Classification and Etiology

Nearly all primary arterial infections result in the formation of aneurysms or pseudoaneurysms. Osler coined the term mycotic aneurysm in 1885 to describe infected aortic arch aneurysms containing “fresh fungal vegetation” in a patient who had concomitant aortic valve vegetations.² While “mycotic” aneurysms apply only to the subset of individuals with infected aneurysms caused by septic emboli, the term has been loosely applied to include all infected aneurysms, regardless of etiology. This practice is confusing and prevents meaningful comparison of the numerous small series of infected aneurysms reported in the modern literature.

The most widely accepted classification of arterial infections was introduced by Wilson et al. in 1978.³ In keeping with the traditional definition introduced by Osler, the authors classified a mycotic aneurysm as one that occurred in an otherwise normal, nonaneurysmal artery as a result of septic emboli of endocardial origin. A preestablished aneurysm that became infected as a result of bacteremia is classified as an infected aneurysm. Microbial arteritis refers to infection of a normal or atherosclerotic (i.e., nonaneurysmal) artery that has become infected as a result of bacteremia. This most often results in rupture with formation of a pseudoaneurysm. Traumatic infected aneurysms include infected aneurysms due to trauma or iatrogenic injury (e.g., complications of arteriography). Contiguous arterial infection is due to direct extension of an adjacent infection into the wall of the artery, such as infected aortitis associated with vertebral osteomyelitis. The specific classification based on etiology will be acknowledged wherever appropriate in this chapter. However, for purposes of clarity and simplification, the generic term infected aneurysm will be applied to include all arterial infections discussed.

The etiology of infected aneurysms has changed in the past 150 years. In the pre-antibiotic era, 86% of patients with arterial infections had evidence of endocarditis.⁴ Following widespread use of antibiotics, the incidence of infective endocarditis has relegated the true mycotic aneurysm to a rare entity. In 1984, Brown and associates reported a collective series of infected aneurysms based on a search of the English literature.⁵ The etiology could be determined in 75% of the 180 subjects. The authors separated the reported experience into cases occurring before 1965 and those occurring since that time. Accuracy of the results suffers because of important differences in diagnosis and reporting frequency between the two periods. Nevertheless, this collective experience remains the largest comparative analysis of infected aneurysms to date. In the earlier part of the series, endocarditis was still the leading cause of infected aneurysms, but arterial trauma of all types became the leading cause after 1965. The authors attributed this etiological shift to a substantial change in the pattern of antibiotic use for treatment of sepsis and trauma.⁵ Other explanations include an increased prevalence of intravenous drug abuse and the widespread application of transarterial interventional procedures. The increase in interventional procedures was particularly notable after the pioneering work of Grunzig and others in the 1970s. The enthusiasm for endovascular technology seen in recent years suggests that arterial trauma may soon become an even more important cause of arterial infection.

Pathogenesis of Infected Aneurysms

The basic mechanisms leading to formation of infected aneurysms have been studied most extensively in the abdominal aorta. Chronic uninfected abdominal aortic aneurysms (AAAs) are thought to form as a result of both destruction of medial elastin and adventitial collagen (see Chapter 37).⁶ Elastolytic matrix metalloproteinases (MMPs) play a central role, leading to initial aortic dilation.⁶ Collagenase MMP leads to collagen failure that eventually leads to gross enlargement and eventual rupture of the AAA. The extensive transmural infiltration typically seen in noninfected AAAs suggests that inflammation and immune responses play a significant role in AAA formation.⁷ Interestingly, infectious causes have also been postulated: histochemical studies have demonstrated that as many as 55% of AAAs harbor Chlamydia pneumoniae.⁷ Thus, it appears that infected and noninfected AAAs may represent two ends of the same spectrum, with progression to infection depending on organism virulence and host resistance.

A number of important clinical differences have been noted between infected and uninfected aneurysms of the abdominal aorta. In contrast to chronic AAA, infected AAAs follow a more rapid course, have a predilection for the suprarenal aorta, and may be isolated to a small segment of an otherwise normal aorta. Recent studies have revealed a number of interesting findings related to the etiology of infected AAA. First, Buckmaster et al. have shown that elastolytic activity is derived from host leukocytes, not from the infectious organisms.⁸ However, infectious organisms play a central role in collagen degradation. Many bacterial isolates produce collagenases,⁹ and bacteria are capable of activating the collagenase promoter in macrophage-like cells.¹⁰ Furthermore, a variety of bacterial proteases activate MMP-1, MMP-8, and MMP-9.⁹ Therefore, infected AAAs appear be the consequence of bacterial proteases causing rapid collagen breakdown in a previously normal aorta.⁹ The collagenase activity may be relatively localized, leading to formation of a saccular AAA or pseudoaneurysm in an otherwise normal appearing vessel. Collagenase activity may also be intensive, which may explain the rapid course associated with infected AAAs. The reason infected AAAs are predisposed to the suprarenal aorta has not been elucidated.

Pathological findings of infected aortic aneurysms have been described by Hsu and Lin.¹¹ Typical findings included aortic atherosclerosis, acute suppurative inflammation, neutrophil infiltration, and bacterial clumps. Two thirds of patients in their series showed acute inflammation superimposed on severe chronic atherosclerosis; the remainder showed atherosclerosis with chronic inflammation or pseudoaneurysms.

Anatomical Location

In their classic 1984 study, Brown and associates documented 243 infected aneurysms in 180 patients in the following distribution: 38% femoral artery, 31% abdominal aorta, 8% SMA, 7% brachial artery, 6% iliac artery, 5% carotid artery, 3% ulnar/radial arteries, 1% hepatic artery, less than 1% subclavian artery, and less than 1% popliteal artery.⁵ Notably, there were no cases involving the suprarenal or thoracoabdominal aorta in this series. More recent reports have documented a much higher prevalence of infected aortic aneurysms involving the segments proximal to the renal arteries,^12–15 suggesting the aorta is the most frequent site of involvement.

Bacteriology

Approximately 75% of clinically infected aneurysms are associated with positive culture results.⁵ There have been significant shifts in the bacteriological patterns of infected aneurysms that have paralleled the changes in etiology. Prior to 1960, gram-positive organisms predominated, particularly Streptococcus pneumoniae, Streptococcus, and Staphylococcus aureus.³ More recent series have reported a higher prevalence of gram-negative organisms, paralleling the increasing number of arterial infections due to bacteremia, particularly Salmonella species.^13,16 Gram-negative sepsis in elderly patients is a frequent clinical scenario in these circumstances.¹⁷ It appears that the bacteriological pattern is continuing to evolve: several reports have identified S. pneumoniae as an increasingly frequent cause of infected aortic aneurysms.^14,18,19 The prevalence of organisms associated with opportunistic infections such as fungus and Mycobacterium species may also be on the rise owing to the increasing prevalence of chronic diseases associated with impaired immunity.

