Popliteal Artery Aneurysm

Popliteal artery aneurysm, trauma and disease.


The popliteal artery crosses the popliteal fossa closely applied to the back of the femur, the knee joint, and the proximal tibia and tethered proximally by adductor magnus, distally by soleus. This arrangement makes it vulnerable to injury when the knee is dislocated or adjacent bone is fractured. Mechanical stresses imposed by muscle contraction and knee movement could also be responsible for some of the other conditions peculiar to this artery described below.

Popliteal aneurysms

Popliteal aneurysms rarely endanger life but may threaten limb survival. They are the most common of peripheral aneurysms but occur 15 times less frequently than aortic aneurysms. Nowadays most are 'atherosclerotic' and 95 per cent occur in men over 60 years. They form part of the spectrum of dilating disease: of those with aortic aneurysms, 10 per cent have popliteal aneurysms; of those with popliteal aneurysms, one-third have aortic aneurysms and 50 per cent have bilateral popliteal aneurysms. Occasionally, mycotic or pseudoaneurysms occur in younger individuals, with pseudoaneurysms sometimes associated with osteochondromas of the distal femur.

The normal popliteal artery measures 0.7 cm in diameter and is often difficult to palpate. A localized expansion over 1.05 cm constitutes a popliteal aneurysm, but may be clinically undetectable until it reaches 2 cm unless ultrasonographic examination is used in patients suspected to harbour the disease.

There are four main complications of popliteal aneurysms:

  1. acute thrombosis;
  2. distal embolization;
  3. rupture;
  4. local pressure effects.

Acute thrombosis

Acute occlusion of the aneurysm is probably the most common complication and has a variable outcome. Some patients are unaware of the event and a thrombosed aneurysm is detected during unrelated investigations at a later stage. At the other extreme a significant number of patients require amputation as a consequence of popliteal arterial thrombosis. The latter we know about: the number who undergo silent thrombosis in the community is unknown.

The classical presentation is of a man in his eighth decade, previously untroubled by claudication or other vascular symptoms, who suddenly develops a cold, painful leg. Examination reveals a pale limb with no pulses below the femoral (the thrombosed popliteal aneurysm is usually undetectable), perhaps loss of sensation and movement distally, and in some cases a pulsatile mass behind the other knee. Differentiation between thrombosed aneurysm, embolization from a proximal source such as the heart, and thrombosis on pre-existing atheroma can be difficult, but the treatment is similar whatever the cause.

Propagated fresh thrombus or previous distal embolization (see later) often impedes run-off from the popliteal artery and may jeopardize the success of bypass grafting. Thrombolysis is a useful adjunct to surgery in this situation. Preoperative thrombolysis in the patient with intact sensation and power can open up some or all of the crural vessels. Some patients, however, are made worse by this procedure, probably as a result of loosening and embolization of thrombus from the aneurysm. When there is a large thrombotic load, perioperative thrombolysis of the run-off vessels alone is probably safer. The patient who has a critically ischaemic limb with loss of sensation and movement, or muscle pain, cannot afford the delayed revascularization that preoperative thrombolysis would inevitably incur. Under such circumstances, surgical exploration, with the use, as appropriate, of on-table angiography, an embolectomy catheter, peroperative thrombolysis, and bypass grafting, is indicated.

The popliteal artery can be explored through a medial approach, exposing it above and below the knee, anastomosing a bypass graft in an end-to-side fashion at these two points, and excluding the intervening aneurysmal artery by ligation. The alternative is a posterior approach to expose the popliteal aneurysm directly: the aneurysm is opened and an inlay graft performed. Overall, 5-year graft patency is about 60 per cent, but it is consistently better with vein than with synthetic grafts.

Distal embolization

Acute or chronic distal embolization from a popliteal aneurysm is a common form of presentation. The patient complains of claudication or pain at rest as pedal and crural vessels silt up. Treatment is surgical exclusion of the aneurysm (see above) but bypass grafting may again be frustrated by poor run-off. Thrombolysis is a useful adjunct, but is often less successful because of the long-standing nature of the distal obstruction.


This is a rare event accounting for fewer than 5 per cent of presentations of popliteal aneurysm. Blood loss is usually relatively small because the leak is tamponaded by the tight musculofibrous planes in this region. The increase in local pressure may lead to venous compression, occasionally with deep venous thrombosis, and nerve damage. Treatment is emergency surgery as above.

