Popliteal artery aneurysm

INTRODUCTION — Aneurysms of the popliteal artery can occur in isolation, or in association with other large vessel aneurysms (eg, abdominal aorta, femoral artery). A popliteal aneurysm is often diagnosed because of screening tests or other imaging studies (other aneurysms, peripheral artery disease) in patients who do not have obvious symptoms of vascular disease. When symptoms are present, they are due to a variable degree of lower extremity ischemic symptoms that can include claudication, distal ischemia due to chronic embolization or acute limb-threatening ischemia due to thrombosis of the aneurysm or acute thromboembolism [1]. Patients with symptomatic popliteal aneurysm should be referred for vascular evaluation and repair. The management of asymptomatic popliteal aneurysms depends upon patient comorbidities, the size of the aneurysm and the presence or absence of arterial thrombus.

Issues related to popliteal artery aneurysms will be reviewed here. The surgical and endovascular management of popliteal aneurysm is discussed separately. (See "Surgical and endovascular repair of popliteal artery aneurysm".)

ANATOMIC ISSUES

Popliteal anatomy — The popliteal artery is in continuity with the superficial femoral artery. Anatomic landmarks include the tendinous insertion of the adductor magnus muscle in the distal femur superiorly, and the bifurcation of the popliteal artery into the anterior tibial artery and tibioperoneal trunk at the level of the tibial tuberosity inferiorly.

Popliteal aneurysms are true aneurysms involving all layers of the vessel wall (intima, media, adventitia). Pseudoaneurysm formation in the popliteal artery has also been described but is rare [2].

Popliteal aneurysms are described as fusiform (ie, diffusely dilated) or saccular (ie, rounded and typically asymmetric). Fusiform dilation of the popliteal artery may be contiguous with fusiform dilation of the superficial femoral artery [3]. Aneurysm shape may have clinical implications. (See 'Rupture' below.)

Definition of popliteal aneurysm — As with any vessel, the popliteal artery is defined as aneurysmal when focal dilation is identified and the diameter of the vessel is increased by more than 50 percent relative to the vessel's normal diameter (figure 1) [4]. The normal diameter of the mid-popliteal artery ranges from 0.7 to 1.1 cm [5,6]. The normal superficial femoral artery (SFA) diameter can be used as a reference if the entire extent of the popliteal artery is aneurysmal. In one ultrasound study, the distal SFA most closely approximated normal mid-popliteal artery diameter [5].

PATHOGENESIS — The media and adventitia provide the strength of the vessel wall. The elements of the extracellular matrix (ECM) of the media, which include elastin, collagen, and glycosaminoglycans (GAGs), bear the circumferential stress imparted by blood pressure on the arterial wall. Smooth muscle of the media (ie, cellular component) produces ECM in response to a variety of factors.

Aneurysm formation — Aneurysm formation is due to a loss of the mechanical integrity of the vessel wall due to an altered balance between the production and degradation of these vascular wall constituents [7]. The etiology of this imbalance is multifactorial and likely a complex interplay of inflammatory, immunologic and potentially mechanical and genetic factors. A common systemic etiology for large vessel (eg, aorta, femoral, iliac, popliteal) aneurysm formation is supported by the occurrence of multiple aneurysms in the same patient.

●Inflammation – Inflammatory infiltrate is seen within the wall of the popliteal artery and is similar to that seen in aortic aneurysms [7,8]. The exact role of the inflammatory process is unknown, although the release of reactive oxygen species and matrix metalloproteinases appears to underlie elastin and collagen degradation. Depletion of medial smooth muscle cells through apoptosis is an important mechanism that reduces extracellular matrix production impairing arterial wall repair [9].

●Immunologic – A dysregulated autoimmune response against components of the aortic wall is postulated to contribute to aneurysm formation. Although autoantigens have been identified within the wall of abdominal aortic aneurysms, the role of autoimmunity in the development of popliteal aneurysms has not been addressed [10].

●Genetic factors – Patients with peripheral aneurysms have a 10 percent familial incidence rate for aneurysms. Males are more likely to be affected than females [11]. Multiple observational studies have also found that patients with arteriomegaly have an increased incidence of aneurysm formation [6,12-15]. These observations, together with an increased incidence of aneurysm formation in multiple genetic conditions, suggest that genetic factors play a role in aneurysmal degeneration of the arterial wall. For abdominal aneurysms, genetic markers for inflammatory mediators have been identified; however, specific mechanisms in the development of popliteal aneurysms are unknown [16].