Salmonella infections deserve special emphasis. For uncertain reasons, Salmonella organisms have a tendency to infect the abdominal aorta. Up to 36% of all infected aneurysms of the aorta are due to Salmonella species; conversely, 65% of Salmonella vascular infections are localized to the aorta.²⁰ Humans become infected by ingestion of contaminated food or water. Of the patients who develop Salmonella gastroenteritis, a small proportion will develop bacteremia that may result in extraintestinal seeding and infection. The interval between the onset of gastrointestinal symptoms and development of aortic infection may be several weeks.²⁰ Diagnosis can be difficult because the signs and symptoms are nonspecific: more than half of patients have ruptured aneurysms before the diagnosis is made.²⁰ Common isolates from aortic wall specimens have included Salmonella choleraesuis, Salmonella typhimurium, and Salmonella enteritidis. Salmonella aortitis is an extremely morbid condition that has historically been associated with mortality rates of 50% and a high rate of reinfection after revascularization.²⁰ However, this trend appears to be reversing: in a more recent series, Hsu et al. documented an 11% mortality rate and showed that Salmonella was a predictor of survival compared to other microorganisms.²¹ Much of this effect may have been due to the fact that the Salmonella infected patients in this series were significantly younger than patients who died with other infections.

Syphilitic aneurysms, once a common cause of death due to aortic arch rupture, are now very rare. In a review of the literature on infected aortic aneurysms, Leon and Mills reported that syphilitic aneurysms occur most commonly in the ascending and arch aorta; they are uncommon below the sixth vertebral body.²² These aneurysms result from the intense inflammatory response associated with the treponemes that lodge in vasa vasorum.

Features

Infected aneurysms of the aorta may involve any segment from the ascending arch to the distal infrarenal area. In a series of 43 patients with infected aortic aneurysms treated at the Mayo Clinic over a 25-year period, Oderich et al. documented a wide distribution of lesions.¹³ No segment of the aorta was spared. As can be seen in Figure 59-1, 40% of infected aneurysms were localized to the infrarenal aorta, and the remaining lesions were almost evenly distributed in the juxta/pararenal, paravisceral, thoracoabdominal, and descending thoracic segments. A similar distribution has been observed by others.^14,28,30

Figure 59-1 Distribution of infected aortic aneurysms in a series of 43 patients treated at the Mayo Clinic.

(From Oderich GS, Panneton JM, Bower TC, et al: Infected aortic aneurysms: aggressive presentation, complicated early outcome, but durable results. J Vasc Surg 34:900, 2001, with permission from the Society for Vascular Surgery and the American Association for Vascular Surgery.)¹³

The majority of aortic infections can be classified as bacterial aortitis.¹¹ Most lesions are saccular and well localized in an otherwise normal-appearing aorta (Fig. 59-2). This appearance is highly suggestive of a ruptured aortic pseudoaneurysm, which is pathognomonic for aortic infection. In a minority of cases, infection of a preexisting aortic aneurysm may make diagnosis difficult. In these circumstances, suspicion of infection is completely reliant on clinical information.

Figure 59-2 Arteriogram of infected aneurysm in infrarenal abdominal aorta.

Note saccular shape of pseudoaneurysm and normal appearance of aorta above and below the lesion.

Diagnosis

The majority of patients with infected aortic aneurysms are symptomatic. In the series by Oderich et al., 93% of patients had symptoms, the most common of which were fever, back pain, and leukocytosis (Table 59-1).¹³ Blood cultures are positive in approximately 75% of cases.¹³ The degree of symptomatology may be an important indicator of prognosis. Recent data suggest that the systemic inflammatory response syndrome (SIRS), a marker for sepsis, is associated with increased morbidity and mortality in patients with infected aortic aneurysms.^14,29 Diagnostic criteria for SIRS include the presence of two or more of the following: body temperature above 38 °C or below 36 °C; heart rate over 90 beats/min; respiratory rate over 20 breaths/min or a partial pressure of carbon dioxide in arterial blood (PaCO₂) less than 32 torr; and white blood cell (WBC) over 12,000 cells/mm³, less than 4000 cells/ mm³, or 10% immature (band) forms.²⁹

^{Table 59-1} Clinical Presentation and Laboratory Findings in 43 Patients Treated at the Mayo Clinic for Infected Aortic Aneurysms

Adapted from Oderich GS, Panneton JM, Bower TC, et al: Infected aortic aneurysms: aggressive presentation, complicated early outcome, but durable results. J Vasc Surg 34:900, 2001.¹³

Diagnosis of infected aortic aneurysms relies on a number of imaging techniques. The presence of a saccular aneurysm in a patient with typical symptoms is pathognomonic, and the diagnosis is confirmed if blood cultures are positive. Gas bubbles and periaortic fat stranding on magnetic resonance imaging (MRI) or enhanced computed tomography (CT) scans are also diagnostic for infection (Fig. 59-3) but are not universally present. More subtle signs include periaortic stranding, proximity to abnormal fluid collections or nearby infections such as vertebral osteomyelitis, and rapid aneurysm expansion over several days.¹⁵ Indium-111-labeled WBC scans have been used in some patients, but the 80% sensitivity and specificity of this test suggest that it has limited usefulness. Angiography has been recommended to localize the infection and plan appropriate operative treatment in all patients. As an alternative, newer imaging techniques such as CT angiography (CTA) can be used to assess periaortic tissues, localize the infectious process, and evaluate vascular anatomy. This technique has the advantage of being minimally invasive compared to standard angiography, and it essentially combines two tests into one.

Figure 59-3 Enhanced computed tomography (CT) scan demonstrating gas bubbles and periaortic fat stranding suggestive of an infected aortic aneurysm.

(From Oderich GS, Panneton JM, Bower TC, et al: Infected aortic aneurysms: aggressive presentation, complicated early outcome, but durable results. J Vasc Surg 34:900, 2001, with permission from the Society for Vascular Surgery and the American Association for Vascular Surgery.)¹³

Clinical Course

The natural history of infected aortic aneurysms depends on the classification. The more common bacterial aortitis is associated with inexorable expansion of the pseudoaneurysm and eventual rupture. Rapid expansion over 2 to 3 days has been documented; in more than half of cases, the pseudoaneurysm has already ruptured at the time of diagnosis. Contiguous and traumatic infections of the aorta, also associated with pseudoaneurysms, have a similar natural history. Urgent repair of these lesions is always indicated. Infections involving preexisting aortic aneurysms are relatively rare, and the natural history is unknown, but because of the potential for rapid expansion and rupture as well as recurrent bacteremia, urgent repair is indicated for these lesions as well. Patients with true mycotic aneurysms have two problems: the aortic aneurysm and the primary cardiac valvular lesion. Treatment may require extensive preoperative stabilization before the aneurysm is repaired.

Treatment

Treatment of infected aortic aneurysms is surgical. Although treatment with broad-spectrum antibiotics may “sterilize” an infected aneurysm, the aneurysm still requires treatment because of the significant risk of rupture. In a series of 22 high-risk patients treated with antibiotics but without resection, Hsu et al. reported that 50% had in-hospital mortality, and 59% of those who survived to leave the hospital died of aneurysm rupture in late follow-up.³⁰

The urgent nature of infected aortic aneurysms cannot be overstated because of the potential for rupture with exsanguination. In a recent series, nearly half of all patients with infected AAAs had already ruptured at the time of surgery, including free ruptures in 20%.³¹ Once the diagnosis is confirmed with appropriate imaging, preoperative preparation should be completed as rapidly as possible—preferably within 2 or 3 hours. Patients with hemodynamic instability should be transported immediately to the operating room. Stable patients should be admitted to an intensive care unit for rapid fluid repletion, institution of broad-spectrum intravenous antibiotics, and placement of appropriate monitoring devices. Blood should be typed and crossmatched, and at least four units of packed red blood cells should be available in the operating room.

