International Journal of General Medicine

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Case report and literature review of popliteal

artery entrapment syndrome
This article was published in the following Dove Press journal:
International Journal of General Medicine
6 July 2015
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Nedaa Skeik 1
Taylor M Thomas 2
Bjorn I Engstrom 3
Jason Q Alexander 4
Vascular Medicine, Minneapolis Heart
Institute, 2Research, Minneapolis
Heart Institute Foundation,
3
Interventional Radiology, Minneapolis
Heart Institute, 4Vascular Surgery,
Minneapolis Heart Institute, MN, USA
1

Abstract: Popliteal artery entrapment syndrome (PAES) is an uncommon condition

resulting from an abnormal anatomic relationship between the popliteal artery and the surrounding musculature. The compression created by this variance in anatomy can lead to ischemia and
vascular claudication. The diagnosis of PAES requires a thorough patient history and physical
exam, a high index of suspicion, and dedicated imaging techniques. Several treatment options
are available, including surgical intervention, thrombolysis, or a combination of these depending
on the clinical indication. We present a case of PAES in a 34-year-old man who presented with
typical symptoms illustrative of the complicated decision making related to this disorder.
Keywords: popliteal artery thrombosis, limb ischemia, revascularization

Case report

Correspondence: Nedaa Skeik,

Department of Vascular Medicine,
Minneapolis Heart institute,
920 E 28th St, Minneapolis,
MN 55407, USA
Email Nedaa.skeik@allina.com

A 34-year-old man presented with abrupt onset of intermittent exercise-induced pain

in the left calf that improved with rest. He denied any trauma to the lower extremity.
Past medical history was significant for 14 years of tobacco abuse, and 1-year use of
electronic cigarette. He denied history or symptomatology concerning for vasculitis,
autoimmune, connective tissue, thrombotic or rheumatologic disorders.
Physical examination revealed normal vital signs with palpable left femoral but
absent popliteal, posterior tibial, and dorsalis pedis pulses. In spite of the absence of
pulses on the left lower limb, the patients foot did not have other findings of critical
ischemia. The remainder of the physical exam was unremarkable.
Arterial duplex ultrasound showed a complete occlusion of the left popliteal artery.
The patient was started on anticoagulation with enoxaparin to bridge to warfarin.
Magnetic resonance angiogram of abdomen and pelvis with three-vessel runoff revealed
widely patent common femoral, profunda femoral, and proximal-mid superficial femoral arteries. However, distal segment of the left superficial femoral and above-knee
popliteal arteries showed abrupt occlusion, with the occluded segment spanning 9 cm
(Figure 1). Mild medical deviation of bilateral above-knee popliteal artery was also
present suggesting extrinsic compression laterally, although with patent right arterial
system (Figure 2). This deviation was concluded to be related to the proximal and lateral aberrant insertion of the medial head of the gastrocnemius muscle in the left leg
and due to a fibrous band or muscle slip in the right leg (Figures 13). Catheter-based
angiogram was performed 3 days later and confirmed the diagnosis of distal superficial
femoral and popliteal artery occlusion with possible popliteal entrapment syndrome as

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2015 Skeik etal. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution Non Commercial (unported,v3.0)
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http://dx.doi.org/10.2147/IJGM.S82067

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Skeik etal

Figure 2 Flash 3D coronal T1-weighted post-contrast magnetic resonance image

of bilateral knees.
Note: The arrow indicates a thin fibrous band of small muscle slip on the contralateral
side with mild medial deviation of the popliteal artery (the asymptomatic side).

Discussion

Figure 1 Fast low-angle shot 3D coronal T1-weighted post-contrast magnetic

resonance image of the left knee demonstrates occlusion of the above-knee popliteal
artery (thick arrow) as well as a lateral aberrant insertion of the medial head of the
gastrocnemius muscle onto the distal femur (thin arrow).

the etiology (Figure 4). It also revealed significant infrapopliteal artery disease suggestive of thromboembolic event
versus Buergers disease (Figure 5).
Management was started with enoxaparin (80 mg)
subcutaneous injection twice daily, aspirin (81 mg) once
daily and Lipitor (40 mg) at night. Due to the severity
of his symptoms, the patient underwent catheter-based
lytic therapy using tissue plasminogen activator at 1 mg/h
delivered through a multi-sidehole infusion catheter with
heparin at 500 units/h through the sidearm of the sheath
over 48 hours (Figure 6), followed by left lower extremity
superficial femoral artery-to-below-knee popliteal artery
bypass using ipsilateral reverse saphenous vein graft
tunneled beneath the sartorius and below-knee popliteal
artery endarterectomy, with good results. Following surgery, the patient was continued on warfarin to complete
at least 3 months of anticoagulation. A repeat duplex arterial ultrasound was performed 2 weeks post-surgery and
showed a widely patent distal superficial femoral artery to
below-knee popliteal vein bypass graft without evidence
of stenosis.

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Popliteal artery entrapment syndrome (PAES) is an important

but infrequent condition that occurs as a result of compression of the popliteal artery by adjacent muscles and tendons,1
often resulting in ischemia and vascular claudication.2 Most
commonly seen in young and middle-aged men,3 PAES
can be a source of significant disability and impairment in
affected patients. According to the Heidelberg classification system, PAES is classified into three types. Type I is
characterized by an atypical course of the popliteal artery,
type II occurs as a result of an abnormal muscular insertion,
and type III exhibits both of these anatomic irregularities.4

Figure 3 Reconstructed flash 3D post-contrast T1-weighted magnetic resonance

image of the left knee in the transverse plane demonstrates the medial head of the
gastrocnemius muscle (thick arrow) between the occluded popliteal artery (short
thin arrow) and the popliteal vein (long thin arrow).