●Mechanical factors – Mechanical factors are also believed to contribute to the formation of popliteal aneurysm. Abnormal arterial wall stress (due to hypertension), vibration and turbulence may contribute to arterial wall degeneration. Repeated flexion and extension of the knee may be another factor [1].

Turbulent flow distal to a relative stenosis is known to cause vessel dilation in the distal segment (ie, post-stenotic dilatation). Within the lower extremity arterial system, the adductor hiatus and arcuate popliteal ligament may represent areas of relative arterial stenosis. As an example, popliteal entrapment due to abnormal insertions of the thigh muscle tendons can lead to popliteal aneurysm formation, which can be bilateral [17].

Expansion and thrombosis — The natural history of popliteal aneurysm growth is not as well-defined as that of abdominal aortic aneurysm. Aneurysm expansion rates similarly depend upon artery diameter; however, in prospective observational studies, expansion of ectatic (ie, dilated but not aneurysmal) popliteal arteries is generally slow, but variable and difficult to predict. Published expansion rates for small (ie, 1.5 to 2.0 cm) popliteal aneurysms range from 0.7 to 1.5 mm/year while expansion rates for larger aneurysms range from 1.5 to 3.7 mm/year [18-20]. A significant number of popliteal aneurysms do not demonstrate expansion. In one study, for example, 60 of 67 popliteal aneurysms did not demonstrate progression [18]. As with abdominal aortic aneurysm, a concurrent diagnosis of diabetes has been correlated with slower expansion rates.

The presence of mural thrombus within the popliteal aneurysm may have clinical implications. Mural thrombus may be associated with aneurysm enlargement, but it is unclear if the thrombus contributes to the etiology or is merely a byproduct of expansion. The mean growth rate of vessels with and without mural thrombus was 1.9 and 0 mm/year, respectively, in one study [18]. Others have suggested that thrombus increases the risk of embolism and thus thrombus, in addition to size and symptoms, is an indicator of the need for treatment. (See 'Management' below.)

In a retrospective review of thrombosed aneurysms, proximal superficial femoral artery occlusion and limited distal runoff were independent factors associated with popliteal artery thrombosis probably due to stagnant flow [21].

EPIDEMIOLOGY — Popliteal artery aneurysms are the most common true peripheral aneurysm (representing approximately three-fourths), occurring more frequently than femoral artery aneurysms, but less frequently than abdominal aortic aneurysm. The prevalence of popliteal aneurysm in the general population is difficult to determine, but appears to be increasing possibly due to more common use of imaging modalities and an aging population [22]. Men are more commonly affected than women and present at a younger age [23,24]. In one study of hospitalized patients, the incidence of femoral or popliteal artery aneurysms was 7.4 per 100,000 males and 1.0 per 100,000 females [23].

A screening study of 1074 men identified popliteal artery aneurysm in 1 percent [25]. In another screening study of men between the ages of 65 and 74, abdominal aortic aneurysms were identified in 4.9 percent of patients [26]. Of these patients, 6.8 percent had femoral artery aneurysm and 9.6 percent had popliteal artery aneurysm. In a screening study that included more than 19,000 Swedish men over the age of 60, 14.2 percent of those with screening-detected abdominal aortic aneurysms had a popliteal artery aneurysm [27]. While the diameter of the popliteal artery did not correlate with aortic diameter, there was a positive correlation with common iliac artery diameter.

RISK FACTORS — The risk factors for popliteal artery aneurysm are similar to those of other large vessel aneurysms (abdominal aorta, iliac, femoral) and include smoking, hypertension, male sex, advancing age, and arteriomegaly. (See "Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Risk factors'.)

Fifty to 75 percent of patients are smokers and 40 to 60 percent have hypertension [28-30]. Ten percent of patients also have cerebrovascular disease and more than 40 percent have significant cardiac disease [28]. Up to 15 percent of patients with popliteal artery aneurysms have diabetes mellitus; however, diabetes appears to provide a protective effect with slower aneurysm growth rates similar to that seen with abdominal aortic aneurysms [18,31]. (See 'Expansion and thrombosis' above.)

