteal artery is located behind the popliteal muscle.

The persistence of the primitive popliteal artery, located anteriorly to the popliteal muscle explains the development of PAES type IV, in which the popliteal artery is entrapped by this muscle.¹⁹

The anomalous formation of the gastrocnemius muscles is another important cause of popliteal entrapment. Around the sixth week, the primitive gastrocnemius muscle, located laterally, is divided into lateral gastrocnemius (which remains inserted in this region) and into medial gastrocnemius (which migrates until it is definitively inserted in the medial femoral condyle). Under normal circumstances, this migration would occur before the development of the popliteal artery, in such a way that this artery would be located in front of the popliteal muscle, preventing its entrapment. A delay in the migration of the medial gastrocnemius muscle or the early formation of the definitive popliteal artery would cause the capture and entrapment of the popliteal artery during the migration of the muscle from the lateral to the medial region, giving rise to PAES types I and II⁵ (Figure 3).

Figure 3 - Migration of the medial gastrocnemius muscle during the embryogenic period and development of the proximal popliteal artery (originated from the femoral plexus), of the medial popliteal artery (as indicative sign of the axial artery) and of the distal popliteal artery (formed by the anastomosis with tibial arteries).

Anomalous, fibrous or muscular bands, formed during the migration of the muscles in the popliteal fossa, are believed to cause PAES type III.^5,20

In 10 to 15% of the cases, the entrapments of the popliteal artery and vein are associated. The presence of an adventitial artery common to both vessels during the embryogenic period could explain this simultaneous entrapment. Consequently, venous entrapment (type V) would be caused by the same anomalies described for arterial entrapment.

The isolated entrapment of the popliteal vein is rare. The anomalies described in this kind of venous entrapment include the semimembranosus and plantaris muscles and the muscle or tendinous bands in the region of the head of the medial gastrocnemius, called by some authors "third head of the gastrocnemius."^15,21,22

PATHOPHYSIOLOGY

In classic PAES, the chronic compression of the popliteal artery, determined by the anomalous anatomic structure initially implies in the reduction of blood flow during muscle work and, later on, in the destruction of the vessel wall, resulting in arterial thrombosis.^1,17,19

These alterations would not occur in the functional form. In this kind of entrapment, the absence of anatomic anomalies led to other pathophysiological mechanisms as the cause of symptoms.^4,11

Rignault et al., after treating an individuals with PAES in 1985,¹⁰ believed this type of disease affected athletes with hypertrophy of gastrocnemius muscles. The anatomic relation of the neurovascular bundle, involved by the muscular and tendinous structures of the popliteal fossa in a restricted space, would render the bundle susceptible to extrinsic compression. Other authors suggested that the internal gastrocnemius tendon could have a more lateral insertion,¹⁶ allowing muscular hypertrophy to compress the popliteal artery.

Turnipseed et al. studied individuals with functional PAES in 1992 ⁴ using magnetic resonance and found out that the entrapment of the popliteal neurovascular bundle occurred during the contraction of the gastrocnemius and plantaris muscles, which laterally pushed the popliteal neurovascular bundle against the femoral condyle and, distally, against the lateral angle of the fibrous loop of the soleus muscle. According to the authors, the symptoms of intermittent claudication are caused by muscular compression of this bundle, resulting in temporary occlusion of the popliteal artery and vein during muscular contractions. Paresthesias that usually occur in the functional form originate from the repetitive trauma to the medial popliteal nerve.

PATHOLOGICAL ANATOMY

In PAES, the pathoanatomical alterations of the popliteal artery are similar to any other form of extrinsic arterial compression. These injuries are caused by the repetitive trauma to the artery, determined by structures adjacent to the vessel. Initially, the injuries are reversible, and are known as adventitious fibrosis. The persistence of the pathological factor produces progressive injury to the tunica media, with rupture of the external elastic layer and, finally, thrombosis due to the degeneration of the arterial intima.^19,23

Early diagnosis is essential, since it allows starting the treatment before arterial thrombosis occurs, and since it restricts the surgical procedure to the removal of the elements that entrap the popliteal artery, without the need for arterial grafts.

