Pathophysiology of Vascular Graft Infections

Mauro Vicaretti

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Fitridge R, Thompson M, editors. Mechanisms of Vascular Disease: A Reference Book for Vascular Specialists [Internet]. Adelaide (AU): University of Adelaide Press; 2011.

Mechanisms of Vascular Disease: A Reference Book for Vascular Specialists [Internet].

Show details

Contents

< PrevNext >

29Pathophysiology of Vascular Graft Infections

Mauro Vicaretti.

Author Information and Affiliations

Introduction

The introduction of prosthetic grafts has revolutionised the management of vascular disease but graft infection although uncommon, remains a dreaded complication with associated significant morbidity and mortality. Mortality occurs in approximately one third of all vascular graft infections,¹ with mortality highest when an aortic prosthesis is involved.²^,³ As many as 75% of survivors of an infected aortic prosthesis require amputation of a limb,³ with the incidence of amputation highest when the infection involves more distal prosthetic grafts.⁴ The incidence of graft infections is difficult to quantify as infection may manifest many years after implantation¹ with many reports being isolated or as part of case series. Nevertheless, the reported incidence is in the order of 5%, varying according to the site of operation, being higher when a groin incision is used, or if the procedure is an emergency or a redo procedure. Infection following endovascular stent deployment has been reported although its incidence is considered to be very low.

Natural History of Prosthetic Vascular Graft Infections

Early prosthetic vascular graft infections typically occurring in the first four months following placement are relatively uncommon (approximately 1%) and are usually caused by the more virulent micro-organisms, such as S. aureus, E. Coli, Pseudomonas, Klebsiella, Proteus and enterobacter.¹ Late prosthetic vascular graft infections are the result of two possible mechanisms. Firstly, by haematogenous seeding from a septic focus elsewhere⁵ or by the prosthetic graft becoming infected with enteric contents following a graft-enteric erosion.⁶ In both the haematogenous and graft-enteric erosion situations the usual causative organisms are those with high virulence and clinical manifestations are signs and symptoms of sepsis. The second mode of presentation is insidious, caused by the less virulent coagulase negative staphylococci such as S. epidermidis with contamination likely occurring at the time of implantation.¹

Mechanisms of Graft Contamination at Operation

Prosthetic grafts most commonly become infected at the time of implantation either by contamination from the surgical team or by colonised microorganisms on the patient. It has been demonstrated that the majority of patients undergoing arterial revascularisation are colonised with coagulase negative staphylococci⁷ and colonisation of patients with nosocomial bacteria is enhanced when the preoperative hospitalisation is lengthy.⁸

The incidence of infection following emergency aneurysmorrhapy has been reported to be increased to 7.5%.⁹ The evidence of other potential mechanisms such as division of lymph nodes,¹⁰^,¹¹^,¹² infected transudated fluid during aortic surgery¹³^,¹⁴^,¹⁵ and infected laminated thrombus⁴^,¹⁴^,¹⁶^,¹⁷ is conflicting.

Pathogenesis of Graft Infections

The exact aetiology of vascular graft infections is not completely understood but is likely to be multifactorial. According to Bandyk and Esses¹⁸ the risk of vascular graft infection as demonstrated by animal models can be predicted by the formula:

\begin{matrix} Risk of biomaterial \\ infection \end{matrix} = \frac{\begin{matrix} Dose of bacterial \\ contamination X virulence \end{matrix}}{Host resistance}

The dose of bacterial contamination is dependent on the infecting microorganism. Experimentation in a canine aortic model has demonstrated that the infective threshold for bacteria to cause graft infection in over 50% of grafts was 10⁷, 10⁹, and 10² for S. aureus, S. epidermidis and P. aeruginosa respectively.¹⁹ Virulence of microorganisms is often associated with the production of secreted toxins and enzymes with a resultant decline in structural integrity of the artery wall¹⁸ and the release of toxins and enzymes to control the perigraft environment and cause graft infection.¹⁹^,²⁰ Many bacterial strains, including S. epidermidis, S. aureus and P. aeruginosa are known to produce extracellular polymer substances (slime), forming a capsule incorporating the bacteria. This is referred to as a biofilm and protects the micro-organism against host defences and antibiotic therapy.²¹ Biofilms allow greater adherence of the microorganism to the biomaterial²²^,²³ and contribute to bacterial virulence. Multiple species of microorganisms may co-exist in a biofilm and unless the biofilm is disrupted and or the microorganism/s become planktonic the microorganism/s identification is limited. Different graft materials have varying susceptibility to infection. Dacron grafts are more likely to become infected than grafts made of PTFE (polytetrafluoroethylene).²⁴ The use of vein grafts instead of prosthetic material greatly reduces the risk of infection.

