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Vascular Infections
Vascular infections represent difficult diagnostic and technical challenges for even the most experienced physicians. Multiple comorbidities frequently afflict the patients, resulting in nutritional and immunologic deficiencies. Patients are often near the end of life as well, further complicating the decision-making for the patients, caregivers, and physicians. Moreover, published series regarding vascular infections are underpowered, which limits the ability for physicians to provide data-driven care.
Vascular infections include both primary and secondary infections. Primary infections often result from bacteremia seeding an underlying vascular pathology, such as atherosclerotic plaque, aneurysm, dissection, or prior injury. Due to multiple, redundant mechanisms that exist to prevent vascular infection, primary vascular infections without an underlying vascular pathology or injury are rare. Secondary infections occur when prosthetic graft or stent material becomes seeded, and cause infection of the adjacent vascular structures. Secondary infections are much more common, due to the lower bacterial inoculum required to cause a prosthetic infection. Theoretically, vascular infections can occur wherever a vascular structure becomes infected; however, there are several anatomic locales where infections occur most frequently. This chapter will describe the definitions, pathophysiology, prevention, diagnosis, and management of some of the more commonly encountered vascular infections in the periphery, excluding those involving the intracranial or coronary circulations. Arterial and venous infections are discussed.
Primary arterial infections
Primary arterial infections (PAIs) were first described by Koch, who detailed the case of a patient who presented with a ruptured mycotic superior mesenteric artery (SMA) aneurysm in 1851. Since then, there have been multiple small case series and case reports of PAI in the literature, affecting multiple vascular beds. The definition of PAIs has been difficult, as there are multiple specific etiologies of PAI. Categorization of PAIs did not occur until 1978 when Wilson et al. described six different variants of PAIs ( Table 59.1 ).
Table 59.1
Variants of Primary Arterial Infections
| Term | Definition |
|---|---|
| Mycotic aneurysm | Area of previously uninfected artery that is seeded by septic emboli, which subsequently undergoes degeneration and aneurysmal enlargement |
| Infected aneurysm | Hematogenous seeding of a preexisting aneurysm |
| Traumatic infected pseudoaneurysm | Area of focal rupture of an artery, which forms a pseudoaneurysm. The associated hematoma becomes infected, likely seeded at the time of injury |
| Contiguous arterial infection | Erosion of an infectious nidus into an adjacent artery |
| Primary aortoenteric fistula | Erosion of an aneurysm into an adjacent gastrointestinal structure, most commonly the duodenum |
| Microbial arteritis | Hematogenous seeding of previously uninfected atherosclerotic plaque |
Mycotic aneurysms describe areas of previously uninfected artery that are seeded by septic emboli secondary to endocarditis. This segment of artery subsequently undergoes degeneration, and becomes aneurysmal. Mycotic aneurysms tend to occur in areas where a septic focus might lodge, though theoretically, these can occur anywhere in the arterial circulation. Microbial arteritis occurs when bacterial seeding of a previously uninfected atherosclerotic plaque occurs without aneurysmal degeneration . Infected aneurysms result from seeding of a preexisting aneurysm secondary to bacteremia. Since the thrombus of aneurysms is rarely sent for culture, the true prevalence of infected aneurysms is unknown. Traumatic infected pseudoaneurysms occur at a site of focal rupture of the artery secondary to iatrogenic arterial access, intravascular drug abuse, or trauma (blunt or penetrating). The surrounding tissues contain the hemorrhage, such that the wall of the pseudoaneurysm is composed of compressed periarterial connective tissue. The hematoma and pseudoaneurysm are likely seeded at the time of the initial insult.
Contiguous arterial infections occur when an infectious nidus erodes into an adjacent artery, resulting in pseudoaneurysm formation and/or rupture. These often occur in the context of resection for neoplasms. The fields are frequently irradiated, with the patient often having undergone chemotherapy, resulting in complex chronic wounds. When wounds are adjacent to major vascular structures, the contiguous infection may compromise the nearby vasculature. A primary aortoenteric fistula (AEF) is thought to form when a mycotic aneurysm gradually enlarges, resulting in repetitive pulsatile pressure upon adjacent gastrointestinal (GI) structures. Over time, iterative pressure and aneurysmal enlargement coupled with weakening of intestinal wall causes a communication between the mycotic aneurysm and GI tract, resulting in an AEF. To limit confusion, and to maintain continuity with prior chapters, the terms infected aneurysm and PAI will be used interchangeably to generally refer to these six entities (see Table 59.1 ).