Local pressure symptoms

A large popliteal aneurysm can impede knee flexion or compress the tibial nerve, causing paraesthesias or foot drop. Popliteal aneurysms over 2 cm in diameter compress and displace the popliteal vein but a collateral venous network usually opens up to allow normal venous function. A few of the larger aneurysms eventually cause venous thrombosis. Such aneurysms are usually repaired electively to avoid further complications but the outcome for nerve and venous function is unpredictable.

Asymptomatic popliteal aneurysms

Twenty years ago, those popliteal aneurysms detected were either large or symptomatic. Ultrasonography has brought to our attention a large number of smaller, asymptomatic aneurysms and raised the question of their management.

Some 15 to 20 per cent of the patients who present with thrombosed aneurysms lose their leg. Increased use of thrombolysis may improve this outcome but will do nothing for the 5 per cent or so who have an unsalvageable leg at presentation. Such data have led many surgeons to advocate prophylactic repair of all asymptomatic aneurysms. They argue that a bypass graft excluding the popliteal aneurysm will guard against future catastrophe and should have good run-off at this stage and therefore good long-term patency. Critics of this approach point to the 60 per cent patency of below-knee femoropopliteal bypass grafts and question the inevitability of complications in all popliteal aneurysms.

The problem is that most of our data on initially asymptomatic aneurysms are drawn from patients with large aneurysms, detected during routine clinical examination, or those with generalized aneurysmal disease in whom the detection of one aneurysm often prompts a search for others. Generalized aneurysmal disease and large size are both known to increase the rate of complications from popliteal aneurysms. Even these data, however, show that some patients with popliteal aneurysms can remain asymptomatic for 15 years. Earlier studies, where aneurysms were detected clinically rather than by ultrasound and tended to be larger, found a complication rate of 30 per cent over 3 to 5 years. More recent studies include aneurysms detected by ultrasound, where the mean size is smaller, and report a complication rate of 8 per cent over 3 years.

Such retrospective studies of asymptomatic aneurysms have shown that those over 3 cm in diameter, tortuous aneurysms with significant narrowing of their lumen, and aneurysms with intraluminal thrombus are more likely to threaten limb viability. Vein bypass of an asymptomatic aneurysm has a 90 per cent 5-year patency. An operative policy based on the above criteria represents a reasonable balance between the risks of surgery and of conservative management.

Developments in treatment

Some centres have reported stenting of patent popliteal aneurysms, using a device covered by synthetic graft material. Antegrade percutaneous placement via the femoral artery adds the risk of distal embolization when the device is negotiated through the aneurysm. This has been addressed by retrograde placement via a surgical approach to the distal popliteal artery. Although appealing in its simplicity, the long-term outcome is yet to be determined. We know that synthetic grafts used conventionally to bypass a popliteal aneurysm have disappointing long-term patency. Use of vein-covered stents may provide a more durable alternative at some future stage.

Trauma to the popliteal artery

Damage to the popliteal artery is associated with a high rate of amputation. There are three categories of injury that have been particularly reported in largely retrospective studies: blunt and penetrating injuries, usually in young adult males as a result of civilian or military violence, and injury incurred as a result of total knee replacement in an elderly population.

Military trauma is likely to be a combination of blunt and penetrating injuries, often with a significant delay between injury and repair because evacuation to hospital proves difficult. The nature of civilian violence depends on environment: in cities in the United States penetrating damage due to gunshot wound is common whereas, in other places, blunt injuries from agricultural, industrial, and road traffic accidents predominate.

Injuries to the popliteal artery were treated in the Second World War by arterial ligation and 70 per cent of cases came to amputation. Reconstruction is usually attempted nowadays, resulting in improved rates of limb salvage. Penetrating trauma is associated with a relatively good outcome: amputation rates of 0 to 18 per cent have been reported. Blunt trauma has a poorer prognosis, with amputation rates ranging from 20 to 35 per cent. The likelihood of amputation depends upon the extent of soft-tissue and bony injury, the size and nature of any open wound, the presence of obvious distal ischaemia or accompanying shock, and the age of the patient. Delayed revascularization of 12 h or more is also a poor prognostic factor but found usually only with military injuries. Attempts have been made through the creation of prognostic scoring systems to decide which patients would benefit from primary amputation. Few of these have been evaluated prospectively and, as one might expect from the number of such systems, none is easily and reliably used in the case of individual patients.