Approximately 40 percent of patients with popliteal artery aneurysms will have an abdominal aortic aneurysm [1,32]. For this reason, patients with popliteal aneurysm should be screened for abdominal aortic aneurysm. (See 'Screening for other aneurysm' below.)

CLINICAL PRESENTATION — The clinical presentation of popliteal artery aneurysm ranges from the finding of an asymptomatic pulsatile popliteal mass on routine physical examination to acute limb-threatening ischemia. (See 'Diagnosis' below.)

Asymptomatic patients — Approximately 30 to 40 percent of patients are asymptomatic at the time of initial diagnosis [1,33]. For some patients, popliteal aneurysm is identified as an incidental finding on a radiologic study (eg, plain film, magnetic resonance imaging) performed for another indication (eg, knee pain) or in the course of evaluating aneurysmal disease elsewhere. (See 'Diagnosis' below.)

Symptomatic patients — Common symptoms related to popliteal artery aneurysm include acute or chronic limb ischemia, and pain or limb swelling related to aneurysm expansion or compression of surrounding structures (algorithm 1). The probability of developing symptoms increases over time, with 60 to 74 percent of patients with popliteal aneurysm developing symptoms these symptoms or experiencing rupture (extremely rare) [1,21,34-38]. Popliteal aneurysms ≥2.0 cm are at a higher risk for thromboembolic events compared with smaller aneurysms [1,39]. Depending upon time course, thrombosis can cause symptoms of acute or chronic limb ischemia as a result of popliteal occlusion, distal embolization, or popliteal stenosis. Symptoms may also develop as a result of localized "mass effect" within the confined space of the popliteal fossa and can include deep vein thrombosis.

Chronic ischemia — Patients can present with claudication to varying degrees as the initial symptom of popliteal aneurysm. Progressive luminal narrowing of the popliteal artery or even occlusion of the popliteal artery from thrombus can cause insidious or more sudden onset of claudication. In one retrospective review, one-third of patients who presented with aneurysm thrombosis had some degree of claudication [21]. Claudication may improve as collateral blood flow develops, or the patient may develop clinical signs of more progressive ischemia (ie, ischemic rest pain, gangrene). Repeated episodes of distal embolization can progressively occlude the outflow vessels (anterior tibial, tibioperoneal trunk), slowing flow and leading to thrombosis of the aneurysm [40]. Some patients initially present with thromboemboli manifested as a "blue toe syndrome". (See "Embolism to the lower extremities", section on 'Blue toe syndrome'.)

If the patient does not develop adequate collateral arterial blood flow around a thrombosed aneurysm, symptoms and signs of chronic limb ischemia will manifest that are indistinguishable from occlusive atherosclerotic disease. Patients with claudication from a thrombosed popliteal aneurysm usually have a more sudden onset of symptoms compared with patients who have atherosclerotic occlusion. Smaller aneurysms may have more of a propensity to thrombose compared with larger aneurysms [41].

Acute ischemia — The most dramatic presentation of popliteal artery aneurysm is acute limb threatening ischemia (ie, pain, pallor, poikilothermia, pulselessness) due to abrupt popliteal aneurysm thrombosis, which occurs in up to one-third of patients who are followed conservatively [1]. Approximately two-thirds of patients with thrombosed popliteal artery aneurysms will present with acute ischemia; the remainder will have chronic symptoms [21]. Embolization of thrombotic debris can also acutely reduce perfusion to the extremity [42]. (See "Clinical features and diagnosis of acute lower extremity ischemia" and "Embolism to the lower extremities".)

Risk factors for popliteal aneurysm thrombosis include diameter >2 cm, the presence of thrombus, and limited distal runoff [1]. The incidence of limb loss ranges between 20 and 60 percent for patients presenting with acute limb ischemia, in spite of timely and adequate treatment [43].

Acute thrombosis of popliteal artery aneurysm has been reported in association with coronavirus disease 2019 (COVID-19) and its multiple variants, likely related to a hypercoagulable state [44]. A COVID-19 test should be obtained in the patient presenting with acute limb ischemia and palpable posterior knee mass. (See "COVID-19: Hypercoagulability" and "COVID-19: Acute limb ischemia".)

Local compressive symptoms — Local symptoms are uncommon unless the aneurysm is large (>3.0 cm). Local pain or a sensation of fullness behind the knee is due to a mass effect from the aneurysm. Patients may experience sensory or motor nerve deficits from compression of the sciatic, tibial, or peroneal nerves [45]. Compression of the popliteal veins can lead to the development of varicose veins, symptoms of phlebitis, or ipsilateral extremity swelling from deep vein thrombosis [46]. (See "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity".)

