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Chapter 88

Vascular Infection

Jayer Chung and J. Gregory Modrall

Key Points

1 The pathogenesis of infected aneurysms involves seeding of a pre-existing aneurysm by bacteremia.

2 The pathogenesis of microbial arteritis involves hematogenous seeding of an atherosclerotic plaque.

3 The pathogenesis of infected aortitis involves direct spread of infection to the aorta by contiguous

septic structures, such as vertebral osteomyelitis.

4 The pathogenesis of arterial graft infections involves seeding of the graft from intraoperative

contamination, erosion of adjacent structures, or hematogenous seeding from a distant source.

5 Characteristics of a prosthetic graft that predispose to graft infection include lowering of the

bacterial bioburden required to cause a graft infection, surface irregularity that permits bacterial

attachment, abrogation of local defense against infection, and creation of the bacterial biofilm that

protects microbes from host defenses and antibiotics.

6 The most common organisms causing arterial graft infections are skin flora, especially Staphylococcus

aureus and Staphylococcus epidermidis.

7 Of the available surgical options for aortic graft infections, treatment with graft excision, aortic

ligation, and extraanatomic bypass is associated with the highest risk of mortality, aortic stump

blowout, and graft occlusion of the available surgical options.

8 Treatment of aortic grafts infections with graft excision and in situ reconstruction with rifampinsoaked Dacron has been associated with the highest rate of reinfection of the available surgical

options.

9 Treatment of aortic grafts infections with graft excision and in situ reconstruction with femoral vein

is the most time-consuming surgical option, but is associated with the lowest risk of reinfection.

10 Treatment of aortic grafts infections with graft excision and in situ reconstruction with

cryopreserved human allograft has been associated with a risk of graft rupture and

pseudoaneurysmal degeneration.

Vascular infections are among the most daunting conditions that a surgeon may encounter in clinical

practice. Vascular infections may afflict native arteries and veins or vascular prostheses. Primary

arterial infections of native arteries are rare, but highly lethal conditions.1 Secondary infections of

prosthetic vascular grafts, albeit rare, are seen more frequently and are often more challenging because

of the adhesions, scarring, and inflammation in the redo operative field.2 These infections commonly

occur in a compromised patient population with significant chronic medical conditions and relative

immune deficiency. The clinical presentations for vascular infections range from indolent infections

detected incidentally to overt sepsis or hemorrhage.1 The management of vascular infections is

individualized, based on the clinical presentation and anatomic location of the vascular infection and the

medical condition of the patient. In recent years, newer therapeutic adjuncts, such as covered stents and

improved cryopreserved grafts, offer additional options to surgeons managing and treating arterial graft

infections. However, the basic tenets of timely diagnosis, antibiotic administration, resuscitation,

operative planning, surgical resection, and revascularization remain the mainstays of therapy in most

cases.

DEFINITIONS AND PATHOGENESIS

Pathogenesis of Primary Arterial Infections

1 2 3 Arterial infections commonly result in aneurysms, or more correctly pseudoaneurysms since there

2523

is disruption of the arterial wall in many infected aneurysms. Aneurysms or pseudoaneurysms related to

infection are often loosely termed “mycotic aneurysms.” However, the term mycotic aneurysm was

initially coined to describe an arterial aneurysm or pseudoaneurysm caused by a septic embolus from

the heart that lodges in a distal artery to create a septic focus that injures the adjacent artery.3 Preexisting aneurysms that are subsequently seeded by bacteremia are “infected aneurysms.” Arteries in

which an atherosclerotic plaque becomes seeded develop “microbial arteritis.” “Traumatic infected

aneurysms” describe those infected aneurysms or pseudoaneurysms that develop secondary to

complications of iatrogenic or other trauma. “Infected aortitis” occurs when the aorta becomes infected

by contiguous septic structures, such as vertebral osteomyelitis.3 For simplicity, we will utilize the term

“primary arterial infection” to refer to all infected arterial infections that occur in the absence of

prosthetic graft or stent material.

Infective endocarditis is no longer the major source of primary arterial infections. Arterial trauma,

particularly due to intravenous drug use, appears to be the most prevalent cause.1 Risk factors for

primary arterial infections include trauma to the arterial wall, atherosclerosis, and pre-existing

aneurysmal degeneration. In an autopsy study, Miller reaffirmed that many of infected aneurysms arise

after pre-existing atherosclerotic lesions are seeded due to an episode of bacteremia, since 75% of the

infected arteries had evidence of atherosclerosis in the resected specimen.4 In Miller’s study, 42% of

arterial infections were located in the infrarenal aorta; the descending thoracic aorta was the next most

common site of infection.4 Immune compromise by systemic conditions or medications, such as chronic

steroid use, malignancy, human immunodeficiency virus syndrome, chronic hepatitis, or malnutrition, is

a common theme among patients with primary arterial infections. Predisposing conditions have been

identified in nearly 70% of patients with mycotic aneurysms.4–7

Pathogenesis of Arterial Graft Infections

Prosthetic grafts are foreign bodies that are either seeded at the time of the operation, or become

infected secondarily due to hematogenous seeding or contiguous infection.8–10 Data from the UK Small

Aneurysm Trial suggest that contemporary rates of aortic graft infections after open aortic

reconstruction are approximately 2%.11 In his study of abdominal aortic aneurysms repaired in

Washington State from 1987 through 2005, Vogel found that the 2-year rate of aortic graft infections

was 0.19%.12 Infrarenal endograft implantation is associated with infection rates of less than 1%.13–15

The infection rate of thoracic aortic endografts is less well defined due to smaller number of thoracic

endografts, compared to infrarenal aortic endografts, but most authorities believe that the rates of

thoracic endograft infection are similar to those described for infrarenal aortic endografts. No particular

endograft design or fabric appears to alter the risk of graft infection.13–15

Lower extremity prosthetic grafts are at the highest risk of infection, which probably relates to the

abundance of skin flora in the groin and the proximity of the graft to the incision. Infections of grafts

originating from or terminating at the femoral artery complicate 4% to 6% of cases.16,17 By comparison,

carotid patches rarely become infected, with Mann reporting a single-center incidence of 0.8% over 20

years.18 Polytetrafluoroethylene (PTFE) may be somewhat more resistant to infection than Dacron, as it

has less porosity to sequester microbes.19 Peripheral bare metal stents appear to be highly resistant to

infection, with a presumed incidence of less than 0.1% based on isolated case reports.20

5 Prosthetic material is at risk for becoming infected for several reasons. First, a 10,000-fold lower

bacterial bioburden is required to cause a graft infection, relative to healthy tissue.21 Irregularly

surfaced materials are also more likely to harbor microbes, as these surfaces create small pockets where

shear stress is decreased to allow bacterial attachment.19,22 Also, the local inflammatory response to

implants abrogates the local defense against infection. Instead of being inert, the prosthetic material

acts as a potent activator of host defenses, which subsequently renders them less capable of defending

the graft from infection. Multiple studies have shown contact with implants causes neutrophils to lose

their ability to produce superoxide and reactive oxygen species, which are critical to their bactericidal

activity.23,24 Finally, communities of bacteria form slime to create biofilms, protecting microbes from

host defenses and antibiotics.19,22,25 Quorum-sensing is prevalent in biofilms, which decreases the

virulence of microorganisms and makes them more difficult to eradicate by host defenses as the bacteria

proliferate.26 This is a critical step in the pathogenesis of prosthetic graft infections caused by

Staphylococcus epidermidis (Fig. 88-1).19,21–26

2524