|Year : 2021 | Volume
| Issue : 3 | Page : 240-243
Popliteal artery entrapment syndrome: Our experience of two patients with bilateral entrapment
Dhanesh R Kamerkar, Nachiket Purandare, Nupur Sarkar, Bhushan Shinde, Shishir Jaiswal
Department of Vascular and Endovascular Surgery, Ruby Hall Clinic, Tertiary Care Centre, Pune, Maharashtra, India
|Date of Submission||04-Jun-2020|
|Date of Decision||25-Jun-2020|
|Date of Acceptance||16-Jul-2020|
|Date of Web Publication||6-Jul-2021|
Department of Vascular and Endovascular Surgery, Ruby Hall Clinic, Tertiary Care Centre, Pune, Maharashtra
Source of Support: None, Conflict of Interest: None
The true incidence of popliteal entrapment cannot be estimated due to a lack of awareness, misdiagnosis, and the relative rarity of presentation. Likely, only the most severe cases present for evaluation and workup and obtain a true diagnosis. We are presenting four legs of popliteal entrapment in two patients at different times.
Keywords: Entrapment release, entrapment, popliteal artery
|How to cite this article:|
Kamerkar DR, Purandare N, Sarkar N, Shinde B, Jaiswal S. Popliteal artery entrapment syndrome: Our experience of two patients with bilateral entrapment. Indian J Vasc Endovasc Surg 2021;8:240-3
|How to cite this URL:|
Kamerkar DR, Purandare N, Sarkar N, Shinde B, Jaiswal S. Popliteal artery entrapment syndrome: Our experience of two patients with bilateral entrapment. Indian J Vasc Endovasc Surg [serial online] 2021 [cited 2022 Nov 26];8:240-3. Available from: https://www.indjvascsurg.org/text.asp?2021/8/3/240/320627
| Background|| |
Popliteal artery entrapment syndrome (PAES) was first characterized in 1879 by Anderson Stuart, which is among one of more unique causes of lower extremity vascular insufficiency., Patients affected by PAES are usually younger active individuals. They typically present with unilateral intermittent symptoms of lower extremity claudication.,,, Other symptoms may include paresthesia, pallor, and pain.,, Symptoms may classically occur during or following activity in the early stages of the disease and may progress to symptoms at rest if the condition is undiagnosed., It has been proposed that the mechanism of a flexed knee with repeated active plantar flexion while driving a vehicle may result in gastrocnemius muscle hypertrophy causing popliteal artery entrapment. To make the diagnosis, a careful history and physical examination are necessary. Physical examination findings in early disease include decreased posterior tibial and dorsalis pedis pulses upon leg hyperextension and active plantar flexion. Duplex ultrasonography of the popliteal artery, computerized tomography (CT) scans, and contrast arteriography may also be used to detect stenosis. The lack of cardiovascular risk factors and active lifestyle can make recognizing PAES challenging; however, it is important to recognize this disease due to the high complication rate in the patient group.
| Case Reports|| |
An 18-year-old male presented in 2001 at the outpatient department with complaints of right foot and leg claudication for 1 month.
On examination, his vital signs were normal, and no cardiac or abdominal abnormality was detected. The right foot was colder than the left foot. There was no tissue necrosis. The ankle and toe movements were present, and the calf was soft and nontender. On the right, pedal pulses were not felt, and the popliteal pulse was weak. There was a full complement of left lower limb pulses.
Buerger's test was positive for the right leg at 30° elevation.
Left leg (contralateral leg) posterior tibial and dorsalis pedis artery flows are decreased on plantar flexion checked on audio Doppler (handheld Doppler).
A clinical diagnosis was B/L popliteal artery entrapment with right lower limb disabling claudication.
The patient was started on low-molecular-weight heparin and aspirin and evaluated further.
Inflammatory markers, rheumatoid workup, coagulation profile, and blood counts were normal.
Duplex examination showed dampened flow at 7 cm/s on the right popliteal artery. No flow was seen in the proximal posterior tibial artery (PTA), with the distal PTA filling through collaterals. The anterior tibial artery (ATA) had a normal triphasic pattern, with low velocities [Figure 1].
|Figure 1: Case 1 Doppler images showing decreased flows in the right popliteal artery|
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The left popliteal and tibial arteries showed normal flow. There was a significant reduction in flow velocity noted in the PTA and popliteal artery on plantar and dorsiflexion on both sides.
Bilateral lower limb conventional angiography (images cannot be retrieved due to old case and angio record not found) was done, and this showed occlusion at the right P2 segment of the popliteal artery with distal runoff into the foot from the ATA; both the PTA and peroneal artery were not seen. The left lower limb showed normal finding when angiogram done at rest.
The patient underwent surgery for a right popliteal entrapment release through the posterior approach. The findings were of a popliteal artery entrapment by an accessory strip and tendon of the medial head of the gastrocnemius muscle which was released (type III popliteal artery entrapment), popliteal artery skeletonized. After the release of entrapment, there was no difference in pulsatility of artery proximal and distal to entrapped part of the artery. The entrapped part of the popliteal artery probably has small anterior wall plaque which is not flow limiting, hence no vascular reconstruction was undertaken.