Bacteriology of Vascular Graft Infections

Gram-positive, Gram-negative, anaerobic and fungal micro-organisms all have the potential to infect a vascular prostheses but in general the majority of infections are the result of a small number of micro-organisms. Staphylococci are the most prevalent organism associated with prosthetic graft infection.²^,²⁵^,²⁶^,²⁷ Of the staphylococci, S. aureus is generally regarded as the most common causative bacteria,²^,²⁶^,²⁸^,²⁹ particularly MRSA.²⁷ S. epidermidis is now being recognised as the leading cause of vascular graft infection, particularly chronic and late onset infections.¹⁷^,²⁹^,³⁰^,³¹^,³²

The Gram-negative organisms, E. Coli, Pseudomonas, Klebsiella, Enterobacter and Proteus, although relatively uncommon causative organisms for graft infections are of particular interest and concern because of their high virulence and their tendency to destroy the vessel wall.¹⁸^,³³^,³⁴

Candida mycobacterium, and Aspergillus infections are uncommon but pose a significant risk to patients who are immunocompromised.² Although uncommon they are all expected to increase in frequency because of their increasing resistance to standard prophylactic antibiotics.³⁵

There is an association between the type of infecting organism, the type of vascular complication and the arteries that are involved in the anastomosis to the prosthetic graft. Bandyk and Bergamini² in a collective survey of 1258 patients who had a vascular graft infection found that the majority of aortoenteric fistulas were the result of either Streptococci or E. Coli and if the anastomosis involved the femoral artery, the thoracic aorta, the subclavian, carotid or innominate arteries S. epidermidis or S aureus was the likely causative organism. E. Coli, Enterococci and Enterobacter were the more likely organisms to be involved in aortoiliac anastomoses.

Investigations for Detection of Prosthetic Graft Infections

The diagnosis of vascular prosthetic infections can be difficult as the presentation may be subtle especially if it is a late onset infection, the prosthesis is intra-abdominal and the micro-organism is one of low virulence. Presentation is thus very dependent on the location of infection and the causative microorganism/s. The diagnosis is aided by multiple available microbiological investigations and imaging but in general is directed more at proving the absence of infection rather its presence. Not only are investigations imperative in the diagnosis of vascular graft infection but they may assist in the planned therapy including vascular reconstruction when required. At times the only means of confirming graft infection is the surgical excision of the graft and further microbiological assessment.

History and physical examination

The clinical clues suggesting graft infection especially those placed superficially include an inflammatory perigraft mass, overlying cellulitus, presence of exposed prosthetic graft, a sinus tract with persistent purulent drainage and/or bleeding and/or a palpable anastomotic pseudoaneurysm, graft thrombosis and distal septic embolisation.²^-⁴^,³⁶^,³⁷ The presence of intra-abdominal prosthetic graft infection may be non-specific, such as fever of unknown origin, septicaemia, or abdominal pain.³ Upper or lower gastrointestinal haemorrhage either of an acute or chronic nature may indicate a graftenteric fistula¹⁷^,³⁷^,³⁸ and can only be excluded when another source of gastrointestinal haemorrhage has been identified.

