Print version ISSN 1677-5449
J. vasc. bras. vol.10 no.4 Porto Alegre Dec. 2011
Marcelo BettegaI; Ariane SzeligaI; Rafael Pereira HagemannII; Antônio Lacerda Santos FilhoIII; Nelson Mesquita JúniorIV
IMedical students in Faculdade Evangélica do Paraná (FEPAR) - Curitiba (PR), Brazil
IIVascular surgeon; former resident in Angiology and Vascular Surgery at the Hospital Universitário Evangélico de Curitiba - Curitiba (PR), Brazil
IIIMaster's degree in Clinical Surgery, Universidade Federal do Paraná (UFPR) - Curitiba(PR), Brazil; Assistant Professor of Angiology and Vascular Surgery at FEPAR - Curitiba (PR), Brazil
IVMaster's degree in Clinical Surgery, UFPR - Curitiba (PR), Brazil; Assistant Professor of Anatomy, Angiology and Vascular Surgery at FEPAR - Curitiba (PR), Brazil
Popliteal artery entrapment syndrome is the compression of the popliteal artery and is the main cause of intermittent claudication in young patients. An 18-year-old man was admitted at our service complaining of right foot paresthesia, coldness, and pallor that appeared 24 hours after physical activity. Posterior tibial and dorsal artery of foot pulses were not present in right lower limb. Diminished posterior tibial and dorsal artery of the foot pulses were found in left lower limb at dorsal flexion and forced plantar flexion. After surgery, both pulses were present. This syndrome is more frequent in men and its prevalence varies between 0.16 and 3.5%. Popliteal artery entrapment type III is most common. Non-treated entrapment can lead to embolism, thrombosis and post-stenotic aneurysms. The syndrome must be considered as a cause of lower limb pain specially in young men with intense sport practice history.
Keywords: popliteal artery; constriction, pathologic; /surgery.
The popliteal artery entrapment syndrome (PAES) is the clinical result of extrinsic compression of the popliteal artery. It can present as an anatomical or congenital anomaly or as an acquired or functional form. The anatomical anomaly is the result of abnormal embryological development of the popliteal artery or the musculotendinous structures around it; in the functional or acquired form, the artery is compressed as a result of hypertrophy of adjacent muscles1.
It was first described in Edinburgh in 1879 by medical student Anderson Stuart, who had dissected the amputated leg of a 64-year-man, victim of gangrene by thrombosis of the popliteal artery2. Hammings described the first case in which this syndrome was surgically treated (section of the medial head of the gastrocnemius muscle), in 19593. Love and Whelan4 proposed the name "popliteal artery entrapment syndrome", which has been used since then.
PAES predominantly affects men (15:1)5,6 and is identified as the main etiology of intermittent claudication in young patients7,8, with symptoms appearing usually after physical activity. As the artery compression results in repeated trauma, the complications, besides causing incapacity for physical exercise, include: stenosis, emboli, post-stenotic aneurysms and thrombosis8,9.
The purpose of this article is to report a case of popliteal artery entrapment, discussing its diagnosis, classification, complications and treatment, and to review the literature for non-experts.
A 18-year-old caucasean male patient, a delivery bicycler, with no medical history, was admitted to our service with right foot paresthesia, coldness and pallor that had appeared when he was riding his bicycle 24 hours earlier. He reported right calf fatigue for over two years and paresthesia when making greater muscular effort while bicycling.
On physical examination, the patient had normal right femoral and popliteal pulses, no pulses in the right posterior tibial and dorsalis pedis arteries and no bruits in the right lower limb. He had paresthesia, coldness and pallor of the right toes, but motor function was normal. Pulses were normal and no bruits were audible in the left lower limb. Reduced left posterior tibial and dorsalis pedis pulses were found on forced dorsal flexion and plantar flexion of the left foot.
Doppler ultrasonography showed no flow in the distal portion of the right anterior tibial and posterior tibial arteries. At forced dorsal flexion and plantar flexion, total compression of both right and left popliteal arteries occurred. The right and left popliteal arteries had a proximal diameter of 0.7 mm, and the right popliteal artery had a distal diameter of 0.9 mm (ectasia).