Surgical treatment of infected aortic aneurysms depends on the location and extent of the infection. The most common operation is ligation and débridement of the infected arterial segment, with revascularization of the lower extremities using grafts brought through uninfected tissues remote from the infected site (extra-anatomical bypass).^28,32 For example, infected aneurysms of the infrarenal aorta can be treated with ligation of the abdominal aorta distal to the renal arteries and revascularization of the lower extremities using axillofemoral bypass grafts. However, proximal aortic aneurysms involving the renal arteries, visceral aorta, or descending thoracic aorta are much more complicated. These aortic segments require direct revascularization to preserve blood flow to the kidneys, intraabdominal organs, and the spinal cord. In these cases, aortic débridement with direct revascularization of the affected segment within the infected bed (in situ reconstruction) is appropriate.

In situ reconstruction has been performed with prosthetic grafts, but the reinfection rate of up to 20% makes this option unattractive except in patients who are unstable at the time of operation.^33,34 Prolonged administration of antibiotics is generally recommended in these patients.³⁵ As an alternative, a rifampin-bonded gelatin-impregnated Dacron has been recommended in patients with arterial infections caused by susceptible organisms such as S. aureus³⁶; however, these grafts are not effective against methicillin-resistant S. aureus or Escherichia coli infections.³⁷ Additional alternatives include human allografts and autogenous vein grafts. The midterm results of cryopreserved human allografts are encouraging: Brown et al. reported a series of 52 patients with infected aortas or aortic grafts who underwent replacement with cryopreserved allografts.³⁸ At 20 months follow-up, three patients had graft thrombosis or stenosis, and one developed a recurrent ilioenteric fistula; the remainder had no evidence of aneurysmal change or reinfection. The experience with autogenous superficial femoral-popliteal vein (SFPV) grafts is also encouraging. Several small series attest to the negligible reinfection rates and excellent durability associated with in situ SFPV reconstruction.^14,39 The early enthusiasm for this option is buoyed by excellent experience using the SFPV to replace infected prosthetic grafts of the aorta (see later discussion).

The modern enthusiasm for endovascular therapy has extended to infected aortic aneurysms. Several small series have suggested that placement of endografts in combination with long-term antibiotics represent definitive treatment of infected aortic aneurysms with similar outcomes to open aortic repair.^40,41 However, these data are countered by reports of a high rate of graft infection requiring removal, or extension of the aortic infection to more proximal segments.^42,43 This appears to be a particular risk in patients with Salmonella infections. Therefore, we suggest that endovascular repair might be a good option to treat acute complications from infected aortic aneurysms such as aerodigestive fistulas. However, these grafts should not be considered definitive treatment, and additional surgical therapy is indicated after resolution of the acute problem.⁴²

Femoral Artery Infections Associated with Invasive Procedures

Compared to alternative approaches involving direct puncture of the axillary artery or the abdominal aorta, the transfemoral approach is associated with the lowest risk of complications. Modern results indicate that the overall arterial complication rate of transfemoral catheterizations is less than 1%; the risk of femoral artery infection is exceedingly rare.^44,45 However, the increasing popularity of transcatheter techniques suggests that the absolute number of patients with catheter-related complications is likely to rise.

In an effort to reduce the incidence of pseudoaneurysms, many interventionalists use percutaneous closure devices to mechanically seal the arterial puncture site. Compared to manual compression, these devices have resulted in earlier mobilization and discharge of patients after arterial catheterization. However, these devices have been associated with a slightly higher risk of femoral artery infection. In a recent meta-analysis, Biancari et al. reported that the risk of access site infection is 0.6% after closure devices, compared to 0.2% without closure devices.⁴⁶ Risk factors for infection include diabetes, obesity, therapeutic intervention, and groin hematoma.

Primary femoral artery infections present as pseudoaneurysms. Common findings include pain at the puncture site, fever with chills, and a pulsatile groin mass. The onset of symptoms may be delayed up to several weeks after the original puncture. Gram-positive organisms predominate, especially S. aureus, but gram-negative bacteria are common isolates. Treatment involves institution of broad-spectrum antibiotics, débridement of the infected arterial segment, removal of all closure device material, and excision of grossly infected adjacent tissues. Direct revascularization with autogenous saphenous vein has been associated with a high risk of reinfection and vein graft blowout.⁴⁷ Alternatively, use of SFPV has been associated with excellent durability and resistance to infection in two small series.^48,49 Simple ligation of the common femoral artery (CFA) may be preferable if the femoral bifurcation is uninvolved.⁵⁰ If revascularization is necessary, the bypass should be routed through extra-anatomical tissues to avoid infected areas. A transobturator bypass is ideally suited to this situation.⁵¹

Femoral Artery Infections in Intravenous Drug Abusers

These complex lesions are extremely difficult to treat. In addition to the acute infection-related problems, many affected patients have serious comorbidities such as seropositivity for HIV and hepatitis B. Psychiatric disorders associated with chronic addiction can cause these individuals to be notoriously unreliable, and most do not return for follow-up after hospital discharge. Therefore, most authorities recommend conservative treatment approaches that emphasize avoidance of reinfection and late complications.

Approximately three fourths of all admissions for accidental intravenous drug injections involve the lower extremity, and the femoral artery is the most common site of involvement.⁵² Most patients present with a painful, pulsatile groin mass, often associated with overlying cellulitis. The most commonly cultured organism is S. aureus. Appropriate treatment involves ligation of the affected arterial segment to reduce the risk of hemorrhage and débridement of all grossly contaminated tissue to remove the septic focus. The advisability of subsequent revascularization remains controversial.

Many authors recommend ligation without revascularization, even if this leads to amputation. Repeated use of superficial veins for drug injection eliminates available autogenous conduits, necessitating the use of prosthetic material in many cases. The incidence of reinfection is extremely high in these circumstances, risking graft disruption and life-threatening hemorrhage.

Avoidance of revascularization rarely leads to amputation. Earlier reports documented an 11% amputation rate when one artery was ligated and a 33% amputation rate after triple-vessel ligation.⁵³ More recent reports suggest that the incidence of amputation is much lower. Ting and Cheng performed routine ligation in 34 infected femoral pseudoaneurysms, including 24 that involved the femoral bifurcation.⁵⁴ The mean postoperative ankle-brachial index was .43 after triple ligation and .52 with single-vessel ligation. Although 88% of patients had some degree of intermittent claudication after discharge, there were no instances of delayed limb loss. Cheng and colleagues reported a similar rate of claudication after single- or triple-vessel ligation, but one patient (5%) required above-knee amputation.⁵⁵ Mousavi et al. reported the results of femoral artery ligation for infected pseudoaneurysms in 134 illicit drug users. There were no amputations in this series.⁵⁶