Laboratory investigations

Routine laboratory studies such as white cell count and differential, erythrocyte sedimentation rate (ESR), C-Reactive Protein (CRP), and blood cultures are routinely obtained but the results may be non-specific and even normal if the organism is S.epidermidis.² Wherever possible pus, exudates, tissue specimens, blood and wound cultures should be analysed microbiologically to aid in microorganism identification and to allow the commencement of appropriate and specific chemotherapy.³⁹ To aid in the diagnosis of S.epidermidis all solid material should be mechanically or ultrasonically disrupted.⁴⁰^-⁴²

Diagnostic imaging

Various diagnostic modalities (Computerised Tomography (CT), ultrasonography, Magnetic Resonance Imaging, Leucocyte or immunoglobulin labelled scanning, Positron Emission Tomography (PET) scanning +/-CT, angiography and/or endoscopy) may assist the vascular surgeon in determining the presence and extent of prosthetic graft infection. Not infrequently, a combination of the diagnostic modalities to improve sensitivity and specificity are utilised to confirm the presence or absence of a vascular prosthetic graft infection.⁴³ These modalities are also helpful in planning definitive surgery. The utility of CT angiography with the capability of vascular three dimensional reconstructions has largely replaced digital subtraction angiography as the method of diagnosis and therapeutic planning. CT guided aspiration is also of benefit in diagnosis. In general the features suggestive of graft infection include perigraft fluid and/or gas, graft disruption, absence of graft incorporation, pseudoaneurysm formation. The pres ence of periprosthetic gas more than six weeks following graft implantation is an abnormal finding and should alert the physician to the likelihood of a graft infection.⁴⁴

Management of Prosthetic Graft Infections

The general principles in the management of prosthetic graft infections are initially preventative, but in the event of a vascular graft infection, therapy needs to be individualised accounting for clinical findings, graft material (prosthetic versus autogenous graft material), site of infection, microorganism/s involved and patient co-morbidities. It is imperative that not only is graft infection eradicated but recurrent infection be minimised with avoidance of significant morbidity and/or mortality.

Prevention

Preventive measures such as the routine use of skin preparations,⁴⁵ the use of a depilatory agent,⁴⁶ limiting the length of preoperative hospitalisation,⁸ operating time and intensive care stay all contribute to the reduction in wound infection and more importantly the chance of developing resistant multiple nosocomial infections.⁴⁵ Antimicrobial prophylaxis has been shown to reduce wound infections in vascular surgery⁴⁷ and ideally should be given as close to the time of incision and repeated in the event of haemorrhage and lengthy operations every four hours. Prophylatic antibiotics are also indicated with percutaneous punctures of existing prosthetic grafts and the implantation of stents. Decolonisation of nasal carriers of S. aureus has been shown to significantly reduce the number of surgical site S. aureus infections especially deep surgicalsite infections.⁴⁸ Institutional prevalence of resistant organism may also dictate antibiotic prophylaxis especially when prosthetic grafts are to be implanted.

As a preventive measure host resistance may be enhanced by the antimicrobial impregnation of grafts. A number of novel combinations of grafts and antibiotic with or without various forms of treatment have been trialled at both the in-vitro and in-vivo levels.

Rifampicin, a known anti-staphylococcal agent, particularly methicillin resistant,⁴⁹ is a hydrophobic semisynthetic substance with a high affinity for gelatin.⁵⁰ It inhibits DNA dependent RNA polymerase activity in bacterial cells without affecting mammalian cells⁵¹ and has been passively incorporated into gelatin sealed Dacron grafts as a mode of staphylococcal protection at the time of implantation. It has been shown to be resistant to experimental bacterial contamination⁵²^-⁵⁵ with in-vivo bioactivity to 22 days,⁵⁶ and in-vitro bioactivity to 4 days.⁵⁷^-⁵⁹ It is these qualities plus its excellent tissue and intracellular penetration⁵⁹ that make rifampicin an ideal antibiotic to be bonded to prosthetic grafts in order to prevent subsequent graft infection.

Reduction of prosthetic vascular graft infection with rifampicin bonded gelatin sealed Dacron

Using an established sheep model⁶⁰ we replaced a segment of sheep carotid artery with a rifampicin soaked Gelsoft graft. At the time of graft removal microscopic assessment (perigraft abscess formation, presence of anastamotic disruption and graft thrombosis) and microbiological assessments (cultures of perigraft tissues, graft external and internal wall and total graft cultures) were recorded. We showed that, following direct inoculation of the rifampicin (1.2mg/ml or 10mg/ml) soaked graft with 10⁸ colony forming units of either methicillin resistant Staphylococcal aureus (MRSA) or methicillin resistant Staphylococcal epidermidis (MRSE), the rifampicin soaked graft offered significant prophylaxis.⁶¹^-⁶³