Ischaemia associated with total knee replacement is rare (less than 0.2 per cent of cases) but associated with a high rate of amputation (death or amputation in 25 per cent). The cause is usually thrombosis of a diseased popliteal artery, especially if a tourniquet is used. There is often no history to suggest a vascular problem, although preoperative examination may reveal absent pulses. In a few cases, musculofascial compression of the artery occurs when a knee previously held in fixed flexion is extended. Distal embolization of plaque or thrombus from the popliteal artery, arterial transection, and pseudoaneurysm formation occasionally occur.


Skeletal muscle does not tolerate more than 6 h of ischaemia, and, although collateral blood supply may maintain viability beyond that time, it cannot be relied upon when there is extensive soft-tissue injury. It is therefore essential to recognize the possibility of trauma to the popliteal artery with particular injuries, and to diagnose and treat as soon as possible.

Bony injuries around the knee are associated with arterial trauma in 2 per cent cases but in knee dislocation the rate increases to 30 to 50 per cent. 'Hard evidence' evidence for disruption of the popliteal artery comes from

  1. local signs of pulsatile bleeding, an expanding or pulsatile haematoma or the palpation of a thrill from an arteriovenous fistula, or 
  2. distal ischaemia with reduction or loss of foot pulses.

It is important to remember that 10 per cent of patients with significant trauma to the popliteal artery have apparently normal foot pulses.

Is preoperative angiography necessary?

Patients with the 'hard' signs noted above are probably best served by immediate surgery. Preoperative angiography provides little more useful information and delays revascularization. The only exception is with multiple gunshot wounds when the site of arterial injury is unclear. If there is doubt during surgery about the site of arterial injury, perioperative angiography can be performed.

When managing patients with 'soft' signs—non-expanding haematoma, nerve damage, or proximity of the wound to the popliteal artery but, by definition, full pedal pulses with no evidence of distal ischaemia—immediate intervention is less important, and angiography or Duplex ultrasonography (if feasible) can be pursued. Some argue that angiography is unnecessary in such cases, but the presence of foot pulses does not rule out arterial injury and in one study 75 per cent patients with 'soft' signs had arterial injury. Narrowing of the popliteal artery on Duplex or angiography should never be ascribed to 'spasm' even in the presence of compartment syndrome: the vessel should always be explored as there is frequently an intimal tear. Even small intimal tears often lead to later thrombosis or the formation of a false aneurysm.


The popliteal artery is usually explored for trauma via a medial incision, with exclusion bypass grafting using vein wherever possible. Some report a posterior approach to the artery but this poses difficulties if a bypass graft to the crural vessels is required. The artery may be completely or partially divided, or have an intimal tear with intact adventitia. It is sometimes possible to perform a direct suture repair of a lacerated or divided artery. Simple endarterectomy for intimal tears rarely provides a satisfactory long-term result. Most cases of arterial trauma require a vein bypass graft, either as an interpositional end-to-end graft or as an end-to-side exclusion graft. Peroperative local or systemic heparinization and even thrombolysis, when necessary, improve the prognosis without a significant increase in risk.

Damage to the popliteal vein from blunt or penetrating trauma occurs in 25 to 50 per cent of cases of trauma to the popliteal artery. The vein should be repaired wherever possible, using saphenous vein from the other leg for both arterial and venous repairs. A third of cases in which the popliteal artery is ligated develop postphlebitic syndrome. In an acutely ischaemic limb with both arterial and venous damage, the insertion of a Javid shunt into the popliteal artery will allow reperfusion of the limb whilst the vein is repaired.

Four-compartment fasciotomy of the calf is required in approximately a third of cases, particularly those with extensive soft-tissue injury or in whom the vein had to be ligated. Fractures may need to be stabilized or drawn out to length. This should be achieved with external fixation to avoid damage to collateral vessels, preferably after arterial reconstruction. Where necessary, primary nerve repair should be performed after vascular reconstruction.