Modern consensus is that infected femoral aneurysms in drug addicts are best treated with ligation alone. Most patients will suffer some degree of claudication, but the risk of early and late amputation is low. Immediate revascularization should be limited to cases in which no Doppler signal is detected at the ankle after femoral artery ligation.⁵⁷ In the vast majority, staged revascularization should be considered in patients with limiting claudication after the infection has been completely cleared. The known propensity for prosthetic graft infection from a remote injection site suggests that autogenous tissue is preferable in these circumstances. In the absence of usable saphenous vein, the SFPV represents an excellent alternative.⁴⁸

Risk Factors and Pathogenesis

The pathogenesis of graft infections is multifactorial and partly related to the site of implantation. Contamination prior to implantation due to failed sterilization techniques or breaks in packaging is thought to occur very infrequently. Likewise, gross breaks in sterile technique are rare. Most graft infections occur as a result of unrecognized bacterial contamination at the time of implantation. Exposure of the graft material to surrounding skin is a likely source; viable bacteria remain in the dermis of the skin despite antiseptic preparation.⁶⁹ Graft contamination can also occur from remote infections such as cellulitis or pyelonephritis. Wet gangrene of a toe can increase the risk of infection in a prosthetic femoropopliteal bypass graft. Similarly, concurrent intraabdominal procedures such as cholecystectomy or appendectomy can expose an aortic graft to the patient’s enteric flora, thereby increasing the risk of graft infection.

A number of specific risk factors have been associated with aortic graft infections. Colonic ischemia following the repair of ruptured and nonruptured aortic aneurysms is associated with a high risk of graft infection due either to direct contamination or to hematogenous seeding from bacterial translocation.⁷⁰ It has long been recognized that graft infections are more common after emergency repair of ruptured aortic aneurysms compared to elective operations.⁷¹ The emergent nature of ruptured AAA repair likely leads to inadvertent breaks in sterile techniques as the surgical team rushes to gain vascular control. In addition, patients presenting with either acute occlusion of the aorta or rupture of an aortic aneurysm are at high risk to develop postoperative SIRS. This SIRS response leads to an initial production of a proinflammatory cytokine response followed by a compensatory antiinflammatory cytokine response. This response renders the patient immunocompromised and at risk for nosocomial infections. Theoretically, this immunocompromised state may contribute to the increased risk of graft infection by hematogenous seeding during episodes of bacteremia.

Aortic grafts are uniquely prone to primary bacterial colonization at the time of aortic aneurysm repair. As already noted, many studies have demonstrated that the mural thrombus found in aneurysms is frequently colonized with bacteria. Macbeth et al. found that up to 43% of arterial walls were culture-positive for bacteria at the time of surgery.⁷² In this series, all of the aortic graft infections (.9%) occurred exclusively in patients with positive aortic wall cultures. The most common isolate was Staphylococcus epidermidis (71%) followed by Streptococcus species (13%) and other isolates (16%).⁷² Similarly, Buckels et al. in 1985 found that graft infection occurred more frequently in patients with positive cultures of aortic contents compared to those with negative cultures.⁷³ More contemporary studies have failed to confirm an absolute association between positive aortic cultures and subsequent graft infections. Farkas et al. reported positive cultures in 37% of 500 aortic aneurysms.²⁴ However, only one patient with a positive culture developed a graft infection. In contrast, 6 of 296 patients with negative cultures developed aortic graft infections during follow-up.²⁴ Based on these observations, it is clear that colonization of the mural thrombus by bacteria plays, at most, a minor role in the pathogenesis of aortic graft infection. Results from more contemporary experiences may be due to the consistent use of perioperative antibiotic therapy.

Local and regional factors may also play a role in development of graft infections. Use of groin incisions (e.g., aortobifemoral bypass) can more than double the risk of graft infection compared to aortic grafts that remain completely intraabdominal (e.g., aortobiiliac bypass or aortic tube graft repairs). This may be related to the local environment of the groin, an area associated with one of the highest concentrations of Staphylococcus species found on the body.⁶⁹ In addition, dissection in the groin disrupts abundant femoral lymphatics, leading to risk of lymph leak, groin wound breakdown, and direct graft contamination. Furthermore, the lymphatic system transports bacteria from distal sites of infection to the groin lymph nodes; opening these channels exposes the graft to potential contamination. Translocated bacteria have been demonstrated in animals and humans. In patients presenting with complex foot infections, positive lymphatic cultures at the time of amputation have been demonstrated in up to 20% of patients.⁷⁴ Cultures of groin lymph nodes at the time of vascular reconstruction have revealed bacteria in 11%. However, these cultures do not correlate with subsequent groin wound infections.⁷⁵

Recurrent operations in the same location, particularly the groin, represent a significant risk for graft infection. Repeated catheter access also increases the overall risk. Aortofemoral bypass grafts placed for treatment of occlusive disease, while durable, do thrombose and are frequently revised by either lysis or thrombectomy. Procedures used to reestablish flow through occluded grafts, whether surgical or endovascular, expose the graft to potential contamination. It is common to find that patients with late graft infections have had multiple procedures to reestablish arterial flow through such grafts.

Graft material also plays a role in the pathogenesis of graft infections. The immune system responds to the foreign body by walling off the offending agent. The initial response is an acute inflammation, with influx of neutrophils followed by macrophages. These inflammatory cells produce cytokines and release proteases in an attempt to eliminate the foreign body. This initial response has a negative effect on bacterial survival; however, if the inoculum is large, some bacteria may survive. The graft interstices may offer a safe haven for bacteria and allow them to survive the initial inflammatory phase. After the acute inflammatory response, a reparative phase begins. This stage is characterized by fibroblasts depositing collagen in response to locally secreted cytokines. A resulting connective tissue barrier shields bacterium from detection and obliteration by immune competent cells. This results in a closed space for the bacteria to thrive and grow on exudative proteins existing in an acidic and ischemic environment. In the absence of infection, the reparative phase culminates in tissue ingrowth and incorporation of the graft. However, if bacterial colonization is present, the graft fails to incorporate, and chronic inflammation continues. Failure to incorporate may be due to fibroblast inhibition by the bacterial components found in the perigraft fluid.⁷⁶ This results in the failure to obliterate the closed space around the graft and failure of incorporation. Bacteria are left to thrive in this closed space, eventually becoming an abscess. This can manifest as perigraft fluid that may express through incisions with sinus tract formation. In addition, the artery may be degraded at suture lines, resulting in pseudoaneurysm formation.

Clearly, multiple factors play a role in establishment of graft infections following vascular reconstructions. Despite this, the incidence of graft infection remains low, at less than 5% for all reconstructions. Vascular graft infections can be categorized into two general groups: aortic graft infections and graft infections following infrainguinal arterial reconstruction. These two broad groups can be further subdivided into prosthetic and autogenous graft infections. Virtually all graft infections following aortic reconstructions are prosthetic graft infections, but infection following infrainguinal reconstructions can occur in both autogenous and synthetic grafts. The anatomical configuration of the graft and the material that composes the graft alter both the diagnostic and therapeutic modalities. Diagnosis and management of aortic and infrainguinal graft infections will be considered separately in the sections that follow.