For the Mr Se arm, in the 10mg/ml rifampicin group there was a significant reduction in graft infection when compared to both the control group (p < 0.05) and the 1.2mg/ml group (p < 0.05).⁶³ Similarly, for the MRSA group, in the 10mg/ml treatment group there was a significant reduction in the total number of positive cultures when compared to the control group (p < 0.05) and the 1.2mg/ml group (p < 0.05).⁶³

Established Infection

Antibiotic therapy

Once the diagnosis or suspicion of prosthetic vascular graft infection is made then broad spectrum antimicrobial therapy is initiated and subsequently converted to organism specific antibiotics.³ The length of antibiotic therapy following excision of the infected graft is unclear but Bergamini and Bandyk² advocate parenteral antibiotics for two weeks and oral for six months.

Operative management

The ‘gold standard’ treatment although technically challenging is the removal of all infected tissue and revascularisation extra-anatomically.⁶⁴ A number of more conservative approaches have been advocated depending on the site of the infection and the microorganism involved. The most conservative of treatments is aggressive local wound care with graft preservation (prosthetic/autologous) providing that the graft and anastomoses are intact and the patient has no systemic features of sepsis.⁶⁵ Calligaro et al³⁴ in a report of a series of patients who had graft preservation concluded that with the exception of Pseudomonas, vascular graft infections could be managed with debridement, antibiotic therapy and wound closure. The skeletonized prosthetic graft can be covered using viable regional rotational flaps.⁶⁶ Others have proposed graft excision and replacement with cadaveric arterial allografts,⁶⁷ venous autografts,⁶⁸ cryopreserved saphenous vein homografts,⁶⁹ autogenous arteries and/or veins⁷⁰ or prosthesis.⁷¹ The major drawback with in-situ reconstruction is recurrent graft sepsis⁷² with potential limb and/or life threatening graft and/or anastomotic disruption.

Schmitt, et al.²² in an in- vitro model comparing the bacterial adherence of four strains of bacteria (S. aureus, ‘mucin’ and ‘non-mucin’ producing S. epidermidis and E. coli) to ePTFE, woven Dacron and velour knitted Dacron found that bacterial adherence was greatest to velour knitted Dacron and least compared to ePTFE. In addition Schmitt, et al.⁷³ found that ‘mucin’ producing S. epidermidis adhered to Dacron in 10 to 100 fold greater numbers compared to PTFE. Bandyk and Bergamini² have postulated that the differential adherence of staphylococci relates to capsular adhesins.

Using the established sheep model⁶⁰ we have set out to determine if the replacement of a staphylococcal infected vascular graft with a graft impregnated with rifampicin would be considered appropriate surgical management in preventing early recurrent infection. Gelsoft grafts without any antibiotic treatment were infected with overwhelming concentrations of either MRSA or MRSE. The grafts were removed at three weeks and replaced with either control (no rifampicin) grafts or grafts soaked in either 1.2mg/ml or 10mg/ml of rifampicin. The replacement grafts were removed 3 weeks following placement.

For MRSA⁷⁴ there were no statistical significant differences between the groups for any of the macroscopic or microbiological parameters recorded.

For S.epidermidis⁷⁴ there were no statistical differences between the rifampicin concentrations for macroscopic findings. There were however, statistically significant reductions in the number of total infected specimens in the 10mg/ml group when compared to both the control, (p<0.001) and the 1.2 mg/ml groups (p<0.005).⁷⁴

The conclusions from the studies⁷⁴ were that established S. epidermidis bacterial biofilm graft infections model can be treated by the in-situ replacement of the infected prosthesis with a 10mg/ml rifampicin impregnated Gelsoft graft. However, such management for MRSA established infections cannot be recommended from the results obtained in this particular animal model.

To date a number of groups⁷⁵^,⁷⁶ have successfully managed prosthetic graft infections with rifampicin impregnated grafts with zero mortality, no requirement for limb amputation and to date no recurrence of infection.

Conclusion

The future management of vascular graft infections will be reliant on a better understanding of the interaction between the micro-organism, the prosthesis and the immune system. This will allow a more directed approach towards prevention and treatment. Possibilities would include more powerful antibiotics either administered parenterally or incorporated into the prosthesis, acting as a local delivery system for prolonged periods of time. The role of the biofilm in the pathogenesis of graft infection needs further understanding from both a molecular and an immune level.

