Results

Results of surgical therapy depend upon the patency of the distal vasculature. More than 80% of

asymptomatic patients have excellent long-term results, whereas 68% of those presenting with lower

extremity ischemia achieve satisfactory long-term outcomes.6

Anastomotic Pseudoaneurysms

Incidence

3 Anastomotic pseudoaneurysms result from a disrupted suture line between a graft and the host artery.

The incidence varies with the location of the anastomosis and the type of graft that is used. Involvement

of the femoral artery accounts for nearly 80% of these lesions, and 3% of all femoral anastomoses or 6%

of femoral anastomoses after aortofemoral bypass develop this complication compared with 0.2% of

aortic anastomoses.14,15 Patient factors that are associated with increased likelihood of developing a

femoral anastomotic aneurysm after aortofemoral bypass include chronic obstructive pulmonary

disease, current smoking, and postoperative groin wound infection.16 After infrainguinal bypass

procedures, the incidence is higher with prosthetic grafts then autogenous vein grafts with 6% of

femoral anastomoses developing aneurysms when Dacron is used compared with 0.9% when a vein

graft is placed.14 Anastomotic pseudoaneurysms are a late complication of bypass procedures; the mean

interval from primary procedure to recognition is more than 6 years.17,18

Pathogenesis

Several factors contributing to anastomotic pseudoaneurysm formation have been identified including

weakness of the arterial wall, the type of graft material and suture utilized, the presence of infection,

the method of construction of the anastomosis, and the stress on the suture line from hypertension, leg

motion, or excess tension on the graft limb.14,17,18 Progressive degeneration of the recipient artery

accounts for most anastomotic pseudoaneurysms, and an increased incidence has been noted following

endarterectomy of the artery at the anastomosis. False aneurysms occur less frequently with saphenous

vein grafts than synthetic vascular grafts, a reflection of more complete healing of autogenous tissue.

With the use of monofilament synthetic suture, anastomotic pseudoaneurysms rarely result from a loss

of suture integrity, although occasionally a broken suture is a factor in pseudoaneurysm formation.

Although most anastomotic aneurysms are not accompanied by overt graft infection, occult infections

with coagulase-negative Staphylococcus species may be an important factor in development of

anastomotic aneurysms.18 A higher incidence is noted in patients with wound healing complications, and

the use of anticoagulants may increase such complications.

Clinical Manifestations

Femoral anastomotic pseudoaneurysms usually present as a pulsatile groin mass, which may or may not

be accompanied by pain, redness, or symptoms of venous obstruction. Acute complications include

hemorrhage, embolization, and occlusion. The latter may cause lower extremity ischemia with

claudication, rest pain, or gangrene.

Diagnosis

The diagnosis of a false aneurysm is usually made on physical examination by the presence of a pulsatile

groin mass in a patient who has undergone a femoral arterial reconstructive procedure. The differential

diagnosis includes nonpulsatile groin masses, such as hernia, lymphocele, or abscess, through which

pulsation is transmitted from an underlying normal femoral artery. Diagnosis of an anastomotic

disruption in one region should raise suspicion of other anastomotic pseudoaneurysms as multiple

lesions are found in at least 30% of patients.17 The presence of multiple anastomotic pseudoaneurysms

suggests infection. Evaluation of an anastomotic aneurysm includes ultrasonography or CT of all

anastomoses of the graft. Angiography done prior to repair of the anastomotic aneurysm is helpful in

defining the proximal and distal arterial anatomy (Fig. 97-2).

Treatment

Because of the progressive nature of anastomotic pseudoaneurysms, surgical treatment is generally

undertaken for all lesions >2 cm except those in high-risk patients. Principles of surgical therapy are

those of primary aneurysms: obtain proximal and distal control and replace the aneurysmal segment.

Securing proximal control often requires dividing the inguinal ligament to isolate the graft limb. Distal

control is most easily obtained using intraluminal balloon catheters. If intrinsic arterial disease requires

extension of the graft distally on the profunda femoris or superficial femoral artery, these arteries can

2780

be identified by dissection through unscarred tissue distal to the previous exposure. After débridement

of the degenerated artery, an interposition graft is placed between the prosthetic graft limb and the

healthy native artery. Cultures of the graft and vessel wall are essential to exclude infection as an

etiologic factor in the development of the anastomotic aneurysm. If infection is obvious at the time of

surgery, the approach is the same as that of any infected graft with removal of infected prosthetic

material and reestablishment of blood flow, if necessary, with a bypass through an uninfected tissue

route, such as an obturator, lateral femoral, or axillofemoral bypass.

Figure 97-2. Arteriogram demonstrating bilateral femoral anastomotic aneurysms after an aortofemoral bypass and a left

femoropopliteal bypass.

Results

Results of elective operations on uncomplicated anastomotic aneurysms are excellent with 2% operative

mortality, 97.5% graft patency at 2 years, and 2% amputation within 2 years of surgery.17 Recurrence is

reported in less than 16% of cases.14,15 Patients presenting with aneurysms complicated by hemorrhage,

occlusion, or embolization have significantly increased operative morbidity and mortality.