Incidence

The exact incidence of graft infection following aortic reconstruction is not precisely known because most series are retrospective and suffer from lack of inclusive follow-up. The best estimates suggested that the incidence of graft infection following aortic reconstructions ranges from 1% to 5%.^77–79 More contemporary data can be abstracted from the U.K. Small Aneurysm Trial, a randomized study of AAA repair in patients with small aneurysms. Although this study did not directly report the incidence of aortic graft infection, a number of graft-related complications were documented. Three patients in the trial had late aortic rupture following AAA repair, and four patients died following development of aortoenteric fistula. Most of these complications can be assumed to represent complications from aortic graft infection and represent 2% of the total patients.⁸⁰ The true incidence of aortic graft infection remains inadequately described, but most authorities agree the incidence is quite low and certainly less than 2% in the contemporary experience.

Classification

To better understand the pathogenesis and natural history of graft infections, classification systems have been developed. Wound complications following vascular reconstruction were first classified by Szilagyi et al. in 1972.⁸¹ The authors characterized wound complications following prosthetic graft placement in terms of anatomical involvement. Grade I lesions involved only the dermis. Grade II lesions extended into the subcutaneous tissue without involvement of the graft, while grade III lesions involved the graft by direct extension.⁸¹ Grade III lesions can be considered technical problems associated with wound closure. Certainly, local factors such as ischemic tissue play a significant role in wound infections, but they may be avoidable. This grading scheme is important only for early graft infections, which account for less than 1% of all graft infections.⁸² It does not take into account graft infections that present during late follow-up after aortic reconstruction. This grading scheme is more relevant to infections that follow infrainguinal arterial reconstructions, which result most frequently from complications of wound infections.

More relevant to the understanding of aortic graft infection is the scheme developed by Bandyk, who categorized aortic graft infections according to time of presentation after graft implantation.⁸² This classification scheme offers better insight into the origin of graft infections and is a better predictor of the type of bacteria that will be found infecting the graft. Bandyk defined an early graft infection as one that occurred less than 4 months after implantation, and late graft infections manifested after 4 months. Graft infections are subcategorized in terms of presentation: perigraft infection, graft-enteric erosion, and graft-enteric fistula. Most early perigraft infections represent the sequela of Szilagyi grade III wound infection; that is, extension of local wound infections to involve the graft. Remote sites of infection (e.g., wet gangrene) or immunosuppression are thought to play a minor role in early graft infections.⁸² The diagnosis of an early perigraft infection is usually obvious: most patients present with purulent drainage from the wound, signs of sepsis with bacteremia, acute pseudoaneurysm formation, or anastomotic disruption with hemorrhage. Early infections will be manifest almost exclusively in wounds located at or below the femoral level. These infections can be expected to contain any one of a variety of organisms including gram-positive and gram-negative organisms. In contrast, late perigraft infections tend to occur months to years following implantation. Most will present more than 1 year following implantation, and the majority result from S. epidermidis infection with biofilm production.

Bandyk further subdivided graft enteric fistulas into graft enteric erosions and graft enteric fistulas. Graft enteric erosions are aortoenteric communications that do not involve an anastomosis. Many affected patients do not have evidence of gastrointestinal bleeding. These lesions appear late and are thought to be the result of erosion of the graft into a contiguous loop of bowel by mechanical forces. Most graft enteric erosions occur in the body of the graft, and some consider the erosions to be a preliminary step in the process that ultimately extends to involve an anastomosis and leads to aortoenteric fistula. Bacterial cultures from these graft infections will yield predominantly gram-negative pathogens. Yeast is also a commonly isolate. Graft enteric erosions are attributed to inadequate retroperitoneal closure over the prosthetic graft at the time of aortic reconstruction. However, graft enteric erosions may be a manifestation of unrecognized perigraft infection. The infective process involves the overlying retroperitoneum with extension to the bowel and eventual graft enteric erosion. Mechanical forces and inadequate coverage of the graft likely contribute, but in the authors’ opinion, most erosions are the result of latent perigraft infections. Regardless of the etiology, the graft associated with enteric erosion should be considered infected.

Graft enteric fistulas communicate with a vascular anastomosis and present with gastrointestinal bleeding. These fistulas rarely occur in the early postoperative period. In contrast to erosions, graft enteric fistulas are the result of a perigraft infection that leads to anastomotic breakdown and pseudoaneurysm formation at a suture line. The pseudoaneurysm then erodes into the overlying bowel, leading to fistula formation and the potential for exsanguinating hemorrhage. Like erosions, cultures of graft enteric fistulas yield predominantly gram-negative enteric pathogens.

These classification systems are not all-encompassing. All aortic graft infections will not fall into a single category, but such systems serve as a useful guide and allow one to anticipate the pathogens likely to be encountered.

Etiology

Most aortic graft infections are thought to occur by direct contamination or extension of adjacent infections. No good evidence exists confirming that bacteremia contributes to aortic graft infection in humans. However, there is ample evidence from animal studies that bacteremia can result in prosthetic graft infections.^83,84 Antibiotic therapy during bacteremia in dog models prevents prosthetic graft infections.⁸⁴ All these models consist of bacteremia immediately following graft implantation. In humans, bacteremia frequently occurs after aortic surgery, yet the rate of acute graft infection is very low. Bacteremia likely plays only a minor role in acute aortic graft infections. The role of bacteremia in late-occurring graft infection is not known, but it is thought to be a rare cause of late graft infection.

Should patients with vascular grafts receive prophylactic antibiotics before procedures associated with bacteremia, such as dental or genitourinary instrumentation? Although past case reports have suggested a possible association, there is little evidence to indicate that these procedures lead to graft infection. Late-occurring graft infections are caused only rarely by organisms found in mouth flora.⁸⁵ Graft incorporation may act as a barrier to bacteremia and prevent late graft infections. In contrast to patients with prosthetic cardiac valves, current American Heart Association (AHA) guidelines do not recommend antibiotic prophylaxis after vascular graft placement for patients undergoing dental, respiratory, gastrointestinal, or genitourological procedures.⁸⁶

Clinical Presentation

The signs of aortic graft infection are highly variable. As noted previously, early graft infections can be easy to identify because they represent complications of wound infections. Affected patients usually present with induration and cellulitis at the wound, purulent wound drainage, and/or wound dehiscence with exposed graft. In patients with aortic reconstructions confined to the abdomen, presenting symptoms tend to manifest without wound involvement. Typical symptoms include failure to thrive, ileus, fever, elevated WBC count, or frank sepsis. Similarly, malaise, weight loss, and vague constitutional symptoms may be the only manifestations of graft infection. Graft infections can be difficult to diagnose in these patients, and the diagnosis is often made fortuitously during workup of more common sources. Alternatively, the patient may present with pseudoaneurysm formation or catastrophic rupture of the aortic anastomosis.

Any patient with a wound infection overlying a prosthetic graft requires careful wound exploration. The authors examine these wounds in the operating room unless the infection manifests solely as cellulitis. Operative exploration is mandatory because the exterior wound can be deceptive; only direct exploration can reveal that the infective process involves the body of the graft. Cellulitis with drainage requires exploration for an underlying abscess. In the operating room, the wound is explored and opened to the deepest depth of involvement. If the deep tissues are unaffected (Szilagyi grade II), most grafts are not contaminated.