Popliteal entrapment syndrome

Congenital anatomical abnormalities of muscle and artery in the popliteal fossa together comprise an uncommon cause of compression of the popliteal artery. Compression occurs most commonly because of an abnormal attachment of the medial head of gastrocnemius to the lateral femoral condyle (type 2), causing the popliteal artery to pursue a more lateral course than normal. Sometimes the popliteal artery itself appears at fault, taking an unusual medial course around a normally attached medial head of gastrocnemius. A variety of other causes, including compression by accessory slips of gastrocnemius, popliteus, or plantaris muscle, are also described.

The prevalence of entrapment of the popliteal artery in post-mortem studies is only 3.5 per cent. Amongst the living it comes to notice when symptoms of restricted blood flow arise. The majority report a cold foot with tingling and cramps following exercise; others report claudication, and relatively few develop rest pain or ulceration. The largest single-centre series amounts to only 30 patients, and entrapment probably accounts for less than 1 per cent patients with claudication. Patients usually present in their late teens or early twenties but some as young as 12 years and as old as 70 years have been described. Males are up to 15 times more likely to be affected than females, and as the entrapment tends to produce symptoms when physical activity is increased, it has been well described in military recruits. The condition occurs bilaterally in somewhere between 20 and 70 per cent of cases.

Post-stenotic aneurysm formation occurs in 15 per cent of patients. Although restricted blood flow at the site of constriction is the usual cause of symptoms, distal embolization of thrombus, from the site of constriction or a post-stenotic aneurysm, leads to impaired run-off in the crural vessels in 30 per cent of patients.


Claudication-like symptoms in a young adult should raise the suspicion of an entrapment syndrome. Duplex ultrasonography or angiography of the popliteal artery during active plantarflexion or passive dorsiflexion of the foot will demonstrate compression of the artery and, in some, an abnormal course of the artery, local thrombus, or post-stenotic aneurysmal dilatation.


Exploration of the popliteal fossa via a posterior approach allows release of the artery by division of any constricting muscle or fibrous band. In patients without mural thrombus, occlusion, or aneurysmal dilatation (between a third and two-thirds of all patients presenting), this will suffice. Those who have significant arterial damage require bypass grafting. Simple thromboendarterectomy was favoured in the past but the long-term patency was poor compared with saphenous vein bypass. The short saphenous vein is more accessible than the long saphenous vein through a posterior approach but may be too small to use. If a distal bypass graft is required because of run-off disease, a medial approach to the popliteal artery is more appropriate.

Functional popliteal entrapment

Reliance on Duplex ultrasonography alone in making the diagnosis has certain pitfalls. Several studies of healthy young adults, both normally active and athletic, have shown that active plantarflexion produces stenosis of the popliteal artery in all and occlusion in 50 per cent, at the level of the soleal sling (the proximal border of the soleus muscle). Turnipseed reported a series of athletes with calf cramping after exercise in whom surgical exploration revealed no anatomical abnormality but whose symptoms were relieved by division of the soleal sling as it crosses the neurovascular bundle. Compression at this level has since been shown to be almost as common in untrained individuals, but usually without symptoms. Functional popliteal entrapment requires active plantarflexion and is rarely seen with passive dorsiflexion, unlike 'anatomical' popliteal entrapment. Turnipseed's work would suggest that in those with convincing symptoms, Duplex evidence of compression of the popliteal artery is sufficient to justify surgical exploration.

Outcome of treatment

Those patients requiring only musculofascial release have a good outcome, with 95 per cent patency at 5 years. Unfortunately, those who require bypass grafting fare less well: 65 per cent are patent at 5 years. For young adults this is a significant problem. Patients who have arterial damage requiring bypass grafting are more likely to have advanced symptoms such as short-distance claudication or rest pain. Patients without arterial damage usually have relatively minor symptoms of cramps and cold feet. It would seem sensible to attempt diagnosis of this condition at an early stage and to take these symptoms seriously in teenage or young adult patients.

Cystic adventitial disease of the popliteal artery

Cystic adventitial disease is a rare disease of uncertain cause. It affects the external iliac, femoral, radial, and ulnar arteries but 85 per cent of cases occur in the popliteal artery. Multiple cysts within the adventitia, perhaps of synovial origin, protrude into the lumen and sometimes impair blood flow.