Femoral Pseudoaneurysms

Incidence

The femoral artery is the preferred site for percutaneous access for both diagnostic and therapeutic

angiography including endovascular grafts. In recent years, diagnostic studies for coronary and

peripheral artery occlusive disease have increased as have the subsequent endovascular interventions,

which have resulted in an increased number of femoral pseudoaneurysms. Because interventional

techniques often require prolonged arterial cannulation, large-bore sheaths, and anticoagulation, they

are accompanied by a higher rate of arterial complications than are diagnostic studies. Review of recent

experience shows that pseudoaneurysms form after about 0.3% of diagnostic catheterizations and about

1.5% of catheter-based therapeutic procedures.4,19 The use of percutaneous closure devices decreases the

risk of developing a pseudoaneurysm at the arterial access site for an interventional procedure by a

factor of 10 to an incidence of about 0.1%.20,21

Pathogenesis

4 Pseudoaneurysms from iatrogenic catheter trauma are classically defined as collections of blood in

continuity with the arterial system that is not enclosed by all three layers of the arterial wall. These

lesions form because of failed hemostasis at the arterial wall defect created by sheath insertion.

Normally, hemostasis, aided by direct focal application of pressure or hemostatic devices, seals the

defect promptly, and the arterial wall repairs itself. When hemostasis is not successfully obtained, blood

under arterial pressure leaks from the artery, dissects surrounding tissue planes, and forms what is

perceived on physical examination to be a pulsatile mass. The gross findings at surgery are a blood2781

filled cavity surrounded by a capsule. Like all pseudoaneurysms, these lesions can cause symptoms by

rupture or compression of surrounding structures.

Diagnosis

The diagnosis of femoral pseudoaneurysm is suspected when a pulsatile groin mass is noted after

arterial catheterization. The differential diagnosis includes hematoma, lymphadenopathy, and abscess.

Arterial duplex scanning or CT is typically used to establish the diagnosis, differentiate pseudoaneurysm

from hematoma, and aid in defining the communication between the mass and the arterial lumen.

Color-flow duplex scanning is the diagnostic test of choice, providing accurate diagnosis, localization,

and sizing of the false aneurysms.

Natural History

Color-flow duplex scanning has been used to define the incidence and natural history of

pseudoaneurysms after percutaneous transluminal coronary angioplasty.21 Many pseudoaneurysms will

thrombose spontaneously within 4 weeks; however, this is less likely to occur in anticoagulated patients

and those with pseudoaneurysms more than 2.0 cm in diameter. About 30% of patients with

pseudoaneurysms will require intervention.22

Algorithm 97-1. Management of femoral pseudoaneurysm.

Treatment

Therapy of femoral pseudoaneurysms is influenced by aneurysm size and symptoms, and whether the

patient requires continuous anticoagulation (Algorithm 97-1). Surgical therapy is mandatory for all

pseudoaneurysms that are acutely expanding, compressing adjacent nerves, or compromising the

overlying skin. Proximal and distal arterial control is obtained, and the arterial defect is repaired

directly, rarely requiring placement of more than one or two sutures.

An excellent alternative to a surgical approach, when urgent evacuation of the hematoma and arterial

repair is not required, is the use of ultrasound-directed compression therapy or thrombin injection into

the false aneurysm. The pseudoaneurysm is identified with a color-flow ultrasound probe, and then

compressed with the scan head.23 Real-time observation of flow in the underlying artery allows

compression of the pseudoaneurysm while maintaining flow in the native vessel to prevent arterial

occlusion. Pseudoaneurysm thrombosis is documented by absence of flow signals on release of scanhead pressure in the case of compression therapy. While effective, this can often be quite uncomfortable

for the patient and take upward of 30 minutes of compression by the vascular technologist.

Another nonoperative treatment option of femoral pseudoaneurysms is percutaneous ultrasoundguided injection of 0.5 to 1.0 mL thrombin (1,000 U/mL) into the pseudoaneurysm away from the neck

of the aneurysm.24–26 Thrombin injection avoids the discomfort of prolonged compression and is

effective in anticoagulated patients. Continuous ultrasonographic imaging is used to monitor thrombosis

2782

of the pseudoaneurysm.

Results

Ultrasound-guided compression therapy for femoral pseudoaneurysms results in thrombosis in 80% to

90% of cases. Initial success rate is similar in patients who are anticoagulated and in those who are not,

though long-term success appears to be better in patients not receiving anticoagulant therapy. In one of

the largest series of pseudoaneurysms treated with ultrasound-guided compression, thrombosis was

achieved in 86% of anticoagulated patients, and in 98% of those not anticoagulated, with a 20%

recurrence rate in less than 24 hours in anticoagulated patients.27 Success using this therapeutic

modality requires a knowledgeable ultrasonographer and meticulous postcompression follow-up.

