- •Vascular Surgery
- •SECTION AND BOARD OF VASCULAR SURGERY
- •Foreword to the First Edition
- •Preface to the First Edition
- •Preface to the Second Edition
- •Preface to the Third Edition
- •Contents
- •Contributors
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •1.1 Commentary
- •1.2 Beta-Adrenergic Antagonists
- •1.3 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitors (Statins)
- •1.4 Percutaneous Revascularization
- •1.5 Coronary Artery Bypass Grafting
- •References
- •2: Abdominal Aortic Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •2.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •Question 12
- •Question 13
- •Question 14
- •3.1 Commentary
- •3.2 Case Analysis Quiz
- •References
- •4: Ruptured Abdominal Aortic Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •4.1 Commentary
- •References
- •5: Thoracoabdominal Aortic Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •5.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •Question 12
- •Question 13
- •6.1 Commentary
- •References
- •7: Aortic Dissection
- •7.1 Dissection: Stanford A
- •Question 1
- •Question 2
- •Question 3
- •7.2 Dissection: Stanford B
- •Question 4
- •Question 5
- •7.3 Commentary
- •References
- •8: Popliteal Artery Aneurysms
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •8.1 Popliteal Artery Aneurysm
- •References
- •9: Renal Artery Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •9.1 Commentary
- •References
- •10: Anastomotic Aneurysms
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •10.1 Commentary
- •10.2 Indications for Intervention
- •10.3 Treatment for Anastomotic Aneurysms
- •10.4 Infection in Anastomotic Aneurysms
- •10.5 Outcome
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •11.1 Commentary
- •References
- •12: Acute Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •12.1 Commentary
- •References
- •13: Arterial Embolism
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •13.1 Commentary
- •References
- •14: Blast Injury to the Lower Limb
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •14.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •15.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Smoking
- •Antiplatelet Agents
- •Blood Pressure (BP)
- •Glucose Status
- •Lipids
- •Emerging Risk Factors
- •Question 4
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •17.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •18.1 Commentary
- •18.2 Clinical Assessment
- •18.3 Imaging Techniques
- •18.4 Revascularization Options
- •18.5 Aortobifemoral Bypass
- •18.6 Iliac Angioplasty and Stenting
- •18.7 Iliac Stenting Combined with Profunda Femoris Artery Revascularization
- •18.8 Rationale for Angioplasty of “Donor” Iliac Artery Prior to Femorofemoral Crossover Bypass
- •18.10 Supervision and Follow-up of the Patient
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •Question 12
- •19.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •20.1 Commentary
- •References
- •21: Bypass to the Popliteal Artery
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •21.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •22.1 Commentary
- •References
- •23: Popliteal Artery Entrapment
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •23.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •24.1 Commentary
- •References
- •25: The Obturator Foramen Bypass
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •25.1 Commentary
- •25.2 Preoperative Measures
- •25.3 The Concept of the Obturator Foramen Bypass
- •25.4 Obturator Foramen Bypass Technique
- •References
- •26: Diabetic Foot
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •26.1 Commentary
- •References
- •27: Chronic Visceral Ischemia
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •27.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •28.1 Commentary
- •References
- •29: Renovascular Hypertension
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •29.1 Commentary
- •29.4 Intra-arterial Angiography
- •29.5 Duplex Ultrasonography (DU)
- •29.6 Treatment
- •29.6.1 Medical Treatment
- •29.6.2 Revascularization
- •29.7 Prognosis
- •References
- •30: Midaortic Syndrome
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •30.1 Commentary
- •References
- •31: Management of Portal Hypertension
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •31.1 Commentary
- •31.2 General Considerations
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •32.1 Commentary
- •References
- •33: The Carotid Body Tumor
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •33.1 Commentary
- •33.2 Clinical Presentation
- •33.3 Treatment
- •33.4 Summary
- •References
- •Question 1
- •Question 2
- •Question 3
- •34.1 Commentary
- •34.2 Vertebrobasilar Ischemia: Low-Flow Mechanism
- •Question 1
- •Question 2
- •34.3 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •35.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •36.1 Commentary
- •References
- •37: Acute Axillary/Subclavian Vein Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •37.1 Commentary
- •References
- •38: Raynaud’s Phenomenon
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •38.1 Commentary
- •References
- •39: Aortofemoral Graft Infection
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •39.1 Commentary
- •References
- •40: Aortoenteric Fistulas
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •40.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •41.1 Commentary
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Questions 7 and 8
- •Question 9
- •Question 10
- •Comment
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •42.1 Commentary
- •References
- •43: Amputations in an Ischemic Limb
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •43.1 Commentary
- •References
- •44: Congenital Vascular Malformation
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •44.1 Clinical Evaluation
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •44.2 Commentary
- •References
- •45: Klippel-Trenaunay Syndrome
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •45.1 Commentary
- •Clinical Presentation
- •Evaluation
- •Treatment
- •References
- •46: Deep Venous Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •46.1 Commentary
- •References
- •47: Endoluminal Ablation of Varicose Veins
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •47.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •48.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •50.1 Commentary
- •References
- •51: Iliofemoral Venous Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •50.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •52.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •53.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •54.1 Commentary
- •References
- •Index
23 Popliteal Artery Entrapment |
241 |
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D. The posterior approach is recommended to expose all the structures causing compression.