The clinical presentation of late graft infection can be subtle. Latent graft infections can present as chronic femoral pseudoaneurysms. At repair, the graft will be poorly incorporated, with surrounding perigraft fluid. These findings are considered diagnostic for graft infection and have been associated with positive cultures in 71% of cases.⁸⁷ Lack of graft incorporation is more sensitive for graft infection; Padberg et al. found that 97% of incorporated grafts were not infected.⁸⁷ Infection may be a primary process for the formation of anastomotic femoral pseudoaneurysm. Up to 60% of clinically uninfected femoral pseudoaneurysms will be culture positive at repair.⁸⁸ The presence of a latent graft infection should be considered in all cases of femoral pseudoaneurysms. Another subtle sign of latent graft infection is graft thrombosis. This is particularly true if the graft has failed in the past, requiring revision either surgically or by thrombolysis. All patients with graft limb thrombosis or femoral pseudoaneurysms should have CT scan imaging of the graft to rule out infection prior to repair or revision. Hydronephrosis may also herald a latent graft infection.⁸⁹ All patients with prior aortic surgery should have a CT to evaluate for latent graft infection when hydronephrosis is encountered.

Less subtle presentations of latent graft infections include draining sinuses from groin wounds (Fig. 59-5) and a history of bleeding from a groin pseudoaneurysm. Bleeding from the groin in the presence of a pseudoaneurysm is a surgical emergency and must be addressed immediately. Such bleeding episodes are herald bleeds and portend life-threatening hemorrhage if not dealt with expeditiously. Graft infection may also present as gastrointestinal bleeding in a patient with prior aortic surgery. All such patients should be considered to have an aortoenteric fistula until proven otherwise. Rupture of a previously repaired aneurysm or pseudoaneurysm at the proximal anastomosis should be considered the sequelae of graft infection. An updated summary of the clinical manifestations of aortic graft infections in 187 patients with aortic graft infections treated at University of Texas Southwestern Medical Center is found in Table 59-2. This experience is similar to other published series.^85,90

Figure 59-5 Draining sinus from the right groin in a patient with a late aortic graft infection.

^{Table 59-2} Clinical Manifestations of Aortic Graft Infections* in 187 Patients: University of Texas Southwestern Medical Center Experience

AE, aortoenteric.

^* Many patients had more than one sign.

Adapted from Ali AT, Modrall JG, Hocking J, et al: Long-term results of the treatment of aortic graft infection by in situ replacement with femoral popliteal vein grafts. J Vasc Surg 50:30, 2009.¹²⁴

Diagnosis

Numerous modalities have been used to diagnose aortic graft infection, including CT, MRI, tagged WBC scans, ultrasound, sinography, percutaneous aspiration, arteriography, and operative exploration. Each method has inherent strengths and weaknesses, and often several tests are used in concert to assure accurate diagnosis.

Computed tomography scan

The CT scan remains the gold standard for diagnosis of aortic graft infections. Findings on CT that are suggestive of graft infections include loss of continuity of the aortic wrap (i.e., the residual native aortic wall closed over the graft at the time of repair), pseudoaneurysms, perigraft fluid, perigraft inflammation with loss of tissue planes, perigraft air, and focal bowel wall thickening. Presence of any of these findings is highly suggestive of aortic graft infection. Figure 59-6 demonstrates the presence of perigraft fluid in a patient with an infected aortic graft. The same patient was found to have bilateral femoral artery pseudoaneurysms (Fig. 59-7). The reported sensitivity and specificity of CT scans to diagnose all graft infections is 95% and 85%, respectively.⁹¹ Sensitivity and specificity approaches 100% when findings of perigraft fluid, perigraft inflammation, or ectopic gas are present.^89,91 However, CT scanning may not be able to accurately diagnose subtle graft infections manifest solely by the presence of perigraft fluid. While CT imaging of low-grade aortic graft infection has a specificity of 100%, the sensitivity is only 55%.⁸⁹ The other disadvantage of CT scanning is the requirement for intravenous contrast. This may be contraindicated in patients with chronic renal insufficiency or dye allergies. However, the CT modality is readily available, safe, inexpensive, and familiar to clinicians; it remains the imaging modality of choice for initial evaluation.

Figure 59-6 Computed tomography (CT) scan of patient with infected aortobifemoral bypass demonstrating presence of perigraft fluid.

Arrow points to perigraft fluid.

Figure 59-7 Magnetic resonance imaging (MRI) with heavily T2-weighted images of patient with infected aortobifemoral bypass.

Perigraft fluid is seen as a bright (white) signal surrounding graft (arrow). Note bright fluid “halo” surrounding infected graft.

Ultrasound

Ultrasonography has a limited role in the diagnosis of aortic graft infection. Although ultrasound can accurately diagnose the presence of perigraft fluid (Fig. 59-8), the intraabdominal portion of grafts is not readily imaged. The primary utility of ultrasound is to diagnose femoral pseudoaneurysms and perigraft fluid around infrainguinal grafts or aortic grafts that extend to the groin.

Figure 59-8 Duplex ultrasound of femoral anastomosis in patient with infected aortofemoral bypass graft.

Note hypoechoic rim surrounding graft, consistent with perigraft fluid (“halo” sign).

Antibiotic Therapy

Limited treatment using lifelong antibiotic therapy or percutaneous drainage and antibiotic therapy are options for the most high-risk patient with a limited life expectancy. There are little data to support such treatment regimens. Roy and Grove reported a series of high-risk patients treated with antibiotic therapy alone for proven or suspected graft infections.¹⁰⁶ Only two of the patients had proven infections of preexisting grafts. All patients were alive at the median follow-up of 36 months without systemic symptoms of infection. Although this appears to be a reasonable option, it should be stressed that this therapy is appropriate only for latent graft infections due to low-virulence organisms, particularly S. epidermidis. This therapy should be condemned in all but the most high-risk patients. Infection by more virulent bacteria has a grave prognosis, and antibiotic therapy alone will have little impact on the natural history of the infection.

Total Graft Excision without Revascularization

In the early experience of management of aortic graft infections, graft excision without arterial reconstruction was commonly done. The infected graft would be excised, and a wait-and-see strategy would be used to determine whether the limbs required revascularization. This approach led to unacceptably high rates of amputation and death. Graft excision alone can be considered in patients with occluded grafts who do not have limb-threatening ischemia. Most patients will tolerate excision of a thrombosed infected graft without worsening of the preexisting ischemia; however, the risk of interrupting important collaterals during graft excision should be borne in mind.

Patients who underwent aortic grafting for claudication may tolerate graft excision without revascularization. Such patients can be expected to return to their preoperative degree of ischemia after graft removal, assuming that important collaterals are not interrupted. This technique should be reserved for patients that have had end-to-side aortic grafting for aortoiliac occlusive disease. Preoperative arteriography must be obtained to determine whether native circulation remains intact. Thrombosis of the native aorta is common following end-to-side aortobifemoral bypass graft and must be ruled out prior to graft excision. In most patients and virtually all patients operated on for aortic aneurysmal disease, graft excision without revascularization can be expected to result in lower-extremity amputation.

Total Graft Excision and Extra-Anatomical Revascularization

Total graft excision with extra-anatomical bypass is the traditional treatment for infected aortic graft. This treatment strategy consists of extra-anatomical bypass by axillary-femoral-femoral bypass or bilateral axillary to femoral bypasses with total graft excision. The sequence of operations is very important to prevent cross-contamination of the new graft. The extra-anatomical bypass should be performed first through noninfected tissues, and the wounds should be closed and dressed prior to exposing the infected graft. In addition to avoiding contamination of the new graft, this sequencing has the advantage of limiting leg ischemia.