Untreated PAI have several sequelae, the most significant of which is the propensity of arterial rupture and exsanguination. Microbes cause degradation of the arterial wall, resulting in aneurysm and pseudoaneurysm formation. Unchecked, the microbial-mediated destruction of arterial integrity will exceed the ability to contain hemorrhage. Second, the site of PAI can serve as a nidus of septic arterial embolus formation, particularly when accompanied by aneurysmal degeneration. Septic emboli can also result in end-organ ischemia, further complicating the management of the PAI. Finally, PAI can serve as a source of bacteremia, resulting in septic complications, and further inoculate previously uninfected sites in the vasculature.
Pathophysiology of Primary Arterial Infections
Destruction of the Aortic Wall
Infected aneurysms are characterized by focal destruction of the arterial wall. They grow more rapidly than their noninfected counterparts, and are considered to have an increased rupture risk. Pathologic specimens of infected aneurysms are infrequently reported. Hsu and Lin showed that 100% of infected aneurysms showed evidence of atherosclerosis. The next most frequent finding was acute suppurative inflammation, found in two-thirds of their specimens. Atherosclerosis and chronic inflammation were found in 15% of their subjects. This suggests that the organisms causing PAI are more likely to be rather virulent, inciting a vigorous acute inflammatory response. This significance of atherosclerosis was affirmed by Miller et al. who found atherosclerosis was present in 75% of their mycotic aneurysm specimens.
Collagenases and elastases appear to play a central role in the development of infected aneurysms. The precise origin of these proteases is unclear, however. Buckmaster et al. isolated the bacteria as well as the aortic tissue from four patients undergoing suprarenal mycotic aortic aneurysm repair. The authors concluded that elastases were produced mainly from host neutrophils, rather than the infecting microorganism, or the host macrophages. The exception was Pseudomonas aeruginosa which was the only microbe to produce elastin-degrading enzymes.
Conversely, other works have shown that bacteria, such as Streptococcus mutans, Bacteroides sp., Escherichia coli, Staphylococcus aureus, and Staphylococcus epidermidis can produce collagenases. Moreover, many microbes are capable of activating matrix metalloproteinases-1, -8, and -9, which can degrade the aortic wall resulting in infected aneurysms. Since collagen provides much of the tensile strength to the aortic wall, the activation of collagenases and subsequent rapid degradation of the aortic wall is significant. While the precise mechanism of infected aneurysm development is unclear, further investigations will prove illuminating when attempting to understand the pathophysiology, and to design novel therapeutics for the management of PAI. The pathophysiology of PAI is summarized in Fig. 59.1 .
Source of Infection and Host Response
The source of bacteria is variable. Infective endocarditis is no longer the most prevalent cause of infected aneurysms. Contiguous spread, bacteremia, and embolization from a septic source represent frequent sources of infection, though many times, the etiology is unclear. Atherosclerotic lesions, areas of preexisting aneurysmal degeneration, and traumatic injury all predispose patients toward the development of infected aneurysms.
Some authors posit that infected and uninfected aneurysms may represent either end of the spectrum of the same disease, with the presentation hinging upon the virulence of the organism and the host immunologic response. These authors cite the fact that approximately half of presumably uninfected aneurysms harbor Chlamydia pneumoniae. While this opinion is not widely held, the concept emphasizes the role of the host immunologic response in the development of infected aneurysms, which does play a significant role in the destruction of the vessel wall. Immunodeficiency (chronic immunosuppressive use, malnutrition, diabetes mellitus, malignancy, human immunodeficiency virus [HIV] syndrome, chronic hepatitis) appears necessary in over 50% of cases, which is logical given the prevalence of bacteremia in everyday life, relative to the infrequency of PAI.