Thrombin injection to induce thrombosis of pseudoaneurysms is successful in 94% to 98% of patients

with thrombosis occurring in less than 1 minute.24–26 This technique can be complicated by arterial

thrombosis if an excessive volume of thrombin is used and may not be appropriate for pseudoaneurysms

with large necks. Remote thromboembolic events are rare and probably are not a result of a systemic

effect of the thrombin. Allergic reactions to bovine thrombin occasionally occur. Large

pseudoaneurysms, greater than 8 cm in diameter, and an associated arteriovenous fistula (AVF) are

predictors of failure with thrombin injection.28

Mycotic Aneurysms

The term mycotic aneurysm is currently used to refer to any infected aneurysm. Mycotic aneurysms

today are often a complication of parental drug abuse, but can follow arterial trauma of any form,

including invasive diagnostic and therapeutic procedures. In the past, septic emboli from bacterial

endocarditis were a major cause of mycotic aneurysmal degeneration, but this is less common today.

With the advent of antibiotics, aneurysms secondary to syphilis or tuberculosis are rare. With the

change in cause, the location of mycotic aneurysms has shifted from central to peripheral arteries with

the femoral artery being the most common site.29,30 The importance of mycotic aneurysms comes from

their propensity to rupture.

Pathogenesis

The pathogenesis of mycotic aneurysms can be divided into four major categories, although other less

common causes also exist.29 First, septic emboli from bacterial endocarditis may lodge in normal

arteries, causing infection that weakens the arterial wall, resulting in aneurysm formation. These lesions

are often multiple. Second, during an episode of bacteremia, microorganisms may lodge in a preexisting atherosclerotic plaque or aneurysm and begin to multiply with the same result. A third cause of

mycotic aneurysms is the contiguous spread of bacteria from a local abscess. The inflammatory process

destroys the arterial wall, causing pseudoaneurysm formation. Finally, trauma to the artery with

concomitant contamination may result in formation of an infected pseudoaneurysm. This mechanism of

mycotic aneurysm formation is being seen more frequently, coincident with the increased use of

catheter-based procedures. Bacteria may be introduced concomitantly with needle puncture or by

migration during prolonged arterial catheterization. Mycotic aneurysms accompanying drug abuse may

be secondary to direct contamination of the arterial wall, or they may result from destruction of the

vessel wall by a local abscess.

The bacteriology of arterial infections depends upon the cause of the lesion. Aneurysms secondary to

bacterial endocarditis grew Pneumococcus, Streptococcus, and Enterococcus species most frequently in the

past; but recently Staphylococci, Salmonella, Escherichia coli, and Proteus organisms also have been

cultured.29 Staphylococcus aureus is the most common pathogen in mycotic femoral artery aneurysms

secondary to trauma and drug abuse, occurring in more than 65% of cases.31 In this population, at least

50% of the S. aureus organisms are resistant to methicillin.

Clinical Manifestations

The typical patient with a mycotic femoral aneurysm presents with a history of chills and fever, and a

tender, enlarging, pulsatile groin mass. The patient may have a history of intravenous drug use, recent

arterial catheterization, penetrating trauma, or bacterial endocarditis. Local signs of infection, including

tenderness, erythema, and warmth are noted on physical examination. Lower extremity edema may

occur secondary to venous or lymphatic obstruction. Petechial skin lesions, splinter hemorrhages,

cutaneous abscesses, and septic arthritis may occur as a result of emboli originating from a mycotic

aneurysm. A “sentinel bleed” may occur and signals impending rupture and life-threatening

2783

hemorrhage. Emergency surgery is indicated.

Diagnosis

The diagnosis of a mycotic aneurysm is usually straightforward, but distinguishing an abscess adjacent

to the femoral artery from a femoral mycotic aneurysm may be difficult. In the patient with a pulsatile

groin mass, laboratory findings including a leukocytosis, elevated erythrocyte sedimentation rate, and

positive blood cultures are suggestive, but not specific, for a mycotic aneurysm. Multiple blood cultures

or downstream arterial blood cultures may be necessary to yield positive results. Ultrasonography and

CT angiography are helpful in establishing the diagnosis of an aneurysm (Fig. 97-3), but lack precision

in distinguishing infected from bland aneurysms. The diagnosis of a mycotic aneurysm is confirmed at

operation by demonstration of organisms on Gram stain or by positive cultures of the aneurysm wall.

Treatment

Mycotic aneurysms represent a serious life- and limb-threatening disease because their natural history is

one of expansion and rupture. Therefore, mycotic aneurysms should be addressed surgically. The goal of

treatment is eradication of the infection by excision of the aneurysm and débridement of adjacent

infected tissue as well as by long-term antibiotic therapy. Second, adequate distal circulation must be

restored. Before operative intervention is performed, the patient is started on antibiotics that are

modified based on sensitivity testing of intraoperative cultures. Stent grafts have been used in selected

cases of mycotic aneurysms when other approaches were not feasible; however, concern about latent

infection of the stent graft oftentimes renders this more of a bridging technique than a long-term

solution.