The patient was discharged after 5 days on a single antiplatelet aspirin.
At 4 weeks, a dorsalis pedis pulse was palpable.
We interpreted the deterioration in the Doppler signal on the contralateral left side to be diagnostic of popliteal entrapment. Two months later, the patient underwent similar decompression of the left popliteal artery through the posterior approach, where the accessory strip of gastrocnemius was divided to release the entrapment of a normal popliteal artery.
The patient was discharged after 5 days, and at 40-month follow-up, he is asymptomatic and has palpable pulses in both feet. There was no change in the Doppler signals on provocation maneuvers.
A 16-year-old male presented with right lower limb pain for 2 days with first and second toe tip discoloration. He gave a history of cycling about 1 h every day for the last 6 months. He had no other risk factors for arterial disease. On general examination, no systemic abnormality was found. His right foot was cold, with first and second toe cyanosis, with normal ankle and toe movement. The calf was soft and nontender. Popliteal and pedals were absent.
All pulses were palpable in the left lower limb, but left popliteal was palpable. Handheld Doppler assessment showed normal flow on the left leg dorsalis pedis and posterior tibial arteries, which were dampened on dorsiflexion and plantar flexion.
Routine blood tests and inflammatory markers and two-dimensional echocardiography were normal.
Magnetic resonance angiography (MRA) showed bilateral gastrocnemius muscle slip resulting in an entrapped popliteal artery on both sides (Type III PAES) [Figure 2].
|Figure 2: Magnetic resonance imaging with magnetic resonance angiography of the second patient showing abnormal slip of the muscle|
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CT angiography showed right proximal popliteal artery occlusion and reformation at distal half of popliteal with the posterior tibial occluded in distal half with no runoff in the foot; ATA seems to be reformed from the origin with runoff in the foot. The left popliteal artery looks medialy displaced no thrombosis anywhere in the left leg. The aorta was normal [Figure 3] axial image, [Figure 4] showing coronal view.
|Figure 3: Computerized tomography angiography of the second patient showing right popliteal artery thrombosis|
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|Figure 4: Computerized tomography angiography of the second patient showing left popliteal medial deviation and right popliteal thrombosis|
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- The patient underwent exploration of the right popliteal artery via posterior approach laterally displaced belly of gastrocnemius was released and the occluded popliteal artery was replaced with interposition reversed long saphenous vein graft along with a tibial thrombectomy.
The patient was discharged after 5 days on dual antiplatelet agents, with good flow in the pedal vessels on Doppler.
One month later, this second patient underwent similar decompression of the contralateral left popliteal artery entrapment (Type III) through the posterior approach, without the need for arterial reconstruction. On follow-up, the patient was asymptomatic with all pulses palpable.
| Discussion|| |
The true incidence of PAES cannot be estimated due to a lack of awareness, misdiagnosis, and the relative rarity of presentation. Both of our patients were <20 years of age and physically active. It is likely only the most severe cases present for evaluation and workup and have a confirmed diagnosis. The pathology often involves abnormal congenital anatomy surrounding the popliteal artery. The different types of PAES are categorized based upon the embryological development of the popliteal fossa. During development, the neurovascular bundle and developing muscle groups are maturing in the popliteal fossa in a dynamic manner. Any disruption of the migration pattern or timing of development can result in abnormal anatomy.
Bilateral PAES is common and is reported in about 70% of cases.,,
However, bilateral popliteal arterial occlusion secondary to PAES is rare. All our four legs operated on had a Type III abnormality.
There are six types of PAES described. The first four describe the anatomical anomalies ultimately causing the entrapment. Type I entrapment is caused by the popliteal artery forming prior to the migration of the medial head of the gastrocnemius muscle. This results in the medial deviation of the popliteal artery, causing the popliteal artery to become entrapped between the muscle and the femoral condyle.,, Type II entrapment involves a disruption in the migration of the medial head of the gastrocnemius by a prematurely formed popliteal artery. In Type III entrapment, abnormal remnants of mesoderm may be present, causing slips of the muscle or fibrous bands to entrap the artery. Type IV entrapment is the result of the popliteal artery remaining in the primitive position, deep to the popliteus muscle. Type V entrapment occurs when both the popliteal artery and the popliteal vein are involved.,, Type VI entrapment is acquired due to gastrocnemius or plantaris muscle tendon hypertrophy causing popliteal artery occlusion during active plantar flexion or leg extension.,,,, Other acquired forms of popliteal artery entrapment can result from compressive masses, local edema, or articular knee disorders. Movements that may exacerbate symptoms include repetitive leg extension and plantar flexion. This repetitive trauma of the popliteal artery may result in arterial injury, atherosclerosis, arterial aneurysm, and thrombus formation.,, The differential diagnosis includes atherosclerotic disease, exertional compartment syndrome, thrombosed popliteal artery aneurysm, and cystic adventitial disease.