References

1.: Back MR and Klein SR. Infections and Antibiotics in Vascular Surgery. In: White RA and Hollier LH, (Eds). Vascular Surgery: Basic Science and Clinical Correlations. Philadelphia: J. B. Lippincott company, 1994: 613–624.
2.: Bandyk DF and Bergamini TM. Infection in prosthetic vascular grafts. In: Rutherford RB (Ed), Vascular Surgery (4th ed.). Philadelphia: W. B. Saunders company, 1995: 588–604.
3.: Moore WS and Deaton DH. Infection in Prosthetic Vascular Grafts. In: Moore WS (Ed), Vascular Surgery: A Comprehensive Review (4th ed.). Philadelphia: W. B. Saunders, 1993: 694–706.
4.: Buckels JA and Wilson SE. Prevention and Management of prosthetic Graft Infection. In: Veith FJ, Hobson II RW, Williams RA and Wilson SE (Eds), Vascular Surgery: Principles and Practice (2nd ed.): New York: McGraw-Hill Inc, 1994: 1081–1089.
5.: Moore WS and Cole CW Infection in Prosthetic Vascular Grafts. In: Moore WS (Ed), Vascular Surgery: A Comprehensive Review (3rd ed.): Philadelphia: W. B. Saunders, 1991: 598–609.
6.: Seabrook GR. Pathobiology of graft infections. Seminars in Vascular Surgery 1990; 3: 81–88.
7.: Levy MF, Schmitt DD, Edmiston CE, Bandyk DF, Krepel CJ, Seabrook, GR, and Towne JB. Sequential analysis of staphylococcal colonization of body surface cultures on patients undergoing vascular surgery. J Clin Micro 1990; 28: 664–669. [PMC free article: PMC267773] [PubMed: 2332464]
8.: Perry MO. Infection in vascular surgery. In: Davis JM and Shires GT (Eds), Principles and Management of Surgical Infections Philadelphia: J. B. Lippincott, 1991: 371–382.
9.: Jamieson G, DeWeese J, and Rob C. Infected arterial grafts. Ann Surg 1975; 181: 850–852. [PMC free article: PMC1343907] [PubMed: 1138635]
10.: Bunt TJ. Synthetic vascular graft infections. II. Graft-enteric erosions and graft-enteric fistulas. Surg 1983b; 94: 1–9. [PubMed: 6857503]
11.: Bouhoutsos J, Chavatzas D, Martin P, and Morris T. Infected synthetic arterial grafts. BJS 1974; 61: 108–11. [PubMed: 4816236]
12.: Rubin JR, Malone JM, and Goldstone J. The role of the lymphatic system in acute arterial prosthetic graft infections. J Vasc Surg 1985; 2: 92–97. [PubMed: 3880833]
13.: Russell HE, Barnes RW, and Baker WA. Sterility of intestinal transudate during aortic reconstructive procedures. Arch Surg 1975; 110: 402–404. [PubMed: 1147757]
14.: Ernst CB, Campbell HC, Daugherty ME, Sachatello CR and Griffin WO. Incidence and significance of intraoperative bacterial cultures during abdominal aortic aneurysmectomy. Ann Surg 1977; 85: 626–633. [PMC free article: PMC1396230] [PubMed: 324416]
15.: Scobie K, McPhail N, Barber G, and Elder R Bacteriologic monitoring in abdominal aortic surgery. Can J Surg 1979; 22: 368–371. [PubMed: 455168]
16.: Brandimarte C, Santini C, Venditti M et al. Clinical significance of intraoperative cultures of aneurysm walls and contents in elective abdominal aortic aneurysmectomy. Eur J Epidemiology 1989; 5: 521–525. [PubMed: 2606181]
17.: O’Brien T and Collin J. Prosthetic vascular graft infection. BJS 1992; 79: 1262–1267. [PubMed: 1486415]
18.: Bandyk DF and Esses GE.. Prosthetic graft infection. Surgical Clinics of North America 1994; 74: 571–590. [PubMed: 8197531]
19.: White JV, Nessel CC and Whang K. Differential effect of type of bacteria on peripheral graft infections. In: Calligaro KD and Veith FJ (Eds), Management of infected arterial grafts St Louis: Quality Medical Publishing Incorporated, 1994: 25–42.