Figure 97-3. Computed tomography scan of an infected femoral anastomotic aneurysm that was diagnosed 5 years after

aortofemoral graft placement.

The complexity of the operative procedure varies with the location and extent of the mycotic

aneurysm. Although a direct approach to the femoral artery may be taken, a retroperitoneal exposure of

the distal external iliac artery for proximal control is sometimes preferred for large or proximal femoral

lesions to avoid excessive hemorrhage. When an infected femoral artery aneurysm is confined to only

one arterial segment (common, superficial, or deep femoral artery), the aneurysm is excised and the

proximal and distal arteries are ligated in emergent situations. In these cases in which an isolated

arterial segment is ligated, severe ischemia resulting in amputation is unusual. In more than 50% of

cases, however, the mycotic aneurysm involves the femoral artery bifurcation, and treatment requires

resection of the femoral bifurcation and débridement to healthy arterial wall. The distal external iliac or

proximal common femoral artery, as well as the superficial and deep femoral arteries, are oversewn

with nonabsorbable monofilament suture. This results in significant ischemia in most patients, but with

the patient heparinized, symptoms gradually improve as collateral circulation increases. The majority of

patients will not need revascularization for limb salvage,31 but up to one-third of patients will have

limb-threatening ischemia.32 In patients in whom sepsis can be adequately controlled at the initial

procedure, aggressive débridement may be followed by immediate revascularization using autogenous

saphenous vein graft as the conduit and covering the graft with a sartorius muscle flap.32 Another

option is to observe patients for 24 hours after arterial ligation and selectively revascularize only those

2784

patients in whom limb-threatening ischemia persists. Use of prosthetic material is avoided because of

the high incidence of early and late septic complications, though can occasionally be necessary through

uninfected tissue planes such as the obturator or lateral femoral route. Antibiotics are begun

preoperatively and continued for at least 6 weeks postoperatively.

POPLITEAL ARTERY ANEURYSMS

5 Popliteal aneurysms are limb-threatening lesions, the vast majority of which are degenerative in

etiology. Occasionally, anastomotic or traumatic popliteal aneurysms, and rarely mycotic aneurysms,

are encountered in contemporary clinical practice. The remainder of this section addresses only

popliteal aneurysms that are degenerative in etiology.

Incidence

Popliteal artery aneurysms are the most common degenerative true peripheral aneurysm. They occur

slightly more frequently than femoral artery lesions; however, popliteal aneurysms are relatively

unusual compared to abdominal aortic aneurysms. Aortic aneurysms are diagnosed with about 10 times

the frequency of popliteal aneurysms.33,34

Pattern of Disease

Like patients with femoral artery aneurysms, multiple aneurysms occur frequently in patients with

popliteal aneurysms. About 60% to 70% of patients have bilateral popliteal aneurysms, and 55% have

extrapopliteal aneurysms.35,36 Abdominal aortic aneurysms are encountered in 40% to 50%, and are

particularly common in patients with bilateral popliteal aneurysms, of whom about 70% have aortic

aneurysms.35–37 Femoral artery aneurysms occur in nearly 40% of patients.36,37 The importance of this

multiplicity of aneurysms is that they may be missed on physical examination. Therefore, their presence

must be determined by other studies, such as ultrasonography or CT, so that potentially life-threatening

abdominal aortic aneurysms and other limb-threatening lesions are identified and managed

appropriately. Even when popliteal aneurysms are initially asymptomatic, patients will develop

symptoms at a mean rate of 14% per year, and one-third will develop complications requiring emergent

intervention within 5 years, resulting in poorer outcomes for both life and limb.38,39

Clinical Manifestations

The typical patient with a popliteal aneurysm is a male in his 60s or 70s with the usual risk factors for

atherosclerosis. Of patients with popliteal aneurysms, 50% to 75% are smokers, 40% to 60% have

hypertension, and about 15% have diabetes mellitus.35–37,40 Other manifestations of cardiovascular

disease are also common, with 10% of patients having manifestations of cerebrovascular disease and

more than 40% having evidence of significant cardiac disease.37

The clinical manifestations of popliteal artery aneurysms range from an asymptomatic pulsatile mass

to severe lower extremity ischemia. About 40% of patients are asymptomatic at diagnosis.7 More than

50% of patients present with symptoms of limb ischemia, usually claudication, but the ischemia may be

more advanced and manifested as rest pain or gangrene. Local symptoms, including sensation of a mass,

local pain, and leg swelling or phlebitis secondary to compression of the adjacent vein, account for the

remainder of symptoms. A popliteal artery aneurysm may be complicated by thrombosis, embolization,

or rarely rupture. Thrombosis is reported in approximately 40% of patients,36 and embolization occurs

in about 25% of cases.36 Some patients present with classic “blue toe syndrome,” but more commonly,

repeated episodes of embolization occlude the outflow vessels and result in thrombosis of the aneurysm.

Rupture occurs in fewer than 5% of popliteal aneurysms;35,36 and in these cases, the hemorrhage is

usually confined to the popliteal space, thus permitting surgical intervention and arterial reconstruction

in a timely fashion.