E. The structure causing PAE must be sectioned completely, as incomplete sectioning may cause recurrence.
Question 5
Which of the following statements regarding the incidence of entrapment are correct?
A. The medial gastrocnemius muscle is involved in almost 80% of cases of PAE. B. Venous entrapment is described more often than arterial entrapment.
C. Venous entrapment is concomitant in 20% of cases of PAE. D. More than one structure may be the cause of arterial entrapment. E. Classification of arterial entrapment includes 12 different types.
The postoperative course was uneventful and the patient was discharged 5 days after surgery, returning back to normal activity after 3 weeks. Follow-up demonstrated complete regression of symptoms. Ultrasound examinations (Doppler and color Doppler) showed normal popliteal flow with negative response to PAE maneuvers 1 month after surgery. The patient is now doing sport (swimming) again without any further complaints.
23.1 Commentary
The first case of PAE was treated surgically in 1959 in a 12-year-old boy complaining of claudicationafterwalking300m.Atsurgicalexploration,Hamming1 atLeydenUniversity in The Netherlands found an occluded artery with an anomalous course medial to the medial gastrocnemius muscle. He transected the muscle and performed a successful poplitealarterythromboendarterectomy.Apreviousdescriptionofthediseasewasreported in 1879 by Stuart,2 a medical student at the University of Edinburgh. During the dissection of an amputated leg of a 64-year-old man, he observed the popliteal artery coursing around the medial head of the gastrocnemius muscle and aneurysmal changes in the popliteal artery distal to the point of external muscular compression.
Since then, many case reports have been published. A few authors have published small series.3–6 Unfortunately, the papers that were collected were missing details and showed poor patient follow-up7
InRomein1998,thePoplitealVascularEntrapmentForumwasfounded.Surgeonsfrom around the world with the greatest experience in this field world were invited as founding members of the forum. Great effort was addressed to collect different series with comparable criteria. The criteria established by the Society for Vascular Surgery (SVS) were reviewed and accepted, with some minor changes. Common opinion was to consider both arterial and venous entrapment as a common disease defined as vascular entrapment. The
242 |
L. di Marzo and N.M. Rich |
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functional form of entrapment was discussed. This was first described by Rignault et al.8 in 1985, and describes cases in which the anatomy of the popliteal fossa is normal. Symptoms are usually caused by hypertrophy of the muscles determining a compartment syndrome.8, 9 Functional entrapment was included in the classification as type F (Table 23.1).