Bacteriology of Infected Aneurysms
The microbes responsible vary depending upon the series, era of publication, and location of the infected aneurysm. In the past, gram- positive organisms were predominantly found in blood and arterial cultures of patients afflicted with infected aneurysms. More recent series have found gram-negative organisms to occur more frequently than in prior reports, perhaps due to the concomitant increased prevalence of gram-negative bacteremia noted in the elderly population. The bacteriology seems to be continually evolving, though this may reflect publication bias, where only novel microorganisms now merit publication. Other microorganisms recently described include Streptococcus agalactiae, methicillin-resistant S. aureus, E. coli , and other gram- negative species. Mycobacterium bovis and other caseating microorganisms are also being reported. However, the broader distribution of causal organisms in PAI may reflect an increased prevalence of immunocompromised hosts. Improvements in culture techniques may also be partly responsible for the increased identification of atypical organisms, such as Campylobacter , Listeria, or Coxiella sp.
Salmonella infections merit special mention in PAI. This is especially true for primary aortic infections, where the prevalence ranges between 17% and 67%. The prevalence of Salmonella appears highest among East Asian populations. Within Western populations, Salmonella causes a higher percentage of PAI compared to secondary arterial infections (SAIs). However, other microorganisms are more prevalent than Salmonella in Western populations. Interestingly, Salmonella infections may be associated with a lower risk of mortality relative to infection with other microorganisms. The significance is that a history of an antecedent gastrointestinal illness may help to heighten a physician’s suspicion of an infected aneurysm caused by Salmonella.
Syphilis was the most common cause of mycotic aneurysms prior to antibiotics. Since the introduction of penicillin, however, the prevalence of cardiovascular manifestations of chronic syphilis has declined to where the description is rare enough to warrant publication as a case report. Previous reports cited that most of these aneurysms occurred in the aortic arch and thoracic aorta. The causal treponemal infection of the vasa vasorum results in significant inflammation which weakens the involved segments of the aorta, resulting ultimately in aneurysmal degeneration. While rare, syphilis must remain in the differential diagnosis, especially in the setting of immunodeficiency and a history of other sexually transmitted diseases.
Common Locations and Presentations of Primary Arterial Infections
Theoretically, PAI can occur anywhere in the arterial tree. Among aortic infections, the suprarenal and thoracic aorta are most common and clinically problematic. Aneurysms of the visceral arteries and carotid arteries are frequently mycotic, and represent significant clinical challenges due to the infrequency of clinical presentation, and the technical challenges associated with repair. Femoral artery pseudoaneurysms, either due to iatrogenic catheterizations or due to intravenous drug abuse, are increasing in prevalence due to the increase in percutaneous coronary and peripheral vascular interventions. Presentations depend upon the location, with infected aneurysms that are more superficial, providing more classic symptoms of hemorrhage, pulsatile mass, overlying erythema, with pain or tenderness to palpation. Conversely, infected aneurysms occurring more centrally, such as those within the visceral arteries or in the aorta, present more insidiously with a significant amount of symptom overlap with other conditions. Aortic and visceral artery infected aneurysms therefore require a higher index of suspicion from the physician.
Primary Infections of the Aorta
More recent European data suggest that there is no significant predilection of infection in any segment of the aorta. Prior American studies, however, suggest that approximately one-third of PAIs occur in the infrarenal aorta. The remainder are found in the ascending aorta, arch, descending thoracic aorta, or suprarenal aorta. The variability in the distribution appears to stem from the variable sample sizes reported in the literature. Mycotic aortic aneurysm comprises approximately 0.7% to 2.6% of all aneurysm diagnoses in the United States.
Symptomatic presentations are common, occurring in up to 84% of patients, with overt rupture exceeding 50%. Rapid expansion is the norm, occurring in as little as 7 days, and likely varies depending upon the virulence of the predominant organisms causing the infected aneurysm, as well as host factors. Saccular morphologies were found in 94% in the Mayo experience, and echoed in other series. Symptoms are likely common at presentation due to the indolent course prior to presentation with rupture, AEF, and/or sepsis. Moreover, due to their infrequency, lack of physician suspicion likely results in delays in diagnosis, until the patient symptoms and extremis necessitate and obviate the diagnosis.