20.: JO Cohen. Staphylococcus. In: Baron S (Ed), Medical Microbiology (3rd ed) New York: Churchill Livingstone, 1991: 203–214.
21.: Richards GK and Gagnon RF. An assay of Staphylococcus epidermidis biofilm responses to therapeutic agents. The International Journal of Artificial Organs 1993; 16: 777–787. [PubMed: 8150524]
22.: Schmitt DD, Bandyk DF, Pequet AJ and Towne JB. Bacterial adherence to vascular prostheses. A determinant of graft infectivity. J Vasc Surg 1986b; 3: 732–740. [PubMed: 2939263]
23.: Malangoni MA, Livingston DH and Peyton MS. The Effect of Protein Binding on the a Adherence of Staphylococci to Prosthetic Vascular Grafts. J Surg Res 1993; 54: 168–172. [PubMed: 8479177]
24.: Sugarman B. In- Vitro adherence to bacteria to prosthetic vascular grafts: Infection 1982; 10: 9–14. [PubMed: 6461608]
25.: Lorentzen JE, Nielson OM, Arendrup H et al. Vascular graft infection: An analysis of sixty-two infections in 2411 consecutively implanted synthetic vascular grafts. Surg 1985; 98: 81–86. [PubMed: 4012610]
26.: Golan JF. Vascular graft infection. Infectious Disease Clinics of North America 1989; 3: 247–258. [PubMed: 2663980]
27.: Fletcher JP, Dryden M and Sorrell TC. Infection of vascular prosthesis. Aust NZ J Surg 1991; 61: 432–435. [PubMed: 2059176]
28.: Bunt TJ. Synthetic vascular graft infections. I. Graft infections. Surg 1983a; 93: 733–746. [PubMed: 6344294]
29.: Bandyk DF. Vascular graft infection. In: Bernhard VM and Towne JB (Eds), Complications in Vascular Surgery, (2nd Ed) Orlando: Grune and Stratton, 1985: 471–485.
30.: Bandyk DF, Berni GA, Thiele BL, and Towne JB. Aortofemoral graft infection due to staphylococcus epidermidis. Arch Surg 1984; 119: 102–108. [PubMed: 6689867]
31.: Bandyk DF. Vascular graft infections: Epidemiology, microbiology, pathogenesis and prevention. In: Bernhard VM and Towne JB (Eds). Complications in Vascular Surgery, (2nd Ed) St Louis: Quality Medical Publishing, 1991: 223–234.
32.: Calligaro KD, Westcott CJ, Buckley RM, Savarese RP and DeLaurentis DA. Infrainguinal anastomotic arterial graft infections treated by selective graft preservation. Ann Surg 1992a; 216: 74–79. [PMC free article: PMC1242549] [PubMed: 1632705]
33.: Geary KJ, Tomkiewicz AM, Harrison HN et al. Differential effects of a gram- negative and a grampositive infection on autogenous and prosthetic grafts. J Vasc Surg 1990; 11: 339–347. [PubMed: 2105400]
34.: Calligaro KD, Veith FJ, Schwartz ML, Savarese RP and DeLaurentis DA. Are gram-negative bacteria a contraindication to selective preservation of infected vascular grafts. J Vasc Surg 1992c; 16: 337–346. [PubMed: 1522635]
35.: Treiman GS. Bacteriology of aortic graft infections. In: Gewartz BL and Schwartz LB (Eds.), Surgery of the Aorta and its Branches Philadelphia: W. B. Saunders company, 2000: 375–383.
36.: Goldstone J and Moore WS. Infection in vascular prosthesis. Clinical manifestations and surgical management. Am J Surg 1974; 128: 225–233. [PubMed: 4602192]
37.: Murray SP, and Goldstone J. Diagnostic Advances. In: Calligaro KD and Veith FJ (Eds), Management of infected arterial grafts St Louis: Quality Medical Publishing Incorporated, 1994: 43–53.
38.: Goldstone J and Cunningham C. Diagnosis, treatment, and prevention of aorto-enteric fistulas. Acta Chirrugia Scandinavia Supplement 1990; 555: 165–172. [PubMed: 2195822]