DIAGNOSIS

The diagnosis of both anatomical and functional forms of popliteal entrapment should be considered in every young patient with intermittent claudication. The pain affects the feet and calf muscles and is felt after strenuous exercises. Spastic claudication might also occur, in which the patient does not have pain when he/she runs, but only when he/she walks. Some individuals complain of pain when they stand on the tips of their toes. In the presence of thrombosis, the patients have symptoms of acute arterial obstruction. After thrombosis, some people develop good collateral perfusion from genicular arteries. These individuals complain of claudication when they walk short distances and of increase in knee temperature due to substitute collateral branches.^24-28

Quite often, problems such as diabetes and atherosclerosis are absent. On physical examination, patients without thrombotic complications have normal pulses at rest (with lower limbs in a neutral position). The diagnosis is confirmed by the reduction in pulses or pulselessness during dorsiflexion and plantar hyperextension.^1,29

The following symptoms are common in the functional form: cramps, transient limb fatigue and occasional paresthesia on the feet. These complaints are intensified when running on inclines or when repetitive jumping is performed. Thrombotic complications in this type of entrapment are rare.³⁰

The development of noninvasive exams and their use in individuals with suspected PAES allowed the diagnosis of popliteal entrapment to be established at an earlier stage.^26,28,29 The continuous waveband Doppler ultrasound of the posterior tibial artery is used as screening exam: at rest, no alterations are observed; in the presence of popliteal entrapment, during dorsiflexion and plantar hyperextension, it is possible to observe alterations to the Doppler curve with loss of the three-phase pattern, classically described as the development of a single-phase curve with reduced amplitude.^24,26,29 Quite recently, duplex mapping (DM) has allowed the dynamic visualization of the popliteal artery, detecting the patency of the vessel at rest and the stenosis or occlusion of the artery during maneuvers.^31,32 Magnetic resonance (MR) can complement the investigation, since it accurately identifies the musculotendinous structures involved in arterial compression.^4,33-35

Arteriography is important for the diagnosis and careful planning of surgical treatment; it is indicated if arterial injuries such as aneurysmal or thrombotic degenerations are suspected. It should be performed in the posteroanterior and lateral positions of the leg, in both lower limbs, with dorsiflexion and active hyperextension of the foot. In types I and II, there is a medial deviation of the popliteal artery, while in the functional form, there is a lateral deviation.^12,19

Any young patient with intermittent claudication of the lower extremities or with symptoms that suggest PAES should be investigated for extrinsic compression of the popliteal artery. Special attention should be paid to differential diagnoses such as orthopedic diseases, cystic degeneration of the popliteal artery and chronic compartmental syndrome. In these cases, the symptoms are basically identical to those of PAES, but no compression of the popliteal neurovascular bundle is observed. On the other hand, the diagnosis of popliteal artery or superficial femoral artery occlusion and minimal atherosclerotic disease in elderly patients can result from the extrinsic chronic trauma to the popliteal artery, caused by its entrapment, being unrelated to the intensity of atherosclerotic disorders of the vessel.^19,36

LIMITATIONS OF EVALUATION TESTS FOR POPLITEAL ARTERY COMPRESSION

In symptomatic individuals, the identification of remarkable occlusion or stenosis of the popliteal artery during maneuvers was accepted as specific to the diagnosis of PAES.^{2,5,9,16,19,23} However, the specificity of these tests was questioned after the observation that asymptomatic individuals, with no anatomic disorders, can have these problems as well.^30,33,37

Rignault et al.,¹⁰ after surgically treating a symptomatic individual diagnosed with PAES, noted that this patient did not present anatomic disorders. The authors questioned whether the identification of positional compression of the popliteal artery (compression during maneuvers) was enough for the diagnosis of the disease or whether this compression was a normal anatomic characteristic found in most individuals. In an attempt to clarify this issue, they used continuous wave Doppler scanning of the posterior tibial artery on both lower limbs of 53 military men and 53 male athletes, all of them asymptomatic. During plantar dorsiflexion, 30% of military men and 50% of athletes showed disorders compatible with proximal popliteal stenosis. The authors observed that the positive results of the Doppler ultrasound did not obligatorily mean a diagnosis of PAES.