Natural History

The natural history of popliteal aneurysms is not well defined because most series are composed

primarily of aneurysms that have been treated surgically. In a review of 29 reports in the English

literature published between 1980 and 1994, subgroups of patients were identified whose aneurysms

had been observed.7 A mean of 35% of patients with conservative follow-up developed ischemic

complications, and 25% of these required amputation even with modern therapy. Thus, a significant

2785

percentage of popliteal aneurysms will develop a complication if left untreated, and although this is no

patients in whom limb-threatening ischemia persists. Use of prosthetic material is avoided because of

the high incidence of early and late septic complications, though can occasionally be necessary through

uninfected tissue planes such as the obturator or lateral femoral route. Antibiotics are begun

preoperatively and continued for at least 6 weeks postoperatively.

POPLITEAL ARTERY ANEURYSMS

5 Popliteal aneurysms are limb-threatening lesions, the vast majority of which are degenerative in

etiology. Occasionally, anastomotic or traumatic popliteal aneurysms, and rarely mycotic aneurysms,

are encountered in contemporary clinical practice. The remainder of this section addresses only

popliteal aneurysms that are degenerative in etiology.

Incidence

Popliteal artery aneurysms are the most common degenerative true peripheral aneurysm. They occur

slightly more frequently than femoral artery lesions; however, popliteal aneurysms are relatively

unusual compared to abdominal aortic aneurysms. Aortic aneurysms are diagnosed with about 10 times

the frequency of popliteal aneurysms.33,34

Pattern of Disease

Like patients with femoral artery aneurysms, multiple aneurysms occur frequently in patients with

popliteal aneurysms. About 60% to 70% of patients have bilateral popliteal aneurysms, and 55% have

extrapopliteal aneurysms.35,36 Abdominal aortic aneurysms are encountered in 40% to 50%, and are

particularly common in patients with bilateral popliteal aneurysms, of whom about 70% have aortic

aneurysms.35–37 Femoral artery aneurysms occur in nearly 40% of patients.36,37 The importance of this

multiplicity of aneurysms is that they may be missed on physical examination. Therefore, their presence

must be determined by other studies, such as ultrasonography or CT, so that potentially life-threatening

abdominal aortic aneurysms and other limb-threatening lesions are identified and managed

appropriately. Even when popliteal aneurysms are initially asymptomatic, patients will develop

symptoms at a mean rate of 14% per year, and one-third will develop complications requiring emergent

intervention within 5 years, resulting in poorer outcomes for both life and limb.38,39

Clinical Manifestations

The typical patient with a popliteal aneurysm is a male in his 60s or 70s with the usual risk factors for

atherosclerosis. Of patients with popliteal aneurysms, 50% to 75% are smokers, 40% to 60% have

hypertension, and about 15% have diabetes mellitus.35–37,40 Other manifestations of cardiovascular

disease are also common, with 10% of patients having manifestations of cerebrovascular disease and

more than 40% having evidence of significant cardiac disease.37

The clinical manifestations of popliteal artery aneurysms range from an asymptomatic pulsatile mass

to severe lower extremity ischemia. About 40% of patients are asymptomatic at diagnosis.7 More than

50% of patients present with symptoms of limb ischemia, usually claudication, but the ischemia may be

more advanced and manifested as rest pain or gangrene. Local symptoms, including sensation of a mass,

local pain, and leg swelling or phlebitis secondary to compression of the adjacent vein, account for the

remainder of symptoms. A popliteal artery aneurysm may be complicated by thrombosis, embolization,

or rarely rupture. Thrombosis is reported in approximately 40% of patients,36 and embolization occurs

in about 25% of cases.36 Some patients present with classic “blue toe syndrome,” but more commonly,

repeated episodes of embolization occlude the outflow vessels and result in thrombosis of the aneurysm.

Rupture occurs in fewer than 5% of popliteal aneurysms;35,36 and in these cases, the hemorrhage is

usually confined to the popliteal space, thus permitting surgical intervention and arterial reconstruction

in a timely fashion.

Natural History

The natural history of popliteal aneurysms is not well defined because most series are composed

primarily of aneurysms that have been treated surgically. In a review of 29 reports in the English

literature published between 1980 and 1994, subgroups of patients were identified whose aneurysms

had been observed.7 A mean of 35% of patients with conservative follow-up developed ischemic

complications, and 25% of these required amputation even with modern therapy. Thus, a significant

2785

percentage of popliteal aneurysms will develop a complication if left untreated, and although this is not

synonymous with limb loss, the amputation rate is high.

Figure 97-4. Computed tomography of large right popliteal aneurysm with significant laminar thrombus present.

Diagnosis

The diagnosis of popliteal aneurysm is usually first suspected on physical examination. Palpation of the

popliteal space with the knee flexed reveals a pulsatile mass in approximately two-thirds of patients.