Popliteal artery entrapment is no longer a rare disease. It is encountered more and more often, particularly in young adults. Athletes practicing sports causing hypertrophy of the limb muscles are at higher risk due to an anomalous relationship of the popliteal artery and its surrounding musculotendineous structures. The artery is compressed each time the leg moves, causingperipheral ischaemia during intensive exercise. With time, thisintermittent arterial trauma may give rise to stable arterial damage, with occlusion or post-stenotic aneurysm. Early diagnosis and treatment play an important role in limiting surgical treatment to the sectioning of the structure causing the arterial compression. [Q1: A, C]
The diagnosis of PAE is based primarily on ultrasound scanning. Both continuouswave Doppler and color Doppler are able to detect the presence of an arterial compression due to entrapment. The maneuvers to be performed are well described and are able to detectsuspectedcases.7 GreatcareshouldbetakentosuspectearlycasesofPAEinpatients complaining of minor symptoms (paraesthesia, cold foot and cramping after intensive physicaltraining).Arteriographyislimitedtocaseswithpositiveultrasoundexaminations, and it requires great care in repeating the maneuvers to confirm the popliteal compression. Both Angio-CT and MRA may be diagnostic, but they need latest-generation apparatus and the input of a radiologist with great experience in both the disease and the imaging method. [Q2: A, B, C, D, E] [Q3: True A, B, C, D, E]
Surgical treatment consists of sectioning the musculotendineous structure causing the entrapment.Theanomalousstructureneedstobesectionedentirelyinordertoavoidrecurrence of the entrapment due to hypertrophy of the remaining anomalous muscle. It is important to remember that complete exposure of the popliteal fossa is obtained through a posterior approach. The medial approach limits the view of the medial gastrocnemius muscle. In our opinion, this exposure should be limited to cases in which the arterial impairment is extended to the tibial vessels and a distal reconstruction needs to be planned. However, early diagnosis allows surgical treatment to be limited to the muscle sectioning, which should be considered the first-choice treatment. When a popliteal severe stenosis, occlusion or aneurysm is present, then an arterial reconstruction is indicated. In this case, we recommend the use of autologous material to reconstruct the artery. This improves the
Table 23.1 Classification of popliteal vascular entrapment
Type features
I Popliteal artery running medial to the medial head of gastrocnemius II Medial head of gastrocnemius attached laterally
III Accessory slip of gastrocnemius
IV Popliteal artery passing below popliteal muscle and medial head of gastrocnemius V Primary venous involvement
VI Variants
F Functional entrapment
23 Popliteal Artery Entrapment |
243 |
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long-term patency rate. Great effort should be paid for alternative vein preparation when the saphenous vein is unavoidable. [Q4: A, B, C, D, E]
The medial gastrocnemius muscle is often the cause of compression. However, more than 20 different anatomical variants have been described, and sometimes multiple and complex structures may be associated with the medial gastrocnemius muscle in causing PAE. The popliteal vein is involved in the compression in 20% of cases affected by PAE. Moreover, isolated popliteal vein entrapment is described with increasing frequency in the literature. [Q5: A, C, D]
References
1.Hamming JJ. Intermittent claudication at an early age due to anomalous course of the popliteal artery. Angiology. 1959;10:369-370.
2.Stuart PTA. Note on a variation in the course of the popliteal artery. J Anat Physiol. 1879;13:162.
3.Bouhoutsos J, Daskalakis E. Muscular abnormalities affecting the popliteal vessels. Br J Surg. 1981;68:501-506.
4.Rich NM, Collins GJ, McDonald PT, Kozloff L, Claget PG, Collins JT. Popliteal vascular entrapment. Its increasing interest. Arch Surg. 1979;114:1377-1384.
5.Di Marzo L, Cavallaro A, Mingoli A, Sapienza P, Tedesco M, Stipa S. Popliteal artery entrapment syndrome: the role of early diagnosis and treatment. Surgery. 1997;122:26-31.
6.Levien L, Veller MG. Popliteal artery entrapment syndrome: more common than previously recognized. J Vasc Surg. 1999;30:587-598.
7.Di Marzo L, Cavallaro A, Sciacca V, Mingoli A, Stipa S. Natural history of entrapment of the popliteal artery. J Am Coll Surg. 1994;178:553-556.
8.Rignault DP, Pailler JL, Lunel F. The “functional” popliteal entrapment syndrome. Int Angiol. 1985;4:341-343.
9.Turnipseed WD, Pozniak M. Popliteal entrapment as a result of neurovascular compression by the soleus and plantaris muscles. J Vasc Surg. 1992;15:285-294.