Chapter 50: Prosthetic Graft Infections

INTRODUCTION

Despite all advancements in antimicrobial treatments and surgical infection control, vascular graft infections remain a major cause of morbidity and mortality. Vascular infections can lead to enteric fistulas, pseudoaneurysm formation, ruptures, septic emboli and limb amputation, bacteremia and sepsis, and ultimately death. With the shift in vascular surgery practice from open to less invasive endovascular and percutaneous methods, more stents and stent grafts are being employed to treat vascular patients. In addition, with the advancement of prosthetic material technology, more prosthetic patches and grafts are being used by vascular surgeons in open surgery. This increased utilization of “foreign” material has increased the potential and amplified the complexity of vascular grafts infections. As such, the management of vascular infections usually requires complex strategies involving substantial human and equipment resources, multidisciplinary approaches, as well as prolonged and multiple interventions. In the chapter, we discuss the etiology, classification, presentation, and diagnostic modalities for the different types of vascular graft infections as well as the suggested treatment strategy for each.

ETIOLOGY AND PATHOGENESIS

Vascular graft infections arise from either a contamination at the time of graft insertion or from hematogenous spread or from direct extension of a nearby infection.^1,2 Vascular infections due to contamination at the time of insertion present in the early postoperative period. They are thought to arise due to sterile field contamination in the operating room, from inadequate sterile techniques, contact with patient’s skin, iatrogenic bowel injury, or from the transection of lymphatic channels in the presence of remote infected organs.^3,4 Vascular infections due to hematogenous spread usually present later in the postoperative course. Bacteremia from distant infections such as genitourinary, gastrointestinal (GI), foot infections, or periodontal infections can seed the vascular graft. The risk of seeding is highest during the first 2 months but extends for up to 1 year, or until the development of a pseudointimal lining and complete endothelization of the graft.⁵ Vascular infections due to extension of a nearby infection occur when a surgical site infection or other nearby infection progresses to the adjacent graft. Examples include a wound infection in the subcutaneous tissue of an infrainguinal bypass that progresses to the deeper planes into the adjacent graft, or a suboptimal coverage of an aortic graft that leads to erosion of the graft into a bowel loop that directly infects the aortic graft.

Gram-positive cocci account for almost two-thirds of vascular graft infections.⁶ While historically Staphylococcus aureus was the most common isolated organism, recent reports found that coagulase negative staphylococcus have taken the lead.⁷ Staphylococcus organisms can establish infection through biofilm and slime production. These biofilms protect the bacteria from the innate immune system and limit the efficacy of antibiotics by preventing them from reaching the bacteria in the biofilm matrix.⁸ Other common isolated organisms include gram-negative bacilli such as Pseudomonas aeruginosa. These are usually associated with aortoenteric fistulas.^9...