Rupture — Rupture leading to severe pain behind the knee has historically occurred in fewer than 5 percent of patients [29,47,48]. However, a multicenter study evaluating urgent popliteal artery aneurysm management from 2010 to 2021 reported that 18 percent to presented as ruptured. In most cases, the hemorrhage was usually confined to the popliteal space (image 1) [49]. Saccular aneurysms are thought to have a higher risk for this complication compared with fusiform aneurysms . Popliteal aneurysm rupture into the popliteal vein causing arteriovenous fistula has also been reported [50]. In a review spanning 25 years involving 45 patients with popliteal artery aneurysm rupture, patients with rupture averaged eight years older, had more lung and heart disease, and had a larger mean popliteal artery aneurysm diameter (6.4 versus 3.1 cm) compared with patients with popliteal artery aneurysm treated for other indications [47]. Interestingly, in this review of the initial diagnosis in 27 of the 45 patients, the initial diagnosis was deep vein thrombosis due to swelling in the affected extremity.

DIAGNOSIS — As a part of a routine vascular examination, the popliteal fossae bilaterally should be routinely palpated, ideally with the knee slightly flexed. Sixty percent of patients with popliteal aneurysm have a pulsatile popliteal mass which is located at or above the level of the knee joint. Bilateral popliteal artery aneurysms are present in approximately 50 percent of patients [1,21]. A popliteal aneurysm may not be palpable if the aneurysm is small (ie, <2 cm), or if thrombosis has occurred. The patient should also be examined for clinical signs of distal embolization. The clinical signs of thromboembolism due to popliteal aneurysm are similar to those due to aortic pathologies, which are discussed in detail elsewhere. (See "Thromboembolism from aortic plaque", section on 'Clinical manifestations'.)

The diagnosis of popliteal aneurysm is confirmed with the noninvasive radiographic visualization of an abnormally dilated (ie, ≥1.5 times normal diameter) popliteal artery. Noninvasive imaging can be accomplished with duplex ultrasound, computed tomographic (CT) angiography (image 2), or magnetic resonance (MR) angiography. The choice of modality depends upon institutional resources and the clinical presentation. These modalities can also exclude other entities that present as a popliteal mass (eg, Baker’s cyst) or cause lower extremity pain. (See "Popliteal (Baker's) cyst".)

Duplex ultrasonography is the first-line imaging modality when popliteal aneurysm is suspected. Ultrasound quickly confirms the diagnosis and diameter (image 3) of popliteal aneurysm, provides information about patency (or occlusion) of the popliteal artery and outflow vessels, and identifies the presence (or absence) and nature of thrombus, as well as the presence of coexisting aneurysmal disease. When duplex ultrasonography is not available, CT or MR angiography can be used. Conventional arteriography does not accurately determine aneurysm size when intraluminal thrombus is present and is largely reserved for patients presenting with acute ischemia as discussed below.

Imaging the inflow and outflow vessels is crucial for planning elective popliteal aneurysm repair (image 4). CT and MR angiography are preferred over conventional arteriography to more accurately measure true lumen arterial diameters if endovascular therapy is under consideration and to define surrounding structures, which may have other anatomic abnormalities (eg, abnormal muscle attachments, tumor). These modalities, like duplex ultrasound, can also be used to evaluate the presence of associated aneurysms.

Conventional arteriography is more appropriate for the patient who presents with acute symptoms because it provides an opportunity for thrombolytic therapy, if indicated. Depending upon the severity of ischemia, urgent or emergent arteriography should be performed to identify a suitable outflow vessel for lower extremity revascularization. For patients with non-critical ischemia, the fluoroscopic suite is suitable; however, patients with immediate limb-threatening ischemia (Rutherford IIb, III) should be evaluated in the operating room or hybrid room to facilitate any number of revascularization options. (See 'Role of antithrombotic therapy and thrombolysis' below.)

Noninvasive vascular testing modalities, such as ankle-brachial index, segmental pressures, and pulse volume recordings, do not establish a diagnosis of popliteal aneurysm., These tests are useful, however, for documenting the baseline severity of lower extremity ischemia suggested by the patient's symptoms and clinical examination, as well as for ongoing evaluation after repair. (See "Noninvasive diagnosis of upper and lower extremity arterial disease".)