The improvement of ultrasonographic techniques allowed for the investigation of asymptomatic individuals without anatomic disorders, increasing the accuracy of studies about popliteal artery compression during maneuvers. Erdoes et al., in 1994,³³ used duplex mapping to assess 36 individuals, and observed positional occlusion of the popliteal artery in 53% of the 36 studied individuals, of whom 21 were men, 15 women, 20 sedentary individuals and 16 athletes. In 1997, Hoffman et al. ³⁷ assessed 42 people, 18 athletes and 24 sedentary individuals. Duplex mapping yielded positive results in 88% of the cases, with no significant differences as to sex or level of physical activity. In a recent study, carried out at the School of Medicine of Botucatu,³⁸ 21 athletes and 21 sedentary individuals were evaluated with anthropometric tests and maximum oxygen consumption tests, being objectively classified according to their level of physical activity. Duplex mapping assessment, using the same method of previous studies, showed positive results in six (14.2%) individuals: two (4.7%) athletes and four (9.5%) sedentary individuals. Although these studies show discrepant results, most asymptomatic individuals without anatomic disorders presented positive evaluations of positional compression of the popliteal artery. These results would be equivalent to those of the thoracic outlet syndrome, in which extrinsic compression of subclavian vessels and of the brachial plexus is positive in 30% of normal and asymptomatic individuals, during arm abduction maneuvers.³⁹

It is not known whether the popliteal artery compression detected in asymptomatic individuals may result in a pathological state. Turnipseed et al.³⁰ reported that "there is no clinical evidence that functional entrapment, in the absence of symptoms, requires surgical intervention." Porter, in 1999,⁴⁰ commented that "positional occlusion of the popliteal artery is normal and should not be used for the diagnosis if abnormal conditions".

On the other hand, the pathoanatomical alterations observed in popliteal entrapment bear resemblance to those of any artery whose wall is submitted to chronic extrinsic trauma.¹⁹ Levien and Veller¹¹ reported three cases of popliteal artery thrombosis in individuals with functional PAES, revealing that chronic trauma in this type of entrapment may lead to arterial degenerations. After considering these facts, individuals with extrinsic compression of the popliteal artery admittedly are at risk for occasional injury to the vessel wall and for thrombosis as well.

The reason why some individuals with positional popliteal artery compression are symptomatic and others are not is still unknown. It is relevant to say that the presence of symptoms is important for the diagnosis of functional PAES, and that, according to the literature, all patients with functional entrapment practiced sports regularly.^4,11,12,30 Based on this fact, Melo et al.⁴¹ suggested that physical activity predisposed to the development of symptoms. In this regard, some individuals with positional occlusion of the popliteal artery are asymptomatic because their physical activity is not enough to produce clinical complaints, but a more strenuous activity could trigger off typical symptoms of functional PAES.

The long-term consequences of positional compression of the popliteal artery in asymptomatic individuals without anatomic disorders are still unclear. By the observation and clinical follow-up of asymptomatic individuals, it might be possible to understand these consequences in the near future.

TREATMENT

In 2002, Araújo et al.¹⁶ proposed an evaluation protocol for individuals with symptoms suggestive of PAES. This evaluation would be based on duplex mapping for the investigation of the compression of popliteal vessels and, in the presence of positive results, digital angiographic examination, magnetic resonance or computed tomography would be used. Surgical treatment would be indicated in cases of anatomic entrapment. In case of functional entrapment and discrete symptoms, clinical treatment with physical therapy and duplex mapping follow-up every six months would be indicated.

Turnipseed et al.³⁰ suggested that in patients with claudication symptoms, in the anatomic and functional forms of popliteal entrapment, surgical treatment should be indicated. The suggestion of the authors for functional PAES is pertinent, as the individuals assessed in their study group were athletes, and therefore long-term rest or interruption of sports activities was undesirable.