Visceral Artery Infected Aneurysms
Visceral mycotic aneurysms include those occurring within the distribution of the celiac axis, SMA, inferior mesenteric artery (IMA), or renal arteries. As a whole, these entities are exceedingly rare. The most frequent arterial distribution for visceral artery infected aneurysms is the SMA, comprising 88% of visceral artery aneurysms in older series. Hence much of the discussion will focus on SMA infected aneurysms.
A recent review of mycotic SMA aneurysms revealed that approximately two-thirds present with epigastric pain, with 60% presenting with fever. Nonspecific malaise, nausea and vomiting, and weight loss also occur in approximately 20% to 25% of patients. The median age is 36 years, with a male predominance of 3:1. An antecedent history of subacute bacterial endocarditis and intravenous drug abuse appear most frequently. Because the symptoms are nonspecific, some have recommended entertaining the diagnosis of infected SMA aneurysms in the differential if patients present with the pentad of abdominal pain, fever of unknown origin, malaise, weight loss, and nausea. The microbiology is somewhat different from mycotic aortic aneurysms, with Streptococcus sp. appearing in almost 50% of case reports. Staphylococcus sp. occur next in frequency, occurring in almost 30% of reports.
Infected aneurysms of the celiac axis are the next most frequently reported. Symptoms are slightly different, with jaundice and hematemesis accompanying the abdominal pain. Reports of septic embolization and infarction have also been reported with celiac axis–infected aneurysms. Microbiology is similar to SMA mycotic aneurysms. Also similar to SMA-infected aneurysms, bacterial endocarditis and intravenous drug abuse histories often precede the discovery of infected celiac axis aneurysms.
Mortality from infected visceral artery aneurysms with antibiotic therapy alone has been reported in up to 50%, with rupture-associated mortality approaching 100%. Therefore surgical intervention is warranted should the patient be physiologically fit enough to tolerate the required procedure. Specific surgical options will be discussed in the ensuing sections regarding management.
Femoral Artery Infected Pseudoaneurysms
Infected femoral artery pseudoaneurysms due to intravenous drug abuse
Intravenous drug abusers can theoretically damage any vessel used to inject illicit substances. Most frequently, the common femoral and superficial femoral artery in the groin are involved ( Fig. 59.2 ). Other less common sites include the axillary and brachial arteries. Iterative puncture without sterile technique results in repetitive intraarterial introduction of microbes. Multiple products are also combined with the illicit substances to augment or dilute the effect, all of which may also be caustic to the artery and the surrounding tissues. Symptomatic presentations, including acute hemorrhage, systemic sepsis, a pulsatile mass, or limb ischemia, are frequent. The most common presentation varies depending upon the series and the location of the mycotic pseudoaneurysm. Without appropriate surgical therapy, hemorrhage, limb loss, and/or death ensues rapidly.
Most patients are young, with the majority presenting in their early 30s. Reports vary in their description of the predominant gender. Bacteriology of mycotic pseudoaneurysms from drug abuse vary among reports. If single microbial isolates are reported, the most common organisms are S. aureus and S. epidermidis. Methicillin-resistant S. aureus may be becoming more prevalent in the United States. However, 18% to 50% of series describe polymicrobial infections, which is intuitive given the repeated arterial punctures without adherence to sterile technique. Concurrent infection with hepatitis C and/or HIV is the norm, occurring in as many as 90% and 67%, respectively. A history of prior iliofemoral deep venous thrombosis is also common, occurring in over 70% of subjects in one series.
Iatrogenic infected pseudoaneurysms of the femoral artery
In spite of advances in the medical management of atherosclerosis, the rates of percutaneous coronary intervention remain largely unchanged. Approximately 600,000 to 1,000,000 procedures per annum are performed in the United States. This number underestimates the true figure, however, as peripheral interventions are not included in these studies. Moreover, percutaneous methods of closure are becoming increasingly prevalent following aortic endografting and structural heart procedures. Thus while iatrogenic catheterization-related infected aneurysms are rare, they remain a clinically significant entity simply due to the volume of catheterizations performed annually in the United States.