Screening for other aneurysm — Patients with a popliteal artery aneurysm have a high risk of new aneurysm formation in the contralateral popliteal artery, femoral arteries (image 5), or abdominal aorta [32]. Thus, patients found to have a popliteal aneurysm should be screened with duplex ultrasound for aneurysms at other locations.

A study that followed 465 patients with abdominal aortic aneurysm found that popliteal artery dilation developed in 19 percent for a diameter >12 mm and in 11 percent for diameter >15 mm. In this study, the sensitivity of clinical examination relative to radiologic evaluation was only 26 percent. The specificity of the clinical examination was 90 percent [51].

The incidence of coexistent abdominal aortic aneurysm is approximately 40 percent overall [22,25,26,34,35,52] but much higher with bilateral compared with unilateral popliteal artery aneurysms (50 to 70 versus 25 to 40 percent) [22,32,34,35]. Screening for abdominal aortic aneurysm is discussed in detail elsewhere. (See "Screening for abdominal aortic aneurysm".)

The presence of abdominal aortic aneurysm, ipsilateral iliac, femoral or contralateral popliteal, iliac, or femoral artery aneurysms may impact the management of the popliteal aneurysm.

Differential diagnosis — The differential diagnosis of pain in the region of the knee takes into account the chronicity and location of pain and includes a variety of conditions. (See "Approach to the adult with unspecified knee pain".)

Etiologies that may present as a posterior knee mass (with or without pain) include sarcomas or glomus tumors, Baker cyst, popliteal lymphadenopathy, and popliteal venous aneurysm. Among these, rupture of a Baker cyst can mimic the symptoms of ruptured popliteal artery aneurysm. These entities are easily distinguished from popliteal artery aneurysm on imaging studies, as are other common etiologies for pain or a mass in the knee region. (See "Popliteal (Baker's) cyst" and "Evaluation of peripheral lymphadenopathy in adults".)

Acute limb ischemia from a popliteal artery is indistinguishable clinically from other etiologies, such as more proximal aneurysms, that might lead to distal embolization. CT angiography of the aorta with bilateral lower extremity runoff is often readily available for emergency imaging in most facilities. It provides an excellent way to image concomitant aneurysmal disease in other locations remote from the popliteal artery, in addition to possible thromboembolic sources. (See "Embolism to the lower extremities".)

Patients with symptoms due to a chronically thrombosed popliteal artery aneurysm may be confused with patients with atherosclerotic vascular occlusion or other vascular etiologies. The etiology of occlusion will be obvious on imaging studies. (See "Clinical features and diagnosis of lower extremity peripheral artery disease" and "Nonatheromatous popliteal artery diseases causing claudication or limb-threatening ischemia" and "Overview of peripheral vascular problems in athletes".)

MANAGEMENT — Depending upon the clinical presentation, size of the popliteal artery aneurysm, presence of other aneurysms, and patient factors, popliteal artery aneurysms can be repaired (surgical or endovascular [53,54]) or managed conservatively (algorithm 2).

All patients with popliteal aneurysm should be treated to manage their risk factors. Risk factor reduction is discussed in detail elsewhere. (See "Overview of established risk factors for cardiovascular disease" and "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk" and "Overview of smoking cessation management in adults".)

When to and not to intervene — Popliteal aneurysm repair is indicated for [55,56]:

●All symptomatic aneurysms that present with acute limb ischemia regardless of size, to relieve symptoms and minimize the risk of limb loss.

●Patients with patent popliteal aneurysms ≥2.0 cm in diameter, as these patients have a 30 to 40 percent risk of developing acute ischemic complications which are associated with a high risk for limb loss [1,39,57].

The decision to perform a surgical repair must be balanced against the operative risk of the individual patient. A conservative nonoperative approach is safe in a subset of asymptomatic higher-risk patients with small popliteal aneurysms [58].The choice of procedure and technical issues are discussed in detail separately. (See "Surgical and endovascular repair of popliteal artery aneurysm".)