Axillary-femoral-femoral bypasses are employed for treatment of infected grafts that do not involve the femoral arteries; bilateral axillary-to-femoral bypasses are used to treat infected aortobifemoral bypass grafts. The approach for infected aortobifemoral bypass requires careful planning and inventive tunneling. To prevent cross-contamination of the new graft, the femoral vessels are approached through uninvolved tissue planes, typically lateral to the sartorius muscle. Bypasses are performed from the axillary artery to the profunda femoris artery or to the superficial femoral artery if it is disease free. Axillary-to-popliteal bypasses have very poor patency and have largely been abandoned.

After completing the extra-anatomical bypass, the infected graft is removed. Timing of the two stages is controversial. The extra-anatomical bypass can be performed just prior to removal of the infected graft during the same operative procedure, or the procedures can be staged with extra-anatomical bypass performed several days prior to removal of the infected graft. Staging procedures give the patient time to recover from the initial bypass and avoid a long procedure. Proponents of the staged procedure purport a lower operative morality and increased limb salvage than the single-stage operative strategy.^107,108

There are several disadvantages to extra-anatomical bypass with total graft excision. The most worrisome complication is infection of the new bypass graft. Reinfection rates can be as high as 20%, but most series report a low reinfection rate of less than 10%.^67,68,108 The notoriously poor durability of the extra-anatomical bypasses is also a concern. The highest reported primary patency rate for axillary-femoral-femoral bypasses is over 75%, but the reported primary patency rates of unilateral axillary-femoral bypasses average approximately 60% at 3.5 years.^107,109 The most devastating complication of this procedure is disruption of the oversewn aortic stump (aortic stump blowout). Fortunately, this lethal complication is rare. Because of these disadvantages, a number of other options for graft excision and revascularization have been introduced.

Total Graft Excision with In Situ Replacement Using Prosthetic Graft

In situ replacement of an infected graft with a new prosthetic graft is technically the simplest method of revascularization and avoids the potential for aortic stump blowout. However, replacing an infected prosthetic graft with a new prosthesis poses the very real potential for recurrent graft infection. In situ prosthetic replacement may be best used as a salvage operation for unstable patients with either aortoenteric fistula or ruptured proximal pseudoaneurysms. Fortunately, the reported rates of clinically apparent reinfection following in situ replacement for aortoenteric fistula is surprisingly low (< 15%).^110,111 Replacement with new graft may be appropriate for localized graft infections such as those found in the setting of aortoenteric fistula. Recurrent infection in the setting of gross graft infection has been disappointing. The authors use in situ replacement with prostheses as a bridge to definitive therapy with autogenous replacement at a later operation.

The advent of antibiotic-bonded Dacron grafts appeared to offer improved results for in situ prosthetic replacement. This modality seems to be most appropriate for treatment of graft infections with biofilm-producing S. epidermidis or S. aureus. Young et al. reported a series of nine patients treated with rifampin-soaked grafts and found that the reinfection rate was 11%.¹¹¹ Bandyk et al. and Hayes et al. both concluded that rifampin-bonded grafts are acceptable for treatment of low-grade biofilm graft infections by S. epidermidis and S. aureus.^112,113 Bandyk et al. found that recurrent infection occurred in less than 10% of patients.¹¹² Hayes et al. only reported reinfection in patients with meticillin-resistant S. aureus (MRSA) infections.¹¹³ It appears that antibiotic-bonded grafts may offer improved results, but only in selected patients with low-grade S. epidermidis and possibly S. aureus infections. They are usually not appropriate in cases involving more virulent organisms. Similar findings have recently been reported using silver-coated polyester grafts for in situ replacement. In a series of 24 patients with a variety of polymicrobial graft infections, Batt et al. documented a 40% prevalence of graft reinfections.¹¹⁴

Total Graft Excision with In Situ Replacement Using Arterial Allograft

An alternative to in situ replacement with prosthetic graft is replacement with arterial allograft. Animal studies have demonstrated the allograft is relatively resistant to infection when antibiotic loaded.¹¹⁵ The experience in humans has confirmed this finding. Leseche et al. reported a series of 28 patients treated with allografts for graft infection or infected aortic aneurysms.¹¹⁶ They reported no recurrent infection. In a series of 49 patients, Vogt et al. reported two patients with recurrent infections that resulted in death.¹¹⁷ However, in this series there were four deaths related to allograft technical complications. In three patients, allograft side branch rupture resulted in three aortoenteric fistulas that were uniformly fatal. A fourth patient died intraoperatively from rupture of a friable allograft. In a recent study of 110 consecutive patients with aortic infections, Bisdas et al. reported a 9% overall operative mortality. During a mean follow-up of 36 months, 6% required reoperation for graft deterioration, but no recurrence of infection was noted.¹¹⁸ Others have noted that reoperation for reinfection or degenerative changes in allografts is common (9%-17%) and that pathological changes are seen in up to 26% of patients.^38,116 In situ allograft and prosthetic graft replacement may be best used a temporizing technique until more definitive therapy can be undertaken.

Total Graft Excision with In Situ Replacement Using Autogenous Veins

Perhaps the best solution for management of prosthetic graft infection is in situ reconstruction with SFPV. This conduit has proven to be the most resistant conduit to infection, has unchallenged patency rates, avoids the risk of aortic stump blowout, and rarely degenerates. Operative mortality following aortic reconstruction with SFPV has been reported as less than 10%.^119–123 Reinfection is very rare. In our experience, only one patient suffered infection of an SFPV graft, and the offending organism was Candida. Franke noted two cases of SFPV infection that occurred in the face of overwhelming Pseudomonas infection.¹²³ In our experience, all patients with pseudomonal infections have been treated successfully, but it should be pointed out that none of our patients presented with overwhelming sepsis. Patients with overwhelming sepsis may be better served by extra-anatomical bypass and graft excision. SFPV is very durable, with primary patency rates of greater than 80% and less than 5% of grafts requiring revision.^122,124 Venous morbidity is minimal.¹²⁵

Most patients are suitable for aortic reconstruction with SFPV regardless of the bacterial pathogen. The only downside to this management strategy is the length of the operative procedure. Harvest of the SFPV requires two teams, and mean operative time is 8 hours. Because of the length of time required, SFPV aortic reconstruction is not appropriate for unstable patients, particularly patients with bleeding aortoenteric fistulas. However, such patients can be treated with in situ prosthetic replacement with delayed conversion to SFPV after a period of stabilization and recovery. We have had very pleasing results with this strategy. Extra-anatomical bypass with graft excision has been the standard for treatment of aortic graft infection, but we believe that autogenous replacement with SFPV has earned a place as the new gold standard for management of such patients.