Surgeons should be aware that there are several types of disorders that could predispose to popliteal entrapment. The decision for surgical treatment, type of surgery, and its approach should be based on clinical history and preoperative tests.

In the absence of thrombosis or of arterial degenerations, the treatment (in both forms of popliteal entrapment) is simpler and is restricted to the elimination of the cause of entrapment, by means of myotomies, debridement and release of the popliteal neurovascular bundle.

Several authors^19,24,28 advocated that, in the presence of thrombotic disorders of the popliteal artery, arterial repair with a saphenous vein interposition graft should be used. According to these authors, the replacement of the injured artery results in longer patency in comparison to endarterectomy, in the presence of severe arterial degenerations. In fact, by analyzing the cases reported in the literature,^{1,5,7,13,17,28,29} endarterectomy, with or without an arterial patch, showed a high rethrombosis incidence.

In classical PAES, the treatment should be as early as possible, in the presence or absence of symptoms, since this could prevent a high rate of arterial degeneration. With regard to the surgical approach, Darling et al.,²⁹ in1974, used the medial approach for the treatment of this syndrome. Review studies on the surgical treatment of PAES^1,41 revealed that most surgeons opted for exploration of the popliteal fossa through the posterior S or bayonet approach. The medial approach for treatment of classic PAES in the presence of popliteal artery thrombosis facilitates the dissection of the greater saphenous vein for interposition venous graft. Nevertheless, it does not allow the identification and correction of the anomalous structure responsible for thrombosis, being regarded as an exception approach for the correction of this syndrome. The authors revealed that a patient with entrapment type I and popliteal artery thrombosis, in whom the medial approach was used, showed occlusion of the interposition graft due to nonidentification of the abnormality and consequent maintenance of the entrapment. On the other hand, the posterior approach has the advantage of identifying different anomalies, which range from the abnormal insertion of the medial head of the gastrocnemius muscle to accessory muscle fascicles and several types of fibrous bands. With the systematic exploration of the popliteal neurovascular bundle and of the entire fossa, it is possible to identify any additional stenotic factor, thus eliminating recurrence.

As for the surgical treatment of functional PAES, the literature describes some peculiarities. Rignault et al.¹⁰ surgically treated an individual with functional entrapment using the posterior S approach and maintained the fascia open, suturing only the skin region. In the postoperative period, symptoms disappeared completely. These authors believed that fasciotomy allowed for a new adaptation of structures of the popliteal fossa, which would be responsible for the patient's cure. Curiously enough, in 1988, Klooster et al.⁴² conducted a similar surgery, deciding on the closure of the fascia. The authors noted that the symptoms had reappeared completely in the postoperative period and then recommended fasciotomy in order to prevent claudication symptoms. Maintaining the fascia open and only closing the skin seems to prevent the recurrence of symptoms in functional entrapment. In 1992, Turnipseed et al.⁴ proposed a new technique for the approach of functional PAES. After carrying out studies with magnetic resonance in athletes and identifying excess development of the soleus muscle with formation of fibrous band in the fascia around its ring, they used the medial approach in the surgical treatment and released the soleus muscles completely and resected the muscle and the plantaris tendon. With this technique, 18 of 20 surgically treated patients had total resolution of symptoms and, according to the authors, the postoperative recovery was quicker, comparatively to the posterior S approach.

We can observe that although the criteria for the diagnosis and treatment of anatomic or classic PAES are well established, it is necessary to have a closer clinical observation of patients with functional PAES, especially in terms of their outcome after treatment. The careful analysis of a larger number of patients can be of help, since it would allow for a better therapeutic planning. However, in view of currently available information, we can make the following suggestions:

" Individuals with intermittent claudication, young and athletes or those at any age with nonadvanced atherosclerotic disease, should be studied in order to rule out PAES.

" The identification of anatomic PAES should include the assessment of the type of abnormality involved in popliteal entrapment with the aim of planning a more appropriate surgical treatment.

Nowadays, no consensus exists as to functional PAES in view of the paucity of studies on this topic. However, the available studies suggest that symptomatic patients have benefited from surgical treatment.

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