Chapter 143 - nonatheromatous popliteal artery disease Flashcards
Popliteal artery entrapment syndrome first described
1879 Anderson Stuart (medical student) 1965 Love and Whelan coined the term
Epidemiology of PAES
1) 80% men 2) median age 32 (20.7-41) 3) bilateral in 30% clinical, 67% anatomical
Embroylogy of popliteal artery
1) umbilical artery –> axial and external iliac arteries 2) external iliac –> femoral artery in anterior compartment 3) axial artery in posterior compartment 4) 42d intrauterine: axial divide to 3 in relation to popliteus: proximal, deep, distal 5) proximal artery joins femoral via ramus communicans superius in adductor hiatus 6) proximal axial artery gives branch that joins distal axial artery 7) deep axial artery involutes
Embryology of the medial head of gastrocnemius
1) Start from proximal tibia 2) migrate cranially end immediately caudal to adductor hiatus
Heidelberg Classes of popliteal artery entrapment syndrome
TYPE 1: popliteal completes development before medial head migration –> pushes artery medially; normal gastroc location TYPE 2: popliteal artery maturation halts gastroc migration; abnormal insertion site on lateral side of medial condyle or intercondylar area TYPE 3: abnormal muscle slip or fibrous band from either of the femoral condyle traps the artery TYPE 4: persistence of axial artery thereby remain deep to popliteus muscle or fibrous bands TYPE 5: both artery and vein involved 10-15% TYPE 6: (functional, type F)
Hypothesis for Type 6 popliteal entrapment
1) hypertrophy of gastroc 2) lateral attachment of medial head of gastroc
Stages of popliteal entrapment syndrome in histology
STAGE 1: fibrosis to adventitia STAGE 2: fibrosis to media with dilatation and aneurysm STAGE 3: fibrosis into intima, thrombogenic
Classification of popliteal entrapment symptoms
0 = asymptomatic 1 = pain, parethesia and cold feet after exercise 2 = claudication with walking > 100m 3 = claudication with walking < 100m 4 = rest pain 5 = necrosis
Nerve and vein impingement in PAES
1) venous entrapment TYPE 5 can have calf cramp, compartment syndrome like and swelling 2) tibial nerve impingement can occur except in TYPE 6
Manuevers that tense the gastroc muscle against entrapped artery
1) passive dorsiflexion 2) active plantar flexion
Ishikawa sign
loss of pedal pulse with sharp knee flexion (adventitial cystic disease)
Angiographic features in PAES
1) medial deviation of proximal popliteal artery 2) focal occlusion of mid popliteal artery 3) poststenotic dilation of the distal popliteal artery
Management options for PAES
TABLE 143.3

Surgical approach in PAES medial vs posterior
Medial: faster return to activity but only good for TYPE 1 and 2 Better exposure to distal popliteal Ease of GSV harvest Posterior: use of SSV
Indications to repair popliteal artery in PAES
1) PSV >250 cm/s 2) velocity ratio >2 3) arterial occlusion 4) aneurysm degeneration
Treatment of TYPE 6
1) monitor if asymptomatic 2) Botox –> paralyze slip of muscle responsible and aid muscle atrophy (controversial) 3) surgical decompression with muscle release 4) continue myectomy until intraoperative duplex show no further changes in velocity
Patency after open bypass PAES
65-100% at 10 years interposition better than long bypass
Adventitial cystic disease first described
1947 Atkin and Key (London) in EIA
First adventitial cystic disease in popliteal
1954 Ejrup and Hiertonn (Sweden)
% of ACD that are in popliteal artery
80.5%
Laterality of ACD
mostly unilateral
Epidemiology of ACD
1) male:female 5:1 2) mid 40’s
5 theories of ACD
1) Repetitive trauma 2) Ganglion 3) Systemic disorder 4) developmental 5) articular/synovial
Repetitive trauma theory key points
1) flexion and extension cause chronic injury and cystic degeneration 2) intramural hemorrhage 3) joint degeneration cause hydroxyproline secretion 4) hydroxyproline acts on intramural hemorrhage poor evidence athletes do not get it more
Ganglion theory key points
1) ganglion and ACD have similar content of high hyaluronic acid 2) synovial cyst enlarge along arterial branch and implant itself poor evidence histology doesn’t match
Systemic disorder theory key points
1) systemic mucinous or myxomatous degenerative condition causes ACD poor evidence bilateral disease rare
Developmental theory key points
AKA cellular inclusion theory 1) mesenchymal mucin-secreting cells implanted in adventia during development 2) mesenchymal cells from joints incorporated into closely adjacent vessels
Articular (synovial) theory key points
1) synovial fluid from joint egresses and dissects along adventitia of vessel branch to parent vessel
Duplex finding of ACD
1) fine bright line that pulsates 2) no flow in cyst
Angiography finding of ACD
1) Eccentric complression (Scimitar sign) 2) concentric compression (hourglass sign) 3) total arterial occlusion
Nonresectional methods of ACD
1) Angioplasty - ineffective 2) cyst aspiration - high failure and high recurrence 3) cyst excision and evacuation
Resectional method of ACD
Useful if extensive arterial degeneration or thrombosis
Recurrence with different methods
Cyst aspiration 10-30% at 15 months Cyst evacuation 15% Cyst resection 6-10% Endo failure 37.5%-50% bypass and recon - less likely