Small (<2.0 cm in diameter) asymptomatic popliteal aneurysms are typically managed conservatively. The optimal approach remains controversial because the natural history of these smaller aneurysms is not well defined and comparative randomized trials have not been performed [53,59]. Patients may become symptomatic during conservative management [1,30,60-62]. In addition, the presence of thrombus within the aneurysm is associated with the development of symptoms and may also increase the risk of expansion [19,30]. Thus, some clinicians feel the presence of popliteal thrombus supports a decision for repair, and that outcomes are improved with elective repair [61,62]. Others argue for conservative management using serial ultrasound and ongoing antiplatelet therapy. (See 'Role of antithrombotic therapy and thrombolysis' below.)

Patients found incidentally to have a chronically occluded popliteal artery aneurysm and who are asymptomatic or minimally symptomatic are managed medically like patients with occlusive atherosclerotic disease with cardiovascular risk reduction, exercise therapy, and possibly a trial of cilostazol. The popliteal artery aneurysm is not intervened upon. (See "Management of claudication due to peripheral artery disease".)

Patients with chronic critical limb ischemia due to chronic popliteal aneurysm thrombosis or chronic embolization may benefit from lower extremity revascularization and are treated like patients with occlusive atherosclerotic disease and chronic ischemia. (See "Management of chronic limb-threatening ischemia".)

For patients with multiple large vessel aneurysms, the approach must be individualized. Abdominal aortic aneurysm is generally treated first, followed by repair of the popliteal aneurysm unless limb-threatening ischemia is present. While it is likely that popliteal artery aneurysm thrombosis is the cause of the limb-threatening ischemia, embolization to the popliteal artery from an aortic aneurysm cannot be excluded. Thus, once the popliteal aneurysm repair is completed, aortic aneurysm repair should be undertaken as soon as possible [63].

In the setting of concomitant ipsilateral common or superficial femoral artery aneurysms, popliteal artery aneurysms are typically repaired at the same time using a bypass procedure. Contralateral peripheral aneurysms are usually treated in a staged fashion. (See "Surgical and endovascular repair of popliteal artery aneurysm".)

Role of antithrombotic therapy and thrombolysis — Systemic anticoagulation, using intravenous heparin (or alternative agent as indicated), should be initiated immediately in patients diagnosed with popliteal artery aneurysm who have evidence of acute thrombosis, distal embolization, or chronic critical limb ischemia. This approach is recommended by the 2012 American College of Chest Physicians (ACCP) guideline on antithrombotic therapy for peripheral artery disease and the 2007 TASC II consensus document for the management of acute ischemia in peripheral artery disease [64].

Intra-arterial thrombolytic therapy (catheter-directed or direct intraoperative) is indicated if arteriography demonstrates no target vessel or multiple distal thrombi are seen [42,65-73]. Many clinicians would not use lytic therapy on a patient who has adequate vein conduit and an appropriate target vessel because dissolution of the thrombus with distal showering can compromise the outflow, which may or may not be recovered [65]. The number of patent tibial arteries, has and continues to remain, significant for long-term limb salvage and survival. (See "Embolism to the lower extremities", section on 'Intra-arterial thrombolysis'.)

A select group of patients who have undergone successful thrombolysis for complications related to a popliteal aneurysm but who are not immediate candidates for surgical or endovascular repair may benefit from ongoing anticoagulation, either as a bridge to definitive treatment or long-term if the patient is not deemed suitable for endovascular or open repair. The use of other novel oral anticoagulants (NOACs), such as rivaroxaban or apixaban, have not been specifically studied in patients with successful thrombolysis of acutely occluded popliteal artery aneurysms. The safety profile of NOACs, however, may make them attractive for consideration in this patient population.

The use of warfarin in patients with asymptomatic popliteal artery aneurysm has not been well studied and is not recommended. Only one small study found a lower incidence of thrombus formation in patients with popliteal artery aneurysm treated with warfarin compared with antiplatelet therapy; however, the number of events was small [19]. It should be noted, however, that with aneurysms in other locations, anticoagulation has not been found to decrease the incidence of distal thromboembolism, and some speculate that it may actually increase the incidence of events.

The role of antiplatelet therapy in the treatment of popliteal artery aneurysm is not defined. Antiplatelet therapy is indicated for secondary prevention in patients with risk factors of cardiovascular disease and could potentially limit the development of luminal thrombus in patients managed conservatively. Randomized trials are needed to determine the role, if any, of antithrombotic therapy in the conservative management of small popliteal artery aneurysms.