The rate of infection varies from 0.01% to 0.9%, depending upon the source. A recent meta-analysis suggests that infection is three times as likely with a vascular closure device versus manual compression alone. The specific mechanisms of action for the vascular closure device does not seem to impact infection rates, though no study is adequately powered to truly address this question. Likely, however, those that leave more foreign material are more likely to become infected, as the inoculum required to infect foreign material is lower. Risk factors favoring infection include a history of diabetes mellitus, therapeutic intervention, obesity, and presence of a groin hematoma.
Patients often present with pain, tenderness, and a pseudoaneurysm of the common femoral or superficial femoral artery in conjunction with fever and/or chills. Gram-positive organisms, such as S. aureus or S. epidermidis , predominate, though gram-negative organisms have also been isolated. Due to the predominance of skin flora, periprocedural contamination is the most likely source. Hence periprocedural adherence to antiseptic technique is critical. Symptoms may occur within days to weeks of the initial procedures. While the presentation is often milder than with infected aneurysm from intravenous drug abuse, the patients are frequently older, with atherosclerotic risk factors.
Primary Carotid Artery Infections
Primary infected aneurysms of the extracranial carotid are exceedingly rare. Over 35 years, only 45 cases had been reported in the world literature. However, due to the anatomic location and importance of the end-organ that the carotid artery supplies, these entities merit special mention. Typical presentations include an enlarging, painful pulsatile mass in the lateral neck associated with fever, dysphonia, and dysphagia. Impingement of nearby nerves can present as palsies of cranial nerves X and XII, Horner syndrome, exophthalmos, or ophthalmoplegia. Untreated, these may result in septic embolization of mural thrombus within the infected aneurysm sac. Alternatively, these may rupture, which may present as oropharyngeal bleeding, airway compromise, and/or stroke.
Frequent responsible microorganisms include S aureus. Case reports of multiple other microbes include Salmonella sp., Klebsiella sp., E. coli, Proteus mirabilis, Yersinia sp., and Corynebacterium sp. Prior to the widespread use of antibiotics, Mycobacterium sp. and Treponema sp. infections were also common. While infrequent, Mycobacteria and Treponema infection remain important in the differential among immunocompromised patients, or among patients without access to modern medical care. Leukocytosis and/or an elevated sedimentation rate may be present, but are often nonspecific. Blood cultures may aid in the diagnosis, but are negative in up to half of cases. The differential diagnosis includes carotid body tumor, peritonsillar abscess, cervical lymphadenitis, or kinking/redundancy of the extracranial carotid vasculature.
Other Primary Infected Aneurysms
The aforementioned sites are the most common sites of PAI. In the lower extremities, there have been infrequent case reports describing primary infected aneurysms of the popliteal, tibial, and pedal vasculature. In the lower extremity vasculature, due to the relatively superficial location compared to the abdomen or chest, presentation is relatively consistent, with a painful, pulsatile enlarging mass with fever and erythema overlying the involved artery. Signs and symptoms of distal ischemia may also be present. The infected aneurysms of the lower extremity vasculature are classically caused by endocarditis with septic emboli, though hematogenous spread from a noncontiguous source, or from direct puncture (iatrogenic, or due to illicit drug injections) are also prevalent. The true frequency of microorganisms causing infected peripheral aneurysms in the lower extremity is unclear due to publication bias, which likely results in underreporting of the more common infections. Gram-positive organisms are most frequently found in the literature, though cases of Salmonella sp. as well as Candida sp. have also been reported.
Upper extremity infected arterial aneurysms are also rare. The most frequently reported are secondary to illicit drug abuse and iatrogenic puncture. Signs and symptoms are similar to infected aneurysms of other superficial sites, with an enlarging, painful, pulsatile mass with overlying erythema and fevers. Signs of distal ischemia may also be present, such as cyanosis, petechiae, and splinter hemorrhages. The microbiology is similar to that of other peripheral infected aneurysms, with gram-positive organisms predominating, but with a significant minority of gram-negative and mixed infections as well.