39.: Gröschel DHM and Strain BA. Arterial Graft infections From a Microbiologist’s View: In Calligaro KD and Veith FJ (Eds), Management of infected arterial grafts St Louis: Quality Medical Publishing incorporated, 1994: 3–15.
40.: Tollefson ED, Bandyk DF, Kaebnick HW, Seabrook GR and Towne JB. Surface biofilm disruption. Enhanced recovery of microorganisms from vascular prosthesis. Arch Surg 1987; 122: 38–43. [PubMed: 3541853]
41.: Bergamini TM, Bandyk DF, Govostis D, Kaebnick HW and Towne JB. Infection of vascular prostheses caused by bacterial biofilms. J Vasc Surg 1988; 7: 21–30. [PubMed: 2961893]
42.: Bergamini TM, Bandyk DF, Govostis D, Vetsch R and Towne JB. Identification of Staphylococcus epidermidis vascular graft infections. A Comparison of culture techniques. J Vasc Surg 1989; 9: 665–70. [PubMed: 2524605]
43.: Bruggink JL, Glaudemans AW, Saleen BR, Meerwaldt R, Alkefail H, Prins TR, Slart RH, Zeebregts CJ. Accuracy of FDG-PET-CT in the diagnostic work-up of vascular prosthetic graft infection. Eur J Vasc Endovasc Surg 2010 Sep; 40: 348–54. [PubMed: 20576451]
44.: Qvarfordt PG, Reilly LM, Mark AS, Goldstone J, Wall SD, Ehrenfeld WK and Stoney RJ. Computerized tomographic assessment of graft incorporation after aortic reconstruction. Am J Surg 1985; 150: 227–231. [PubMed: 3161350]
45.: Cruse PJ and Foord R. A five year prospective study of 23,649 surgical wounds. Arch Surg 1973; 107: 206–210. [PubMed: 4719566]
46.: Seropian R and Reynolds BM. Wound infections after preoperative depilatory versus razor preparation. Am J Surg 1971; 121: 251–4. [PubMed: 5546329]
47.: Bandyk DF, Bergamini TM, Kinney EV, Seabrook GR and Towne JB. In situ replacement of vascular prosthesis infected by bacterial biofilms. J Vasc Surg 1991; 13: 575–583. [PubMed: 2027196]
48.: GMB Lonneke, Kluytmans JA, Wertheim HF, Bogaers D et al. Preventing Surgical-Site infections in Nasal Carriers of Staphylococcus aureus. NEJM 2010; 362: 9–17. [PubMed: 20054045]
49.: Turnbridge J and Grayson ML. Optimum Treatment of Staphylococcal Infections. Drugs, 1993; 45: 353–366. [PubMed: 7682906]
50.: Ashton TR, Cunningham JD, Patan D and Maini R. Antibiotic loading of vascular grafts. Proceedings of the 16th Annual Meeting of the Society for Biomaterials 1990; 13: 235.
51.: Farr B and Mandell GL. Rifampicin. Medical Clinics of North America 1982; 66: 157–168. [PubMed: 7038325]
52.: Powell TW, Burnham SJ and Johnson G Jr. A passive system using rifampicin to create an infection resistant vascular prosthesis. Surg 1983; 94: 765–769. [PubMed: 6415831]
53.: MacDougal EG, Burnham SJ and Johnson G. Jr. Rifampicin protection against experimental graft sepsis. J Vasc Surg 1986; 4: 5–7. [PubMed: 2941596]
54.: Avramovic J R and Fletcher JP. Rifampicin impregnation of a protein sealed Dacron graft: an Infection Resistant Vascular Graft. Aust NZ J Surg 1991; 61: 436–440. [PubMed: 1829350]
55.: Chervu A, Moore WS, Gelabert HA, Colburn M and Chvapil M. Prevention of graft infection by use of prosthesis bonded with a rifampicin/collagen release system. J Vasc Surg 1991; 14: 521–525. [PubMed: 1833564]
56.: Chervu A, Moore WS, Chvapil M and Henderson T. Efficacy and duration of antistaphylococcal activity comparing three antibiotics bonded to Dacron vascular grafts with a collagen release system. J Vasc Surg 1991; 13: 897–901. [PubMed: 1828092]
