Year : 2002 | Volume
: 12 | Issue : 1 | Page : 91--93
Popliteal artery entrapment syndrome : Diagnosis by MRI
Dept. of Radiology, Amrita Institute of Medical Sciences, Cochin, Kerala, India
Dept. of Radiology, Amrita Institute of Medical Sciences, Cochin, Kerala
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Pillai A. Popliteal artery entrapment syndrome : Diagnosis by MRI.Indian J Radiol Imaging 2002;12:91-93
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Pillai A. Popliteal artery entrapment syndrome : Diagnosis by MRI. Indian J Radiol Imaging [serial online] 2002 [cited 2019 Sep 21 ];12:91-93
Available from: http://www.ijri.org/text.asp?2002/12/1/91/28427
Vasculogenic claudication is uncommon in young patients. Although accelerated atherosclerosis is the commonest cause, a differential diagnosis includes less common entities, such as popliteal artery entrapment, adventitial cystic disease, and arterial embolism. Accurate diagnosis is imperative since treatment differs considerably. Calf claudication caused by atherosclerosis can be treated nonoperatively by angioplasty. Operative treatment is recommended, however when an anomalous band of the gastrocnemius muscle entraps the popliteal artery. Magnetic resonance imaging (MRI) has been used to display the anatomic relationship of soft tissue structures in the popliteal fossa. The following case illustrates the use of MRI in the evaluation of a patient with popliteal artery thrombosis caused by the entrapment syndrome.
A 21-year-old man presented with a 1-year history of slowly progressing claudication of the left calf. Four months prior to admission, he noted a distinct worsening of his symptoms, with the claudication distance reduced to less than 500 meters. His right leg was asymptomatic, and there was no history of lower extremity trauma. There was no family history of lipid disorders or accelerated atherosclerosis, and no history of cardiac diseases. He was normotensive, nondiabetic, did not smoke, and was taking no medications.
Physical examination revealed absent popliteal, posterior tibial, and dorsalis pedis pulses in the left leg. The left femoral pulse was normal, and no masses were palpable in the popliteal fossa in either leg. Examination of the other vascular systems was unrevealing. Neurologic examination was normal.
Hematologic evaluation for coagulation disorders did not reveal any abnormality. There were no arrhythmias detected on 24-hour electrocardiographic monitoring, and the echocardiogram was normal. Triglyceride and cholesterol determinations were within normal limits. Color Doppler ultrasound confirmed the clinical finding of left femoropopliteal occlusion.
A DSA angiogram was performed through the right transfemoral route which revealed a normal aortoiliac and right femoropopliteal system. The left popliteal artery was occluded just above the knee [Figure 1], with collateral reconstitution of the distal popliteal artery and patent infragenicular vessels. There was no angiographic evidence of embolism, aneurysm, or adventitial cystic disease.
Considering the patient's clinical profile and the angiographic findings, the possibility of a popliteal artery entrapment syndrome (PAES) was considered. 2D TOF axial MRI of both popliteal regions was performed. No presaturation pulses were used in order to display both the popliteal artery and vein. The MRI demonstrated a distinct anatomic asymmetry in the left popliteal fossa. The medial head of the left gastrocnemius muscle had its origin more laterally on the medial femoral condyle, between the popliteal artery and vein [Figure 2]. The popliteal artery was occluded where the musculotendinous band compressed it against the femur. This was clearly different from the right popliteal fossa, where the muscular and vascular anatomy was normal [Figure 3]. The MRI findings were diagnostic of type 2 popliteal artery entrapment syndrome, as classified by Whelan.
Popliteal artery entrapment, although rare, should be considered in any healthy young patient with complaints of claudication. Stuart described the syndrome of popliteal artery occlusion as a result of an anomalous relationship to the origin of the gastrocnemius muscle in 1879. It was not until 1959, however, that Hamming  reported the first successful surgical treatment of this lesion. The true incidence of the popliteal artery entrapment syndrome is unknown. Bouhoutsas et al reported an incidence of 0.165% in young males entering the Greek military service, and Gibson et al, in a postmortem study found a prevalence of 3.5%,.
The embryological popliteal artery in the developing limb bud is the continuation of the primitive axial or ischiadic artery. The definitive popliteal artery develops from 3 sources. Proximal portion is derived from fusion of the developing femoral arterial plexus and the popliteal remnant of the axial artery. Mid portion of the definitive popliteal artery is directly derived from the remnant axial artery. The primitive distal popliteal axial artery, which lies deep to the popliteus muscle disappears at about 9 weeks and the definitive distal popliteal artery forms superficial to the popliteus muscle by the fusion of two new vessels after the medial head of the gastrocnemius has migrated across the politeal fossa.