Preoperative arteriography at rest showed bilateral medial deviation of the popliteal artery, as illustrated in Figure 1. At forced dorsal flexion of the foot, bilateral popliteal artery compression occurred at the knee joint line. Such compression was more pronounced in the right limb. In addition, segmental occlusion of the distal anterior tibial and posterior tibial arteries were observed, as previously reported by Doppler ultrasonography. Computed tomography showed bilateral extrinsic compression of the popliteal artery at forced dorsal flexion, with no identification of the structure that caused the compression.
With the diagnosis of popliteal artery entrapment, the patient underwent surgical treatment. The posterior approach, using the italic S incision was selected (Figure 2). The right limb was operated first. The surgical findings were the same in both limbs, i.e., the popliteal artery was displaced medially of its usual course, not running along the popliteal vein and the posterior tibial nerve between the heads of the gastrocnemius muscles, but medially to the medial gastrocnemius muscle tendon, as illustrated in Figure 3. The popliteal artery was dissected proximally and distally to the compression site and partial myectomy was performed in the medial gastrocnemius muscle, with popliteal artery release (Figure 4). After myectomy in the medial head of the gastrocnemius muscle and popliteal artery release, intraoperative arteriography was performed, with dorsal flexion of the foot, which did not show any compression (Figure 5). The patient presented normal right dorsalis pedis pulse in the immediate postoperative period. The posterior tibial pulse was also present at follow-up.
The patient is under clinical follow-up with pulses prevent even at forced dorsal foot flexion. The same operation was performed on the left lower limb 90 days after the first surgical intervention.
Popliteal artery entrapment syndrome is more frequent in men, and most cases are unilateral1. Imaging exams are decisive for the diagnosis of this syndrome 10-12, and may include Doppler ultrasonography10,11, computed axial tomography12, magnetic resonance10 and angiography12. The latter are more useful for allowing better surgery planning10,12. The combined use of more than one imaging exam can be more effective than just one exam12.
The prevalence of PAES in the general population ranges from 0.16 to 3.5%, and type III is the most common form, affecting 35% of all cases11. The patient PAES is young, with a recent history of intense sport practice13.
A Brazilian study investigated the presence of this syndrome in 42 asymptomatic individuals, half of whom were athletes and half were sedentary subjects. Popliteal compression was detected in 6 individuals (14.2%), 2 (4.7%) in athletes and 4 (9.5%) in non-athletes, with no statistically significant relation between PAES and physical activity14. In this study, pocketDoppler exam of the posterior tibial artery and the ankle-brachial index were compared to the Doppler ultrasonography for the diagnosis of PAES. Both showed good sensitivity and specificity and were suggested as diagnostic screening instruments in individuals suspected of having the syndrome14.
The importance of correct diagnosis and treatment of PAES is reflected on the differential diagnosis and the resulting complications of the disease. The physician should distinguish PAES from arteritis, neurogenic claudication, muscle diseases, adventitial tumors in the popliteal artery, cystic disease of popliteal artery and traumatic causes of lesion in the popliteal artery11. Non-treated popliteal artery entrapment can lead, in the anatomical form, to complications, such as stenosis, embolism, post-stenotic dilatation and arterial thrombosis, and in the functional form, to incapacity to practice physical exercises9,15.
The most common symptoms are: intermittent claudication9,11,12,16, in 40% of the patients11, and feet and calf pain, which appear after physical exertion9,17. Intermittent claudication - complaints of pain only while walking - can occur9. Our patient reported calf fatigue and toe paresthesia during intense cycling, being asymptomatic in the left side, despite the popliteal artery compression at forced dorsal flexion.
It should be observed that the patient had no other diseases, such as diabetes and atherosclerosis9. Patients without thrombotic complications have normal pulses with the lower limbs in neutral position and may have reduced or no pulses at forced dorsal foot flexion9. In the case presented here, there were no posterior and dorsal tibial pulses in the right foot, without popliteal artery thrombosis; what probably happened was an intense artery spasm, due to repeated trauma, as the intraoperative control arteriography after partial myectomy in the medial head of the gastrocnemius muscle showed normal flow in the posterior and dorsalis pedis arteries and pulses were detected at digital palpation.