Small aneurysms may not be palpable on physical examination, and if thrombosis has occurred the mass

may be nonpulsatile. Radiographs of the knee demonstrating a calcified arterial wall occasionally

suggest the diagnosis of a popliteal artery aneurysm, but it must be confirmed by duplex

ultrasonography, CT (Fig. 97-4), or MRI. These diagnostic modalities can establish diagnosis of popliteal

artery aneurysms and exclude other entities that could be responsible for a nonpulsatile popliteal fossa

mass (tumor or Baker cyst). Ultrasonography, CT, or MRI is also useful in the detection of associated

aneurysms, particularly abdominal aortic and femoral artery aneurysms. Angiography can be misleading

in the diagnosis of aneurysms because intraluminal thrombus may obscure the true size of the vessel

(Fig. 97-5); however, it is essential for visualization of the inflow and outflow vessels necessary for

revascularization. CT angiography can be a noninvasive way to provide this information (Fig. 97-6).

Treatment

Indications

Surgical treatment is indicated for all symptomatic and many asymptomatic aneurysms. Controversy

exists regarding the optimal management of small asymptomatic popliteal aneurysms because the

natural history is not well defined. The incidence of complications with popliteal artery aneurysms is

high, and the occurrence of complications does not correlate with the size of the aneurysm because the

most common complications are embolization and thrombosis, which are not size related. In fact, in

some reports the average diameter of symptomatic aneurysms is smaller than asymptomatic lesions.40

These considerations, and the significantly higher limb loss rate after complications even when

intervention is undertaken, has resulted in the recommendation for operative treatment when a

popliteal aneurysm is diagnosed.

The goals of surgical treatment are to eliminate the potential for complications and to preserve or

restore adequate blood flow to the limb. In patients with multiple aneurysms, the operative approach

must be individualized. Generally, the life-threatening aortic aneurysm is treated first, followed by

repair of the popliteal aneurysm. On the other hand, if a limb-threatening complication has occurred,

treatment of the popliteal aneurysm usually takes precedence, followed by expeditious aortic aneurysm

repair.

2786

Figure 97-5. Arteriogram demonstrating a popliteal aneurysm associated with occlusion of the outflow tract presumably from

repeated episodes of embolization. A bypass to the distal posterior tibial artery was successful.

Figure 97-6. Computed tomography arteriogram demonstrating right popliteal artery aneurysm and associated inflow and outflow.

Surgical Technique

Most popliteal aneurysms are easily approached through standard medial thigh and calf incisions for

exposure of the distal superficial femoral artery and the distal popliteal artery, respectively. The

proximal anastomosis will need to originate from the common femoral artery if the entire superficial

femoral artery is aneurysmal. Occasionally, the posterior approach is preferred for lesions confined to

the popliteal fossa, especially when accompanied by symptoms due to compression of adjacent

structures. Most aneurysms are left in situ, bypassed using a segment of saphenous vein, and ligated

proximally and distally. The conduit of choice for bypass is autologous saphenous vein, which is

harvested from the thigh, reversed, and tunneled along the course of popliteal artery. The proximal and

2787

distal anastomosis may be either end-to-end or end-to-side in configuration, with the aneurysm excluded

from the circulation by proximal and distal ligatures. Ligation should be adjacent to the aneurysm to

minimize the number of patent collaterals that are in continuity with the aneurysm.41 Late expansion

and rupture of a bypassed and ligated popliteal aneurysm can occur when patent geniculate arteries

continue to perfuse and pressurize the aneurysm. When the distal popliteal and proximal tibial vessels

are occluded with recent emboli, they can sometimes be cleared using a balloon catheter or

intraoperative thrombolytic therapy. Frequently, bypass grafts must be carried to the distal tibial

arteries. Extensive femoral and popliteal aneurysms may require a femoral-popliteal or femoral-tibial

bypass using in situ saphenous vein that originates from a prosthetic graft replacing a common femoral

artery aneurysm.

Popliteal aneurysms have been treated by an endovascular approach. Small series show a primary

patency rate of about 50% at 14 to 18 months,42,43 and a cumulative patency of 74%,44 suggesting that

this approach should be reserved for the more high-risk patient who requires intervention.

6 The patient who presents with an acutely ischemic extremity secondary to popliteal aneurysm

thrombosis is a management challenge. Popliteal aneurysms often thrombose because of repeated

episodes of emboli to the outflow vessels, which result in their occlusion. An expeditious arteriogram

may identify a suitable outflow vessel for the bypass graft. If no target vessel is identified, intra-arterial

thrombolytic therapy should be initiated with the goal of lysing thrombus in the tibial arteries to

identify a suitable outflow vessel for vascular reconstruction. Although the embolic process may be

chronic, results with thrombolytic therapy followed by bypass of the aneurysm have been much better

than surgical therapy alone for the patient with an acutely occluded aneurysm and severe leg ischemia.