The second patient (cases 3 and 4) was seen in 2018, and we had all imaging modalities available. We initially opted for CT angiography which confirmed right popliteal artery occlusion.
Subsequently, the patient underwent MRA for confirmation of diagnosis, to know the abnormal insertion of muscle slips.
The diagnosis of popliteal artery entrapment early in its course is crucial and relies upon disease awareness and suspicion based on the history and physical examination. Noninvasive and sometimes invasive tests are needed to demonstrate both the anatomic and functional aspects of the disease. Tests including arterial duplex or angiography with provocative maneuver scan show the functional result of compression. CT or magnetic resonance imaging may demonstrate the anatomic variant causing the compression.
In the first patient, operated for right leg popliteal entrapment release, there was a small anterior wall plaque in the popliteal artery with no pressure gradient across the lesion, so the popliteal artery was totally skeletonized with no bypass or interposition graft. This has subsequently proved to be a durable approach for this patient.
However, the second case we operated was presented with acute limbthreatening ischemia. The occluded popliteal artery damaged due to repetitive trauma required replacement with an interposition vein graft.
The treatment of PAES is based on the type of entrapment and degree of arterial pathology. It can range from simple myotomy of the medial head of the gastrocnemius to vascular repair or grafting if arterial damage is present, to endarterectomy in the presence of a thrombus., Young athletes may be advised to limit or stop contact sports to reduce the chance of trauma to the popliteal artery until definitive therapy. However, surgical treatment is indicated in all symptomatic patients.,
| Conclusion|| |
PAES is uncommon, and early recognition based on history, physical examination, and imaging results is paramount to initiate treatment and avoid the severe late presentation of acute limb ischemia.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
O'Leary DP, O'Brien G, Fulton G. Popliteal artery entrapment syndrome. Int J Surg Case Rep 2010;1:13-5.
Gourgiotis S, Aggelakas J, Salemis N, Elias C, Georgiou C. Diagnosis and surgical approach of popliteal artery entrapment syndrome: A retrospective study. Vasc Health Risk Manag 2008;4:83-8.
Radonic V, Koplic S, Giunio L, Bozic I, Maskovic J, Buca A. Popliteal artery entrapment syndrome diagnosis and management, with report of three cases. Tex Heart Inst J 2000;27:3-13.
Duwelius PJ, Kelbel JM, Jardon OM, Walsh WM. Popliteal artery entrapment in a high school athlete. Am J Sports Med 1987;15:371-3.
Gokkus K, Sagtas E, Bakalim T, Taskaya E, Aydin AT. Popliteal entrapment syndrome. A systematic review of the literature and case presentation. Muscles Ligaments Tendons J 2014;4:141-8. eCollection 2014 Apr.
Turner GR, Gosney WG, Ellingson W, Gaspar M. Popliteal artery entrapment syndrome. JAMA 1969;208:692-3.
Levien LJ, Veller MG. Popliteal artery entrapment syndrome: More common than previously recognized. J Vasc Surg 1999;30:587-98.
Murray A, Halliday M, Croft RJ. Popliteal artery entrapment syndrome. Br J Surg 1991;78:1414-9.
McAree BJ, O'Donnell ME, Davison GW, Boyd C, Lee B, Soong CV. Bilateral popliteal artery occlusion in a competitive bike rider: Case report and clinical review. Vas Endovascular Surg 2008;42:380-5.
Gibson MH, Mills JG, Johnson GE, Downs AR. Popliteal entrapment syndrome. Ann Surg 1977;185:341.
Rich NM, Collins GJ, McDonald PT, Kozloff L, Clagett GP, Collins JT. Popliteal vascular entrapment: its increasing interest. Arch Surg 1979;114:1377-84.
Hirokawa M, Iwai T, Inoue Y, Sato S. Surgical treatment of popliteal vein entrapment causing symptoms. Phlebology 2002;17:103-7.
Tercan F, Oguzkurt L, Kizilkilic O, Yeniocak A, Gulcan O. Popliteal artery entrapment syndrome. Diagn Interv Radiol 2005;11:222-4.
Vilás RO, Rodriguez LÁ, Campos MY, Moran Ade L, Mas FL. Exercise-related bilateral leg atypical claudication in female olympictae kwon do player: A case report. J Sports Sci Med 2011;10:768-70.
Cavallaro A, Di Marzo L, Gallo P, Cisternino S, Mingoli A. Popliteal artery entrapment. Analysis of the literature and report of personal experience. Vasc Endovasc Surg 1986;20:404-23.
Insua JA, Young JR, Humphries AW. Popliteal artery entrapment syndrome. Arch Surg 1970;101:771-5.
Servello M. Clinical syndrome of anomalous position of the popliteal artery. Differentiation from juvenile arteriopathy. Circulation 1962;26:885-90.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]