Secondary arterial infections
Prosthetic conduits have extended the ability of physicians to manage arterial pathologies. Unfortunately, the advent of prosthetic conduits has given rise to the rare, though devastating, complication of SAIs, where the conduit and the adjacent artery become infected. While multiple advances have occurred over the last several decades, SAIs remain a difficult diagnostic challenge, and among the most challenging technical and emotional problems a surgeon may encounter.
Prosthetic graft infections are classified by extent of graft involvement, timing since initial implantation, and severity of graft involvement when associated with surgical site infections. While not widely used clinically, these classifications are helpful when studying SAIs, and ensure equitable outcome comparisons. Bunt described graft infections as cavitary and extracavitary. A P0 infection involves a cavitary (intraabdominal or intrathoracic) graft, or the cavitary portion of a graft. Examples include infections of an aortic tube graft or infections of the aortic portion of an aortobifemoral bypass graft. P1 infections are extracavitary only, such as prosthetic lower extremity bypass graft infections. P2 infections are those that involve the extracavitary portion of a graft that has both intracavitary and extracavitary components. An example is an isolated infection of the femoral limb of an aortobifemoral bypass graft. P3 infections involve prosthetic patches, such as an infected femoral artery patch after a common femoral endarterectomy. Bunt’s classifications also include qualifiers for aortoenteric erosions (AEE), and AEF, which he termed graft-enteric erosions and fistulae, respectively. AEE and AEF are similar in that both involve a communication between an enteric structure and infected aortic prosthesis. They differ in that AEE do not involve the suture line between the aorta and the infected prosthetic. Finally, there is a qualifier for an aortic stump infection, where there is an infection of the distal prosthetic stump after ligation and extra-anatomic bypass for a prior aortic graft infection.
Early graft infections are those that occur with 4 weeks of implantation of the prosthetic. When these are associated with surgical site infections, these wounds are classified by the Szilagyi classification, which has since been modified by Samson and colleagues. Szilagyi class I and II infections are superficial wound infections, and do not pertain to vascular infection. Szilagyi class III infections are those that involve the vascular graft and native artery. Samson and colleagues further classified those that involve the graft into several categories. Group 3 infections involve the graft, but do not involve the graft- arterial anastomosis. Group 4 infections are complicated by an exposed anastomosis, but do not have bacteremia or bleeding. Group 5 infections are the worst, and involve the anastomosis and are associated with bleeding from the suture line and/or bacteremia. The Szilagyi and Samson classifications are not necessarily named when describing surgical site infections involving vascular prostheses. However, these definitions do aid in risk stratification and clinical decision-making.
Pathophysiology of Secondary Arterial Infections
Immunodeficiency and nutritional deficiency that exist for PAI also occur in the SAI populations, thereby acting as a cofactor for prosthetic graft infections. Infectious sources include intraoperative contamination, hematogenous spread, or spread from a contiguous source. The role of collagenases and elastases upon the pathogenesis of SAI is similar to PAI, and have been discussed previously. Hence this section will highlight the mechanisms underlying the increased susceptibility to infection with prosthetic materials.
Prosthetic arterial grafts become infected more easily than native arteries, and require a 10,000-fold lower inoculum to become infected. The most common prosthetic materials include polyethylene terephthalate (Dacron) and polytetrafluoroethylene (Gore-Tex). Specific to SAI, there are three separate factors that potentiate SAI: graft factors, ineffective host immune responses, and bacterial biofilm formation. Microbes preferentially adhere to prosthetic graft relative to the host tissue for several reasons. Synthetics are irregularly surface fomites, that create relatively avascular pockets that may harbor microbes. Upon implantation, prosthetic grafts are also coated almost immediately by multiple host proteins, the most notable of which are fibrinogen, fibronectin, and laminin. These each increase the risk of prosthetic infection as they mediate bacterial binding. Charged prosthetics, in contrast to electrically neutral materials, also increase the propensity for bacterial adherence. Hydrophilic materials exhibit decreased bacterial adherence relative to hydrophobic materials.