In Brazil, the first case reports on PAES were made by Ximenes and Ristow et al.19,20. Gallicchio and Schaffer21 and Castiglia22 were the first to publish Brazilian book chapters on the subject,
Created in 1971 by Delaney and Gonzáles, the classification of the various types of popliteal artery entrapment initially included only types I, II, III and IV3,9. In 1979, type V was added by Rich et al.18. In 1999, Levien and Veller8 stated that 50% of the population can have functional compressions and that, in these cases, the treatment should be primarily clinical. Then, type VI was added8. Therefore, the most frequent popliteal artery entrapment classification used today is:
TYPE I - Medial deviation of the popliteal artery, medially to the medial tendon of the gastrocnemius muscle that is inserted in the internal condyle of the femur.
TYPE II - The popliteal artery is normal, running anteriorly to the medial tendon of the gastrocnemius muscle that, for having its insertion more laterally than usual, compresses the artery.
TYPE III - The gastrocnemius muscle has an additional tendon, which is inserted more laterally, compressing the artery.
TYPE IV - The popliteal muscle compresses the popliteal artery, with normal anatomy of the gastrocnemius muscle.
TYPE V - The popliteal artery and the popliteal vein are simultaneously compressed.
TYPE VI - Muscle hypertrophy with normal structure, resulting in functional compression of the popliteal artery and the popliteal vein.
Figure 6 shows types I, II, II and IV of popliteal artery entrapment and the normal anatomical relation. The case reported was classified as type I.
The treatment of PAES caused by muscle insertion anomalies has a formal surgical indication, even in the asymptomatic patient12, thus preventing vascular complications that cause limb loss. In these cases, the operation eliminates the factor that causes entrapment and repairs the artery. We have two approached to the popliteal fossa: medial and posterior accesses3,9,12. The posterior approach, made through a S shaped incision, allows a better view of the structures, making it easier for the surgeon12. The medial approach, which was used for the first time in a functional entrapment case in 1974 by Darling et al.23, is indicated in the presence of artery thrombosis, to allow dissection of the great saphenous vein to be used as a graft9,12,15, as well long occlusions, in which a femoropopliteal bypass is required9. The question of surgical access to the popliteal fossa is still not a consensus3. In the case reported here, the posterior approach was used, with perfect view for treatment of the anomaly. We believe that, in cases of PAES without stenosis or post-aneurysmatic dilatation and with compression only, the posterior access is the best option, as we could explore the whole popliteal fossa without anatomical anomalies going unnoticed and exclude the presence of other factors for stenosis3.
1. Levien LJ. Popliteal artery entrapment syndrome. SeminVasc Surg. 2003;16(3):223-31. [ Links ]
2. Stuart TP. Note on a variation in the course of the popliteal artery. J. Anat Physiol. 1879;13(Pt 2):162-5. [ Links ]
3. Araújo JD, Araújo Filho JD, Ciorlin E, et al. Aprisionamento de vasos poplíteos: diagnóstico e tratamento e o conceito do aprisionamento funcional. J Vasc Bras. 2002;1(1):22-31. [ Links ]
4. Love JW, Whelan TJ. Popliteal artery entrapment syndrome. Am J Surg. 1965;109:620-4. [ Links ]
5. Collins PS, McDonald PT, Lim RC. Popliteal artery entrapment: an evolving syndrome. J Vasc Surg. 1989;10(5):484-90. [ Links ]
6. Wright LB, Matchett WJ, Cruz CP,et al. Popliteal artery disease: diagnosis and treatment. Radiographics. 2004;24(2):467-79. [ Links ]