Results

Excellent results are obtained in asymptomatic aneurysms with intact distal vasculature. Patients with

thrombosed aneurysms or those in whom multiple episodes of embolization have occluded the tibial

arteries have less optimal results. Operative mortality is in the 0 to 2% range, with asymptomatic

patients fairing better than those presenting with acutely symptomatic lesions.45,46 In patients

undergoing revascularization before ischemic complications occur, 5- and 10-year graft patency rates

are greater than 80% and limb salvage is 93% to 98%.35,47 Graft patency rates in patients undergoing

surgery after developing complications of their aneurysms are 60% and 48% at 5 and 10 years,

respectively, and limb salvage rates are 60% to 80%.35,47–49 Thrombolytic therapy, when successful,

improves primary graft patency in patients presenting with acute limb ischemia.50

References

1. Ashton HA, Buxton MJ, Day NE, et al. The Multicentre Aneurysm Screening Study (MASS) into the

effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial.

Lancet 2002;360:1531–1539.

2. Diwan A, Sarkar R, Stanley JC, et al. Incidence of femoral and popliteal artery aneurysms in

patients with abdominal aortic aneurysms. J Vasc Surg 2000;31:863–869.

3. Trickett JP, Scott RA, Tilney HS. Screening and management of asymptomatic popliteal aneurysms.

J Med Screen 2002;9:92–93.

4. Lange P, Houe T, Helgstrand UJ. The efficacy of ultrasound-guided compression of iatrogenic

femoral pseudo-aneurysms. Eur J Vasc Endovasc Surg 2001;21:248–250.

5. Calligaro KD, Dougherty MJ, Ryan S, et al. Acute arterial complications associated with total hip

and knee arthroplasty. J Vasc Surg 2003;38:1170–1177.

6. Lawrence PF, Lorenzo-Rivero S, Lyon JL. The incidence of iliac, femoral, and popliteal artery

aneurysms in hospitalized patients. J Vasc Surg 1995;22:409–415; discussion 415–416.

7. Lawrence PF, Harlander-Locke MP, Oderich GS, et al. The current management of isolated

degenerative femoral artery aneurysms is too aggressive for their natural history. J Vasc Surg

2014;59(2):343–349.

8. Dawson I, Sie RB, Van Bockel JH. Atherosclerotic popliteal aneurysm. Br J Surg 1997;84:293–299.

9. Faggioli GL, Gargiulo M, Bertoni F, et al. Parietal inflammatory infiltrate in peripheral aneurysms

of atherosclerotic origin. J Cardiovasc Surg (Torino) 1992;33:331–336.

10. Thompson RW, Liao S, Curci JA. Vascular smooth muscle cell apoptosis in abdominal aortic

2788

aneurysms. Coron Artery Dis 1997;8:623–631.

11. Cutler BS, Darling RC. Surgical management of arteriosclerotic femoral aneurysms. Surgery

1973;74:764–773.

12. Jarrett F, Makaroun MS, Rhee RY, et al. Superficial femoral artery aneurysms: an unusual entity?. J

Vasc Surg 2002;36:571–574.

13. Dent TL, Lindenauer SM, Ernst CB, et al. Multiple arteriosclerotic artery aneurysms. Arch Surg

1972;105:338–344.

14. Szilagyi DE, Smith RF, Elliott JP, et al. Anastomotic aneurysms after vascular reconstruction:

problems of incidence, etiology, and treatment. Surgery 1975;78:800–816.

15. Szilagyi DE, Elliott JP Jr, Smith RF, et al. A thirty-year survey of the reconstructive surgical

treatment of aortoiliac occlusive disease. J Vasc Surg 1986;3:421–436.

16. Ylönen K, Biancari F, Leo E, et al. Predictors of development of anastomotic femoral

pseudoaneurysms after aortofemoral reconstruction for abdominal aortic aneurysm. Am J Surg

2004;187:83–87.

17. Dennis JW, Littooy FN, Greisler HP, et al. Anastomotic pseudoaneurysms. A continuing late

complication of vascular reconstructive procedures. Arch Surg 1986;121:314–317.

18. Seabrook GR, Schmitt DD, Bandyk DF, et al. Anastomotic femoral pseudoaneurysm: an

investigation of occult infection as an etiologic factor. J Vasc Surg 1990;11:629–634.

19. Kresowik TF, Khoury MD, Miller BV, et al. A prospective study of the incidence and natural history

of femoral vascular complications after percutaneous transluminal coronary angioplasty. J Vasc Surg

1991;13:328–333; discussion 333–335.

20. Knight CG, Healy DA, Thomas RL. Femoral artery pseudoaneurysms: risk factors, prevalence, and

treatment options. Ann Vasc Surg 2003;17:503–508.

21. La Perna L, Olin JW, Goines D, et al. Ultrasound-guided thrombin injection for the treatment of

postcatheterization pseudoaneurysms. Circulation 2000;102:2391–2395.

22. Kent KC, McArdle CR, Kennedy B, et al. A prospective study of the clinical outcome of femoral

pseudoaneurysms and arteriovenous fistulas induced by arterial puncture. J Vasc Surg 1993;17:125–

131; discussion 131–133.

23. Hertz SM, Brener BJ. Ultrasound-guided pseudoaneurysm compression: efficacy after coronary

stenting and angioplasty. J Vasc Surg 1997;26:913–916; discussion 916–918.

