Despite antibiotic prophylaxis and the development of more refined surgical tecniques, microbial infection of the vascular prostheses are well known, not rare and redutable coplications.
The literature-reported incidence may vary between 0,2 and 5% and it is influenced by: the site of the implant, the underlying disease and the host defense mechanism.
Infection affects especially prosthetic grafts which are implanted during emergency procedures (for example emergency surgery for the ruptured abdominal aortic aneurysm) and prostheses anastomosed to the femorala artery or placed into an subcutaneous tunnel (for example the axillofemoral or axillobifemoral grafts).
Vascular graft infections are classified by their appearance time (early infections-which appear earlier than 4 months after graft implantation; late infections-which appear after 4 months), their relationship to the postoperative wound and the extent of graft involvement.
Szilagy’s classification  is reffering to the grades of postoperative’s wound infection. So we have three
grades,as follows:

  • grade I: cellulitis involving wound;
  • grade II: infection involving subcutaneous tissue;
  • grade III: infection involving the vascular prosthesis.

An early infection correlates with a Szilagyi grade III wound infection. These infections are caused by virulent hospital-acquired bacteria and present with sepsis signs  like: fever, leukocytosis, bacteremia and easy noticeble  signs of an infected wound (inflamated tissues around it, pus emerging from it).
Late infections are a result of graft colonization by “low-virulence” organisms such as: Staphylococcus epidermidis  or Candida spp. They are characterized by the fact that  they are indolent and have no signs of sepsis and cultures  of the perigraft tissues are not growing any germs.

Pathogenesis of graft infection 
The initiating event is the bacterial afherence to the biomaterial surfaces, followed by colonization and development of a bacterial biofilm that resist host  defenses and antibiotic penetration.
The presence of a foreign body potentiates the infectivity of bacteria. Elek  and Cone demonstrated in 1957 that a  single-braided silk suture significantly reduced the  inoculum of staphylococci recquired to produce a local  infection. The risk of foreign body infection can be  predicted by the formula:

Risk of biomaterial infection = (Dose of bacterial contamination× virulence)/Host resistance 

Bacterial adherence to polyester grafts is 10 to 100 times  greater than to PTFE grafts. Gram-positive bacteria  produce an extracellular glycocalix made out of mucine  which makes them much more adherent than, for
example, Gram-negative ones. Etiologic factors involved in graft colonization:  perioperative contamination; bacteremia seeding of the  biomaterial; mechanical erosion into bowel or genitourinary tract or through skin.
The risk factors for graft infection are:

  1. Bacterial contamination of the graft (Faulty sterile  technique; Prolonged preoperative stay; Emergency  surgery; Extended operative time; Reoperative vascular  procedure; Simultaneous gastrointestinal procedure;  Remote infection; Postoperative superficial wound  infection/skin necrosis/seroma/lymphocele).
  2. Altered host defenses  Local factors (Biomaterial foreign body reaction: Bacterial  slime producing a protective biofilm).  Systemic factors (Malnutrition; Leukopenia/ lympho- proliferative disorders; Malignancy; Corticosteroid  administration; Chemotherapy; Diabetes mellitus; Chronic  renal failure; Autoimmune disease).

Vascular infections can be minimized if some simple  principles are applied:
• avoid a prolonged preoperative stay to minimize the  development of skin flora resistent to commonly used  antibiotics;
• have patients shower or scrub with an antibacterial soap  the night before the operation;
• control the remote infections before an elective  operation;
• remove operative site hair immediately before surgery  using scissors rather than razors, to minimize skin  trauma;
• protect vascular grafts from contact with contaminating  sources, especially the exposed adiacent skin, using  iodine-impregnated plastic drapes or antibiotic-soaked  towels;
• avoid simultaneous gastrointestinal procedures during  garfting;
• use prophylactic antibiotics whenever a graft or stent is  implanted;
• longer duration of perioperative antibiotics (>48 hours)  may be considered whenever patients present more than  two risk factors for wound infection, including extremes  of age, malnutrition, chronic illnesses such as diabetes,  remote infections or prior irradiation of the surgical site.

Antibiotic prophylaxis protocols for vascular procedures  are as follws:
• Cefazolin 1-2 g IV slowly prior to induction of  anesthesia and repeated (1-2g) each 8 hours for 24-48  hours, or cefuroxime 1,5 g IV and each 12 hours for a  total of 6 g; a single dose of cefazolin 1 g IV is  recommended prior to endovascular stent implantation;
• When MRSA (methycillin-resistant Staphylococcus  aureus) is cultured from body surfaces or is a known  important pathogen in hospitalized patients, add  vancomycin 1 g IV infused over 1 hour;
• If the patient has a cephalosporin allergy, give aztreonam  1g IV each 8 hours for 24 hours;
• If the patient has a vancomycin allergy, give  clindamycin 900 mg IV over 20-30 minutes followed
by 450-900 mg IV each 8 hours for 24 hours.  In some vascular centers, prophylactic antibiotics are
continued for 3 to 5 days in patients being at high risk for  infection from bacteremia, prolonged preoperative  hospitalization or high institutional wound infection rates (>10%).
S. aureus is the most prevalent pathogen, one fourth of  prosthetic infections being caused by it.  Lately, prosthetic infections caused by S. Epidermidis or  Gram-negative bacteria have emerged.  This change in the microbiology of graft infections is the  result of reporting both early and late infections and of  surgeons becoming more aware of the false-negative  microbiological results taken from many late infections,  owed to the low bacteria numbers present within the graft  surface biofilm.
Garft infections associated with negative culture results are  caused by S.epidermidis or other coagulase-negative
staphylococci, or by Candida species.  Infections due to Gram-negative bacteria as E.Coli,
Pseudomonas, Klebsiella, Enterobacter and Proteus spp are  very virulent.
The incidence of anastomotic dehiscence and artery rupture  is high and is due to the ability of these organisms to  produce destructive endotoxins.  Fungal infections are very rare and most of the patients  having them are immunosuppressed or have an established  fungal infection elsewhere.
MRSA is responsible for one fourth of early graft  infections, nowadays. This recent increase in MRSA graft
infections may justify the use of specific antibiotic  prophylaxis for all vascular implant procedures.
Infection diagnosis is reached upon clinical examination,  microbiology findings and intraoperative aspects.
Clinical evaluation includes: patient history, physical  examination and vascular imaging( arteriography,ultarsonography, contrast-enhanced CT, endoscopy).
Surgical therapy is mandatory, antibiotic therapy alone not  being enough.  General principles of the overall management strategies:  Determining the extent of graft infection; ± removing the  graft; Debridement of the arterial wall and perigraft tissues;  Draining and antibiotic therapy.
Calligaro and colegues reccomended specific criteria for  selective graft preservation:
• patent graft that is not construcetd of polyester:
• anastomoses are intact and not involved in the

• patient has no clinical signs of sepsis.

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