The disease probably accounts for 1 in 1200 cases of calf claudication. It usually presents in young or middle-aged males who have a history of relapsing and remitting calf claudication over several years but who are completely asymptomatic between episodes. During a symptomatic phase, pedal pulses may be absent, the foot cool, and ankle/brachial pressure indices reduced, but during remission the pulses return and the limb appears normal. Eventually, thrombosis of the popliteal artery may occur, with the development of permanent symptoms and signs. Sometimes there are also symptoms of nerve compression by the cyst.


In addition to the peculiar history of 'disappearing' claudication, 'Ishikawa's sign' may be positive—flexion of the knee causes the pedal pulses to disappear and the foot to become cold and pale.

During a symptomatic phase, Duplex ultrasonography or angiography reveal smooth, rounded, luminal compression—the 'scimitar sign'. A large cyst may produce an 'hour-glass' compression of the lumen. In 30 per cent of cases the artery is occluded, with a smooth proximal taper by the time of investigation.

Computed tomography or magnetic resonance imaging usually confirm the diagnosis by demonstrating cystic changes within the arterial wall.


Balloon angioplasty is ineffective because of the compliant nature of the cyst. It may be possible to relieve a stenosis by percutaneous aspiration of the cyst under ultrasonographic control. If this fails, or the artery has thrombosed, the affected segment needs to be excised and replaced by vein graft.

Further reading

Popliteal aneurysm

Dawson I, Sie RB, van Bockel JH. Atherosclerotic popliteal aneurysm. British Journal of Surgery 1997; 84: 293–9. [Systematic review of recent studies since 1980 of patients with popliteal aneurysms.] 

Ramesh S, Michaels JA, Galland RB. Popliteal aneurysm: morphology and management. British Journal of Surgery 1993; 80: 1531–3. [Review of experience with popliteal aneurysms presenting to one hospital and including factors predictive of thrombosis.] 

Varga ZA et al. A multicenter study of popliteal aneurysms. Journal of Vascular Surgery 1994; 20: 171–7. [A multicentre prospective study looking at presentation, management, and outcome of patients with popliteal aneurysms.] 

Popliteal artery trauma

Degiannis E, Velmahos GC, Florizoone MGC, Levy RD, Ross J, Saadia R. Penetrating injuries of the popliteal artery: the Baragwaneth experience. Annals of the Royal College of Surgeons of England 1994; 76: 307–10. [Study of popliteal artery trauma due to civilian violence in South Africa.] 

Faris IB, Raptis S, Fitridge R. Arterial injury in the lower limb from blunt trauma. Australia and New Zealand Journal of Surgery 1997; 67: 25–30. [Retrospective study of patients presenting with lower limb injury to a single hospital with the purpose of devising a scoring system predictive outcome.] 

Holmberg A, Milbrink J, Bergqvist D. Arterial complications after knee arthroplasty: 4 cases and a review of the literature. Acta Orthopaedica Scandinavica 1996; 67: 75–8. [Literature review and four case reports of arterial complications after total knee replacement.] 

Popliteal artery entrapment syndrome

Di Marzo L, Cavallero 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. [Retrospective study of patients presenting with popliteal entrapment syndrome to one institution, looking at presentation, management, and outcome.] 

Erdoes LS, Devine JJ, Bernhard VM, Baker MR, Berman SS, Hunter GC. Popliteal vascular compression in a normal population. Journal of Vascular Surgery 1994; 20: 978–86. [Study of young asymptomatic subjects, either normally active or athletically trained, looking at the effect of active and passive dorsi flexion and plantar flexion of the foot on Duplex detected blood flow in the popliteal artery.] 

Turnipseed WD, Pozniak M. Popliteal entrapment as a result of neurovascular compression by the soleus and plantaris muscle. Journal of Vascular Surgery 1992; 15: 285–93. [Review of trained athletes presenting with popliteal artery entrapment to one institution, looking at the usefulness of various investigations and the results of surgery.] 

Cystic adventitial disease

Parks RW, D'Sa AA. Critical ischaemia complicating cystic adventitial disease of the popliteal artery. European Journal of Vascular Surgery 1994; 8: 508–13. [Description of two cases presenting with cystic adventitial disease of the popliteal artery and a review of the subject.]