Whelan classified this syndrome into 5 types based on the embryology of the popliteal fossa. When the definitive distal popliteal artery forms before the migration of the medial head of the gastrocnemius, two possible abnormalities may result: The normally developing medial head of the gastrocnemius will push the distal popliteal artery medially resulting in type 1 PAES. This is the most common variety of PAES accounting for approximately 50% of cases. Alternatively prematurely formed definitive distal popliteal artery may partially arrest the migration of the medial head resulting in a type 2 entrapment. The medial displacement of the artery is less pronounced than in type 1 and the muscle has a variable attachment from the lateral surface of the medial femoral condyle to the intercondylar region. Normally the attachment of the medial head of the gastrocnemius is to the posterior surface of the medial femoral condyle.
When the artery develops within the muscle mass, this is classified as type 3 PAES. When the distal primitive axial artery, which is located deep to the popliteus muscle, persists as the definitive distal popliteal artery, type 4 PAES results.
When the popliteal vein is also involved it is classified as type 5 PAES. Any of the types of entrapment (with the possible exception of type 1) may include the tibial nerves, resulting in neurological paresthesia in addition to claudication as a presenting symptom.
In some individual, there is compression of the popliteal artery and accompanying claudicating symptoms without an associated anatomic abnormality. This phenomenon may be related to hypertrophy of the medial head of the gastrocnemius impinging on the artery resulting in a functional entrapment. This may explain the higher prevalence of this condition in young athletic males. It has been proposed that this functional type of popliteal entrapment be termed type 6. Color Doppler performed with the patient's leg in hyperextension will demonstrate occlusion of the proximal popliteal artery in the stress position, and establish the diagnosis of popliteal entrapment. Angiography will in addition demonstrate the medial deviation of the proximal popliteal artery in the stress position. However, when entrapment has produced popliteal artery thrombosis, these diagnostic maneuvers are of limited value. Angiographic evaluation alone in these circumstances might result in overlooking the underlying cause of the arterial occlusion, which in turn leads to unsuccessful therapeutic procedures such as balloon angioplasty.
A few reports have described MR findings in popliteal artery entrapment syndrome ,. Magnetic resonance (MR) imaging can noninvasively demonstrate the anatomic relationships between the popliteal artery and the muscles within the popliteal fossa, making it an ideal test for popliteal artery entrapment. Awareness of this rare entity in young patients with popliteal artery occlusion is important to come to the correct diagnosis and thereby prompting the correct therapeutic procedure.
|1||McCready RA, Vincent AE, Schwartz RW, Hyde GL, Mattingly SS, Griffen Jr WO Atherosclerosis in the young: A virulent disease, Surgery 1984; 96: 863-9.|
|2||Genant HK, Wilson JS, Bovill SG, Brunelle FO, Murray WR, Rodrigo JJ. Computed tomography of the musculoskeletal system. J Bone Joint Surg [Am] 1980; 62: 1088-94.|
|3||Whelan TJ. Popliteal artery entrapment syndrome. In: Haimovici H ed. Vascular surgery: Principles and techniques, ed 2. New York: Appleton-Century-Crofts, 1984: 557-67.|
|4||Stuart TPA. A note on a variation in the course of the popliteal artery. J Anat Physiol 1879; 13: 162.|
|5||Hamming JJ. Intermittent claudication at an early age, due to an anomalous course of the popliteal artery. Angiology 1959; 10:369-71.|
|6||Atilla S, Akpek ET, Yucel C, Tali ET, Isik S. MR Imaging and MR angiography in popliteal artery entrapment syndrome. European Radiology 1998; 8: 1025-1029.|
|7||MCGuinness G, Durham J, Rutherford RB, Thickman D, Kumpe DA. Popliteal artery entrapment: finding at MR Imaging. J vasc intervent radiol 1991; 2: 241-245.|
|8||Levien LJ, Veller MG Popliteal artery entrapment syndrome: More common than previously recognized. J vasc surg 1999; 4: 587-598.|
|9||Bouhoutsos J, Daskalakis E. Muscular abnormalities affecting the popliteal vessels. Br J Surg 1981 1981; 68: 501-506.|
|10||Gibson MHL, Mills JG, Johnson GE, Downs AR. Popliteal entrapment syndrome Ann Surg 1977; 185: 341-348.|