Surveillance ultrasound — Patients who do not have an indication for popliteal aneurysm repair should be followed with serial physical examination and duplex ultrasonography. Surveillance duplex scanning should be performed every 6 to 12 months in patients with a popliteal aneurysm who are managed conservatively. A scanning interval of 12 months has been suggested for patients with popliteal arteries <1.69 cm and every 6 months for those ≥1.7 cm [19]. Rather than basing ultrasound frequency only on strict size criteria, clinicians can be flexible around this diameter threshold. Intervals can be customized with other factors influencing the surveillance interval such as risk factors for aneurysm expansion (eg, hypertension, contralateral popliteal aneurysm repair, presence of other large vessel aneurysm), or decreased aneurysm expansion (diabetes) [18]. (See 'Expansion and thrombosis' above.)

In a review of 65 patients with popliteal artery aneurysms, a multivariate analysis identified presenting size >20 mm in diameter, presence of luminal thrombus, or atrial fibrillation as factors that may indicate a need to scan at more frequent intervals [74]. While expansion rates are heterogenous in patients with popliteal artery aneurysms, patients with known abdominal aortic aneurysm (AAA) have faster expansion compared with those who do not have coexistent AAA (about 3.5 mm/year versus about 0.8 mm/year) [75]. Patients with AAA and popliteal artery aneurysm may also warrant closer follow-up. While popliteal aneurysms are seen less frequently in women, women were less likely to have bilateral popliteal aneurysms, but more likely to develop symptoms even if the popliteal artery was <2.0 cm [76].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Aortic and other peripheral aneurysms".)

SUMMARY AND RECOMMENDATIONS

●Popliteal artery aneurysms are the most common true peripheral aneurysm. The popliteal artery is defined as aneurysmal when a localized diameter is 1.5 times normal artery diameter. Risk factors for popliteal aneurysm include smoking, hypertension, male sex, advancing age, other large vessel aneurysm, and arteriomegaly. (See 'Epidemiology' above and 'Anatomic issues' above.)

●Arterial obstruction as a complication of a popliteal artery aneurysm may be due to popliteal artery thrombosis or distal embolization of intraluminal thrombus. The time course of ischemic symptoms can be acute presenting as limb-threatening ischemia (a surgical emergency), or chronic if sufficient collateral flow is established around areas of occlusion. (See 'Clinical presentation' above.)

●The diagnosis of popliteal aneurysm is based upon noninvasive radiographic visualization of an abnormally dilated (ie, ≥1.5 times normal diameter) popliteal artery. Duplex ultrasound is the initial test of choice, although CT angiography or MR angiography may also be appropriate depending upon availability of ultrasound, and the urgency of the clinical situation. Conventional arteriography alone does not reliably demonstrate the presence of an aneurysm but is essential for performing endovascular repair or thrombolysis, if indicated, and is helpful if CT angiography does not adequately define inflow and outflow arterial targets. (See 'Diagnosis' above.)

●For patients with acute lower extremity ischemic symptoms due to popliteal aneurysm (any size), we recommend emergency popliteal aneurysm repair due to the high risk of limb loss without treatment (Grade 1A). We suggest thrombolytic therapy prior to repair for patients with absent or limited distal runoff; restoration of outflow improves the long-term patency of revascularization (Grade 2C). Thrombolytic agents can be administered intraoperatively or using catheter-based techniques depending upon the clinical scenario. The patient should be systemically anticoagulated while awaiting repair. (See 'Management' above.)

●For patients with patent popliteal aneurysm ≥2.0 cm (algorithm 2), we suggest elective repair of the aneurysm over conservative management for patients at low risk for perioperative surgical morbidity (Grade 2B). Elective aneurysm repair is associated with a lower long-term risk of limb-threatening ischemia and limb loss. (See 'Management' above.)

●Patients with popliteal aneurysm <2.0 cm are typically observed. However, the presence of mural thrombus may increase the propensity for artery expansion and risk of thromboembolic complications. The role of antiplatelet and anticoagulant therapy in the conservative management of small popliteal artery aneurysms, and particularly those with mural thrombus, has not been defined. As such, some clinicians prefer to repair popliteal aneurysm <2.0 cm when they are associated with significant thrombus. (See 'Management' above.)

●We perform serial physical examination and duplex ultrasonography every 6 to 12 months for patients who are managed conservatively. The time interval between examinations depends on the risk factors for expansion. (See 'Surveillance ultrasound' above.)