7. Schurmann G, Mattfeldt T, Hofmann W, et al. The popliteal artery entrapment syndrome: presentation, morphology and surgical treatment of 13 cases. Eur J Vasc Surg. 1990;4(3):223-31. [ Links ]
8. Levien LJ, Veller MG. Popliteal artery entrapment syndrome: more common than previously recognized. J Vasc Surg. 1999;30(4):587-98. [ Links ]
9. Almeida MJ, Yoshida WB, Melo NR. Síndrome do aprisionamento da artéria poplítea. J Vasc Bras. 2003;2(3):211-9. [ Links ]
10. Ikawa MH, Natour J, Jannini MG, et al. Síndrome do entrelaçamento da artéria poplítea: um diagnóstico diferencial de claudicação de membros inferiores: contribuição da ressonância magnética para diagnóstico e avaliação. Rev Bras Reumatol. 2007;47(6):442-5. [ Links ]
11. Oliveira FM, Santos ACB, Takito AM, et al. Bilateral popliteal artery entrapment syndrome: case report. J Vasc Bras. 2008;7(2):159-62. [ Links ]
12. Gourgiotis S, Aggelakas J, Salemis N, et al. Diagnosis and surgical approach of popliteal artery entrapment syndrome: a retrospective study. Vasc Health Risk Manag. 2008;4(1):83-8. [ Links ]
13. Bonamigo TP, Becker M, Zylberstein S. Síndrome de aprisionamento da artéria poplítea: diagnóstico e tratamento. Relato de caso. Rev Bras Ortop. 1996;31(11):952-6. [ Links ]
14. Almeida MJ,Bonetti Yoshida W,Habberman D,et al. Extrinsic compression of popliteal artery in asymptomatic athlete and non-athlete individuals. A comparative study using duplex scan (color duplex sonography). Int Angiol. 2004;23(3):218-29. [ Links ]
15. Imtiaz N. Popliteal artery entrapment syndrome. J Coll Physicians Surg Pak. 2011;21(6):376-8. [ Links ]
16. Lamb CM, Davies CG, Whitbread T. Two cases of mis-diagnosed popliteal artery entrapment syndrome. Eur J VascEndovasc Surg. 2010;20(2):e16-8. [ Links ]
17. Yamaguchi H, Miura T, Eishi K, Tsuda N. A case of popliteal artery aneurysm associated with popliteal artery entrapment syndrome. Ann Vasc Dis. 2010;3:140-3. [ Links ]
18. Rich NM, Hughes CW. Popliteal artery and vein entrapment. Am J Surg. 1967;113:696-8. [ Links ]
19. Ximenes JOC. Síndrome de enlaçamento da artéria poplítea: relato de um caso e revisão da literatura. Rev Col Bras Cirur. 1975;2:74-77. [ Links ]
20. Ristow AVB, Arruda AM, Baptista H. Síndrome de compressão da artéria poplítea. Med Hoje. 1979;5:80-82. [ Links ]
21. Gallicchio VG, Schaffer NT. Síndrome do aprisionamento da artéria poplítea. In: Bonamigo TP, Burihan E, Cinelli M, et al. Doenças da aorta e seus ramos: diagnóstico e tratamento. São Paulo: Fundo Editorial Byk; 1991. p. 324-44. [ Links ]
22. Castiglia V. Síndrome do aprisionamento da artéria poplítea. In Maffei FHA, Lastória S, Yoshida WB, et al. Doenças vasculares periféricas. Rio de Janeiro: Medsi; 1995. p. 701-15. [ Links ]
23. Darling RC, Buckley CJ, Abott WM, et al. Intermittent claudication in young athletes: popliteal artery entrapment syndrome. J Trauma 1974;14(7):543-52. [ Links ]
Correspondence Submitted on: 06.27.11. Author's contributions
Nelson Mesquita Júnior
Rua Deputado Heitor Alencar Furtado, 1.819 apto 1.302 - Mossunguê
CEP 81200-110 - Curitiba (PR), Brazil
Accepted on: 09.13.11.
Financial support: none.
Conflict of interest: nothing to declare.
Conception and design: MB, AS, RPH, ALSF, NMJ
Analysis and interpretation: N/A
Data collection: MB, AS, RPH, ALSF, NMJ
Writing the article: MB, AS, RPH, ALSF, NMJ
Critical revision of the article: ALSF, NMJ
Final approval of the article*: MB, AS, RPH, ALSF, NMJ
Statistical analysis: N/A
Overall responsibility: NMJ
*All authors have read and approved the final version submitted at the J Vasc Bras.
Submitted on: 06.27.11.