24. Fram DB, Giri S, Jamil G, et al. Suture closure of the femoral arteriotomy following invasive

cardiac procedures: a detailed analysis of efficacy, complications, and the impact of early

ambulation in 1,200 consecutive, unselected cases. Catheter Cardiovasc Interv 2001;53:163–173.

25. Mohler ER 3rd, Mitchell ME, Carpenter JP, et al. Therapeutic thrombin injection of

pseudoaneurysms: a multicenter experience. Vasc Med 2001;6:241–244.

26. Maleux G, Hendrickx S, Vaninbroukx J, et al. Percutaneous injection of human thrombin to treat

iatrogenic femoral pseudoaneurysms: short- and midterm ultrasound follow-up. Eur Radiol

2003;13:209–212.

27. Cox GS, Young JR, Gray BR, et al. Ultrasound-guided compression repair of postcatheterization

pseudoaneurysms: results of treatment in one hundred cases. J Vasc Surg 1994;19:683–686.

28. Kumins NH, Landau DS, Montalvo J, et al. Expanded indications for the treatment of

postcatheterization femoral pseudoaneurysms with ultrasound-guided compression. Am J Surg

1998;176:131–136.

29. Anderson CB, Butcher HR Jr, Ballinger WF. Mycotic aneurysms. Arch Surg 1974;109:712–717.

30. Brown SL, Busuttil RW, Baker JD, et al. Bacteriologic and surgical determinants of survival in

patients with mycotic aneurysms. J Vasc Surg 1984;1:541–547.

31. Gan JP, Leiberman DP, Pollock JG. Outcome after ligation of infected false femoral aneurysms in

intravenous drug abusers. Eur J Vasc Endovasc Surg 2000;19:158–161.

32. Reddy DJ, Smith RF, Elliott JP Jr, et al. Infected femoral artery false aneurysms in drug addicts:

evolution of selective vascular reconstruction. J Vasc Surg 1986;3:718–724.

33. Szilagyi DE, Schwartz RL, Reddy DJ. Popliteal arterial aneurysms. Their natural history and

management. Arch Surg 1981;116:724–728.

34. Ramesh S, Michaels JA, Galland RB. Popliteal aneurysm: morphology and management. Br J Surg

2789

1993;80:1531–1533.

35. Anton GE, Hertzer NR, Beven EG, et al. Surgical management of popliteal aneurysms: trends in

presentation, treatment, and results from 1952 to 1984. J Vasc Surg 1986;3:125–134.

36. Vermilion BD, Kimmins SA, Pace WG, et al. A review of one hundred forty-seven popliteal

aneurysms with long-term follow-up. Surgery 1981;90:1009–1014.

37. Whitehouse WM Jr, Wakefield TW, Graham LM, et al. Limb-threatening potential of

arteriosclerotic popliteal artery aneurysms. Surgery 1983;93:694–699.

38. Michaels JA, Galland RB. Management of asymptomatic popliteal aneurysms: the use of a Markov

decision tree to determine the criteria for a conservative approach. Eur J Vasc Surg 1993;7:136–143.

39. Bowyer RC, Cawthorn SJ, Walker WJ, et al. Conservative management of asymptomatic popliteal

aneurysm. Br J Surg 1990;77:1132–1135.

40. Lowell RC, Gloviczki P, Hallett JW Jr, et al. Popliteal artery aneurysms: the risk of nonoperative

management. Ann Vasc Surg 1994;8:14–23.

41. Ascher E, Markevich N, Schutzer RW, et al. Small popliteal artery aneurysms: are they clinically

significant? J Vasc Surg 2003;37:755–760.

42. Henry M, Amor M, Henry I, et al. Percutaneous endovascular treatment of peripheral aneurysms. J

Cardiovasc Surg (Torino) 2000;41:871–883.

43. Gerasimidis T, Sfyroeras G, Papazoglou K, et al. Endovascular treatment of popliteal artery

aneurysms. Eur J Vasc Endovasc Surg 2003;26:506–511.

44. Tielliu IF, Verhoeven EL, Prins TR, et al. Treatment of popliteal artery aneurysms with the

Hemobahn stent-graft. J Endovasc Ther 2003;10:111–116.

45. Varga ZA, Locke-Edmunds JC, Baird RN, et al. A multicenter study of popliteal aneurysms. Joint

Vascular Research Group. J Vasc Surg 1994;20:171–177.

46. Reilly MK, Abbott WM, Darling RC. Aggressive surgical management of popliteal artery aneurysms.

Am J Surg 1983;145:498–502.

47. Roggo A, Brunner U, Ottinger LW, et al. The continuing challenge of aneurysms of the popliteal

artery. Surg Gynecol Obstet 1993;177:565–572.

48. Dawson I, Van Bockel JH, Brand R, et al. Popliteal artery aneurysms. Long-term follow-up of

aneurysmal disease and results of surgical treatment. J Vasc Surg 1991;13:398–407.