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Popliteal artery entrapment syndrome

Figure 5 Lateral view from digital subtraction left lower extremity arteriogram
demonstrates reconstitution of the posterior tibial artery (thick arrow) into the foot
from a collateral vessel (thin arrow) and a diseased anterior tibial artery (block arrow).

Figure 4 AP image from digital subtraction left lower extremity arteriogram demonstrates thrombosis of the majority of the proximal runoff vessels.
Abbreviation: AP, anterior-posterior.

This abnormal anatomy creates extrinsic compression which

can over time cause vascular compression that can lead to
damage.5 Symptoms often occur as a result of arterial wall
degeneration and compression, depending on the degree of
compression, magnitude of forces acting on the popliteal
artery, and duration of compression.6 If untreated, the compression mechanism frequently results in deterioration of
the popliteal artery which may progress to an occlusion.7
Recurrent popliteal artery compression can cause intimal
damage, thrombosis,8 distal embolization, post-stenotic
dilation, and formation of true aneurysm,6 which makes

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accurate diagnosis and timely management imperative. 7

Unfortunately, delayed diagnosis due to young patient age
and lack of atherosclerotic risk factors is common, making
progressive deterioration more frequent. The diagnosis is
further complicated because PAES can be difficult to separate
from other causes of lower limb pain.9 Clinical diagnosis is
made with careful history, physical exam, imaging testing
including ultrasonography, magnetic resonance angiography (MRA), computed tomography angiography (CTA), or
catheter-based angiography.7 The most common presentation
is intermittent claudication in young or middle-aged athletic
patients without any context of atherosclerosis.4 Doppler
ultrasound is a non-invasive modality that provides a good
overview of the popliteal fossa, popliteal artery, and arterial
flow at a reasonable cost.10 Magnetic resonance angiography
and CTA allow physicians to visualize the popliteal fossa and
arterial anomalies, providing better arterial depiction than
ultrasonography with excellent visualization of stenosis, dilation, and arterial wall abnormalities.9 Furthermore, magnetic
resonance angiography with high-contrast resolution offers
precise analysis of muscle courses and their potential con-

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Figure 6 Digital subtraction angiographic (DSA) images following lytic therapy.

Notes: (A) post-lytic therapy, anterior-posterior view from digital subtraction
angiography (DSA) of left lower extremity demonstrates a persistent web and
irregularity in the above-knee popliteal artery near the joint (thin arrows, marking
the distal end of the previously seen clot in this location) and significant improvement
of the thrombus in the tibioperoneal trunk (thick horizontal arrow) and diseased
proximal runoff which is mainly collateral vessels and a diseased anterior tibial artery
(thick vertical arrow). (B) Image from completion DSA of left lower extremity
(lateral view) demonstrates improved filling of the posterior tibial artery (thick
arrow) and dorsalis pedis artery (thin arrow, not filling prior to tPA) at the ankle
via collaterals and a highly diseased anterior tibial artery into an intact pedal-plantar
loop (not shown).

flict with popliteal vessels as well as allowing classification,

making it ideal for diagnosis.11 However, CTA is less expensive and more available, making it a close second. Once the
diagnosis of PAES has been made, several treatment options
are available, with the treatment objective being to release
the popliteal artery from compression and preserve popliteal
arterial flow.5 Conventional surgery, endovascular surgery,
thrombolysis, or a combination of these modalities are all
reasonable treatment options depending on the patients
clinical symptomology and anatomy.9 This decision making
can be very challenging. If the artery is occluded, stenotic, or
aneurysmal, vascular reconstruction is mandatory in addition
to the division of any entrapping structure. In patients with
an acute occlusion, thrombolysis and angioplasty prior to
surgery are appropriate, but have a high risk of reocclusion
and will not be effective without removing the underlying
reason for the popliteal artery entrapment.12

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Our patient represents a typical case of PAES in that he

is a middle-aged man presenting with acute progressive calf
claudication. He was progressively symptomatic for 2 weeks
before seeking treatment, resulting in a total occlusion.
Diagnosis was confirmed using MRA and catheter-based
angiography. Patient has irregularity of the infrapopliteal
arteries mostly consistent with thromboembolic disease
and less likely to represent Buergers disease. This is based
on the repeat catheter-based angiogram images showing improvement of the infrapopliteal arteries following
lytic therapy. A diagnosis of Buergers disease made via
angiography is based on the presence of segmental occlusions and corkscrew collaterals around the area of the
occlusion.13 As these observations were not made in the
repeat angiography, it was concluded that the diagnosis
of Buergers disease was less likely. Options for treatment
included release of compression and arterial repair versus
bypass alone. The final decision was made for bypass alone
since the patients artery had been damaged over time, and
since muscular release surgery is a significant surgery posing more risk to the patient.
Although other cases of PAES have been published,14,15
this case remains relevant due to the severity of presentation.
The patient presented with complete occlusion of the left
popliteal artery, which required multidimensional treatment.
A combination of catheter-based lytic therapy, anticoagulation therapy, and surgical intervention was successfully
implemented.

Summary
We present a challenging case of PAES with complicated
decision making regarding an appropriate revascularization
option with lowest risk.
We would recommend considering PAES in young
patients with calf claudication. If untreated, the compression caused by this abnormal anatomy frequently results
in damage to the popliteal artery which may give rise to
an occlusion,8 making timely diagnosis and management
essential.4

Disclosure
The authors have no conflicts of interest related to this work.

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