Partial Graft Excision

With the improvement in imaging techniques, some authors have advocated partial graft excision if the aortic graft infection can be localized to the femoral portion on preoperative imaging. Reconstruction can be carried out by extra-anatomical bypass or in situ grafting. This technique is most appropriate for patients with late S. epidermidis infections. It is not appropriate for patients with early graft infections because the entire graft is almost invariably involved.⁸² Towne et al. described treating 14 patients with confirmed S. epidermidis or S. aureus infection using partial graft excision, wide local débridement, and in situ replacement with PTFE graft.¹²⁶ Only 2 of the 14 patients ultimately developed infection in the remaining graft, but the new PTFE grafts remained uninfected. Calligaro et al. demonstrated that graft patch remnants on infrainguinal vessels can be safely left in situ at the time of graft excision in over 92% of patients.¹²⁷ Reilly et al. have described good results with partial graft excision and extra-anatomical bypass.⁷⁷ In the authors’ most recent experience, only 63% of patients require total graft excision. In our experience, subtotal graft excision can be attempted if the body of the graft is found to be incorporated at the time of surgical exploration. In these situations, planned reconstruction with SFPV has a real advantage. The body of the graft can be explored prior to violating the clearly infected portion. If the entire graft is infected, total graft excision and reconstruction with SFPV can be undertaken. If the body of the graft is not infected, the graft can be divided and sewn to the SFPV. The wound is closed, the infected portion of the graft is removed, and the reconstruction completed. Subtotal graft excision should only be considered in high-risk patients with late-occurring graft infections. Such patients should be followed closely, and infection of the residual graft should be anticipated.

Graft Infection Following Endovascular Repair

Graft infection following stent graft repair of aneurysm is becoming more frequently reported. As of 2010, there have been 102 reports of abdominal endograft infections in the literature.¹²⁸ In a series of 494 consecutive stent grafts (389 abdominal aorta and 105 thoracic aorta), Heyer et al. reported a prevalence of abdominal endograft and thoracic endograft infection of 0.26% and 4.8%, respectively.¹²⁹ All affected patients suffered significant morbidity. While rare, endograft infections are extremely difficult to diagnose. The typical clinical presentation and radiographic finding associated with stent graft infections are not well described and await a more mature experience with these endovascular techniques. Infected grafts have been associated with highly virulent organisms including Propionobacterium, Staphylococcus, Streptococcus, and Enterobacter.¹²⁹ Treatment for infected abdominal aortic endografts includes complete graft excision and extra-anatomical or in situ bypass. We have used the SFPV for in situ replacement with gratifying results in these circumstances. On the other hand, treatment of infected thoracic endografts should include graft excision and bypass with antibiotic-soaked prosthetic graft or cryopreserved allograft if more virulent organisms are present.

Peripheral Vein Suppurative Thrombophlebitis

Thrombophlebitis is the most common complication of peripheral vein infusion, occurring in up to a fourth of hospitalized patients receiving intravenous therapy via veins of the forearm or hand.¹³⁶ Pathogenesis has been related to irritation of the vein from the catheter material, infusate, or bacteria. Thrombosis occurs as a result of localized stasis and prostaglandin-mediated activation of the coagulation cascade.¹³⁷ Suppurative superficial thrombophlebitis results from infection of the thrombus, which is estimated to occur in 0.2% to 2% of peripheral vein catheter insertions.¹³⁸ Onset of infection is a serious development, resulting in significant morbidity and prolonged hospital stay. Development of life-threatening infections such as osteomyelitis or endocarditis may occur after a single episode of superficial suppurative thrombophlebitis. This complication is more common with plastic catheters than with steel (“scalp vein”) cannulas and is related to duration of intravenous catheterization.¹³⁹ Prolonged catheterization is the most important predictor of peripheral vein infusion thrombophlebitis; this has led to the recommendation by the Centers for Disease Control and Prevention (CDC) that short peripheral intravenous catheters should be changed every 72 hours.

Although there is a higher risk of suppurative superficial thrombophlebitis from catheters inserted in the lower extremity, upper-extremity involvement is the more common presentation. Affected patients have signs of local inflammation, including tenderness, erythema, induration, and warmth over the involved superficial vein. Differentiation between noninfected and suppurative thrombophlebitis may be difficult. Systemic signs of infection such as fever, tachycardia, and leukocytosis are not universally present. Bacteremia occurs in the majority of patients, and gross pus within the vein lumen may be found in up to half the cases.¹³⁹ Diagnosis often relies on a positive culture of the indwelling catheter tip. S. aureus is the most common isolate, but gram-negative organisms are becoming more frequent. Antibiotic resistance is common.

Treatment of superficial suppurative thrombophlebitis involves removal of the intravenous catheter, institution of broad-spectrum antibiotics, and excision of the involved vein. The involved vein should be explored proximal to the highest anticipated site of involvement—usually several centimeters above the inflamed area. The infected vein segment and its tributaries should be completely excised using a patent noninflamed vein segment as the endpoint. Incisions should be left open to heal by secondary intention. Postoperatively, antibiotics should be continued for an undetermined period of time. Empirical recommendations suggest continuation of culture-directed antibiotics for at least 2 to 3 weeks.

Central Vein Suppurative Thrombophlebitis

Two classic scenarios have been described for suppurative thrombophlebitis of central veins: (1) residual central thrombosis following central line sepsis and (2) pelvic suppurative thrombophlebitis associated with gynecological complications. Suppurative thrombophlebitis of thoracic veins occurs in the chronic setting, whereas suppurative pelvic thrombophlebitis occurs more acutely.

Suppurative Thrombophlebitis of the Portal Vein (Pylephlebitis)

Suppurative thrombophlebitis of the portal vein usually follows infection of an organ drained by the portal vein or a contiguous structure. Historically, pylephlebitis was most commonly due to appendicitis.¹⁴³ Widespread use of antibiotics and early diagnosis and intervention for abdominal infections have made the condition rare. Most modern cases occur as a complication of diverticulitis, but it has also followed other intraabdominal infections such as appendicitis, acute cholecystitis, and foreign body perforation.¹⁴⁴ However, some are due to secondary infection of portal vein thrombosis associated with a hypercoagulable disorder such as cirrhosis or malignancy.¹⁴⁵

The clinical presentation of patients with pylephlebitis is nonspecific: most have fevers of unknown origin with variable signs of systemic toxicity. Abdominal pain occurs in about three fourths of affected patients, and up to 20% have severe sepsis.¹⁴⁴ Ultrasound may be helpful to detect thrombus within the lumen of the portal vein, but CT is the more common test to confirm the diagnosis. Magnetic resonance imaging with angiography may be able to discern acute from chronic thrombus.^144,145 Many patients have other intraabdominal processes such as abscesses or common bile duct stones. Small intrahepatic liver abscesses may also be present.

Treatment of pylephlebitis involves use of broad-spectrum intravenous antibiotics and eradication of the underlying infection. Early treatment is critical to reduce the risk of ischemic bowel infarction from mesenteric vein thrombosis. Although systemic administration of broad-spectrum antibiotics is usually adequate, catheter infusion of antibiotics directly into the portal vein may result in more prompt improvement.¹⁴⁶ Intraabdominal infections should be treated promptly by percutaneous drainage or surgical intervention. In rare cases, laparotomy and thrombectomy of the portal system have been used in severely ill patients.¹⁴⁴ In all cases, antibiotics should be continued until complete resolution or cavernous transformation of the thrombus, as confirmed with CT or MRI.¹⁴⁴ This usually requires at least 4 to 6 weeks. Fortunately, development of acute portal hypertension with variceal hemorrhage is uncommon.