The host response can also paradoxically abrogate immune cells ability to eradicate pathogens. For instance, contact with the prosthetic causes neutrophils and natural killer cells to degranulate. Hence when they do contact bacteria, even if favorably opsonized by complement, these cells are less likely to be bacteriocidal, as they no longer have sufficient respiratory burst to act upon the bacteria. Similarly, phagocytic cells exhibit impaired activity against bacteria in the presence of prosthetic material. Attenuation of the immune cell response is worsened with increased complement activation against the foreign material, which increases inflammation and further attracts phagocytes and neutrophils to the area of implantation. Neointimal formation along the graft is critical to decreasing infection rates, and requires a minimum of 2 weeks to form.
Bacteria have also developed several mechanisms to evade the host immune response, the most notorious of which is the formation of biofilm. This occurs after adhesion of the bacteria to the graft, which then begin to form exopolysaccharide matrix, or “slime.” The slime improves adherence, and protects the bacteria from immune cells and antibiotics in the serum. Within the biofilm, the metabolic rate is altered via quorum-sensing, or the ability to decrease the metabolic rate when other microbes are in close proximity. Quorum-sensing decreases the ability of host defenses to detect and eradicate microbes. Biofilms also serve as a method to more efficiently transport nutrients and waste to and from the colony.
Finally, bacteria may reside within the cells of the host. Certain microorganisms are obligate intracellular organisms. Other microorganisms, however, are traditionally considered extracellular bacteria, but develop the capacity to live within the host cells in the presence of prosthetic materials. When intracellular, the microorganisms dramatically decrease their metabolic rate, and are protected against the immune response by the host cell. These small intracellular colonies can then proliferate slowly over the course of years, until they reach a sufficient density, become extracellular, and infect the prosthesis.
Common Locations and Presentations of Secondary Arterial Infections
SAI can theoretically occur wherever a prosthetic graft, patch, or stent is placed in continuity with the artery. Hence these infections will be localized to where prosthetics are frequently utilized. The presentation depends upon the virulence of the microorganisms, the extent of graft involvement, and anatomic locale involved. These will be described in further detail in the following subheadings. There are three main locations where prosthetic arterial infections occur: the aorta, the lower extremity, and the carotid artery.
Aortic Graft Infections
Aortic graft infections are highly lethal and represent some of the most diagnostically, technically, and emotionally challenging cases that surgeons may face. The inflammation that is frequently encountered with infection is worsened by the scar tissue and adhesions from the prior surgery, which obliterates anatomic dissection planes. Each case requires individualized management that matches the patients’ and caregivers’ wishes with the anatomic and surgical requirements for appropriate therapy.
While significantly more prevalent than primary aortic infections, aortic graft infections remain underdiagnosed, with significant diagnostic delays translating into treatment delays with markedly diminished chances of successful outcome. Data from the United Kingdom Small Aneurysm Trial suggest that 2% of open aortic reconstructions are complicated by infection. More contemporary registry data, however, portray a lower rate of aortic graft infections, with both open and endovascular aortic graft infections occurring in less than 1%. Large single center cohort data from Baylor College of Medicine also confirm the < 1% rate of graft infection after open thoracoabdominal aortic aneurysm repairs. The rates after thoracic endograft placement are difficult to measure, as the series in the literature are significantly smaller than those describing infrarenal aortic endograft infections. Logically this follows, since the prevalence of thoracic endograft placement is significantly lower than infrarenal aortic endograft placement. No particular manufacturer or stent graft design is associated with an increased risk of aortic endograft infection.
The microbiology of aortic graft infections belies the most likely causes of aortic graft infections, and differs somewhat from that of primary aortic infected aneurysms. Staphylococcal and Streptococcal sp. are responsible for up to 55% of aortic graft infections. These microorganisms are consistent with the theory that intraoperative contamination is responsible for many, and perhaps most, aortic graft infections. Gram-negative organisms and anaerobes are the next most frequent organisms. Candida sp. are particularly prevalent with AEF. Hence their presence should raise one’s suspicion of an AEF. The causal organisms are not cultured many times, due likely to the lack of cultures prior to the institution of antibiotic therapy. Moreover, culture techniques are biased against slow-growing organisms so that the prevalence of anaerobes, fungi, and fastidious organisms is likely underrepresented.
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