Figure 97-1. Arteriogram demonstrating bilateral femoral artery aneurysms that extend into the superficial femoral arteries. Unlike many patients with femoral artery aneurysms, this patient did not have an associated aortic aneurysm or popliteal aneurysms.
Surgical Strategy. The operative approach is individualized based on associated aneurysmal disease. In patients with multiple asymptomatic aneurysms, treatment is staged. The life-threatening aortic lesions are treated before limb-threatening femoropopliteal lesions. Femoral artery aneurysms are addressed after popliteal lesions unless the femoral aneurysm is repaired in combination with treatment of the aortic or popliteal aneurysm. If an aortofemoral bypass is necessary, the femoral aneurysm should be treated at the same time, to avoid later anastomotic aneurysm formation. The graft limb can be anastomosed into an interposition graft that has replaced the femoral aneurysm. Similarly, if a stent graft is placed for treatment of an abdominal aortic aneurysm in a patient with femoral artery aneurysms, the aneurysm should be repaired with an interposition graft. In patients with severe lower extremity ischemia, the femoral aneurysm is treated with an interposition graft, from which the proximal anastomosis of the required femoropopliteal or femorotibial bypass is based.
Technique. The operative procedure for treatment of an isolated femoral artery aneurysm is determined by aneurysmal involvement of the superficial and deep femoral arteries as well as by the existence of lower extremity occlusive disease. The femoral artery aneurysm is usually approached through a longitudinal groin incision. When addressing an unusually large aneurysm or a ruptured aneurysm, however, initial proximal control of the external iliac artery through a retroperitoneal approach is advisable. After proximal and distal arterial control is obtained, the aneurysm sac is opened and the atheromatous debris removed. Small aneurysms may be excised, but routine excision of large aneurysms is not recommended as these lesions can often be adherent to the adjacent vein and nerve. For type I aneurysms, the preferred treatment is reconstruction with an interposition graft of Dacron or expanded polytetrafluoroethylene with the proximal anastomosis at the distal external iliac artery or proximal common femoral artery and the distal anastomosis at the femoral bifurcation.
For type II aneurysms with patent superficial and profunda femoris arteries, an interposition graft to the profunda femoris artery with reimplantation of the superficial femoral artery is one standard configuration. If the superficial femoral artery is chronically occluded and the patient has minimal symptoms, an interposition graft to the profunda femoris artery alone is sufficient. If the patient has severe lower extremity ischemia, this is typically followed by a standard distal reconstruction. If recent emboli or in situ thrombosis have occluded the outflow tract, percutaneous mechanical thromboembolectomy or catheter-directed thrombolytic therapy is useful before open arterial reconstruction is undertaken.
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
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.17,18Anastomotic 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.
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.
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.
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).
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 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 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.
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
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 blood-filled cavity surrounded by a capsule. Like all pseudoaneurysms, these lesions can cause symptoms by rupture or compression of surrounding structures.
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.
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
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 scan-head 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 ultrasound-guided 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 of the pseudoaneurysm.
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
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.
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 pre-existing 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.
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 hemorrhage. Emergency surgery is indicated.
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.
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.