57.: Goeau-Brissonniere O, Leport C, Bacourt F, Lebrault C, Comte R Pechre JC. Prevention of vascular graft infection by rifampicin bonding to a Gelatin sealed Dacron graft. Ann Vasc Surg 1991; 5: 408–412. [PubMed: 1835641]
58.: Lachapelle K, Graham AM and Symes JF. Antibacterial activity, antibiotic retention, and infection resistance of a rifampicin- impregnated gelatin- sealed Dacron graft. J Vasc Surg 1994; 19: 675–82. [PubMed: 8164283]
59.: Gahtan V, Esses GE, Bandyk DF, Nelson RT, Dupont E and Mills JL. Antistaphylococcal activity of rifampicin- bonded gelatin-impregnated Dacron grafts. Journal of Surgical Research 1995; 58: 105–110. [PubMed: 7830398]
60.: Fletcher JP, Dryden M, Munro B, Xu J H and Hehir MD. Establishment of a vascular graft infection model in the sheep carotid artery. Aust NZJ Surg 1990; 60: 801–803. [PubMed: 2144960]
61.: Sardelic F, Ao PY, Taylor DA and Fletcher JP. Prophylaxis against Staphylococcus epidermidis vascular graft infection with rifampicin-soaked, gelatin-sealed Dacron. Cardiovasc Surg 1996; 4: 389–92. [PubMed: 8782944]
62.: Fletcher JP, Avramovic JR, Kenny J and Sardelic, F. Increased resistance to Staphylococcal graft infection by rifampicin impregnation of gelatin sealed Dacron. In: Chang JB (Ed). Modern Vascular Surgery (vol 6) New York: Springer Verlag, 1994: (483–487).
63.: Vicaretti M, Hawthorne, WJ, Ao PY and Fletcher JP. An Increased concentration of rifampicin bonded to gelatin-sealed Dacron reduces the incidence of subsequent graft infections following a staphylococcal challenge. Cardiovasc Surg 1998; 6: 268–73. [PubMed: 9705099]
64.: Curl GR and Ricotta JJ. Total Prosthetic Graft Excision and Extraanatomic Bypass. In: Calligaro KD and Veith FJ (Eds), Management of infected arterial grafts. St Louis: Quality Medical Publishing Incorporated, 1994: (82–94)
65.: Calligaro KD, Veith FJ, Schwartz ML, Savarese RP, GoldsmithJ, Westcott CJ and DeLaurentis DA. (1992b). Management of infected lower extremity autologous vein grafts by selective graft preservation. Am J Surg 1992; 164: 291–4. [PubMed: 1415932]
66.: Turnispeed WD and Dibbell DG Sr. Rotational Muscle Flaps in Localized Infections. In: Calligaro KD and Veith FJ (Eds.), Management of infected arterial grafts St Louis: Quality Medical Publishing Incorporated, 1994: (142–159).
67.: Kieffer E, Bahnini A, Koskas F, Ruotolo C, Le Blevec D and Plissonier, D. In situ allograft replacement of infected infrarenal aortic prosthetic grafts: Results in forty three patients. J Vasc Surg 1993; 17: 349–356. [PubMed: 8433430]
68.: Clagett GP, Bowers BL, Lopez-Viago MA, Rossi MB, Valentine RJ, Myers SI and Chervu, A. Creation of a neo-aortoiliac system from lower extremity deep and superficial veins. Ann Surg 1993; 218: 239–249. [PMC free article: PMC1242955] [PubMed: 8373267]
69.: Fujitani RM, Bassinouny HS, Gewertz BL, Glagoz S and Zarins CK. Cryopreserved saphenous vein allogenic homografts: An alternative conduit in lower extremity arterial reconstruction in infected fields. J Vasc Surg 1992; 15: 519–526. [PubMed: 1538509]
70.: Seeger JM, Wheeler JR, Gregory RT, Snyder SO and Gayle RG. Autogenous graft replacement of infected prosthetic grafts in the femoral position. Surg 1983; 93: 39–45. [PubMed: 6849186]
71.: Towne JB, Seabrook GR, Bandyk D, Freischlag JA and Edmiston CE. In situ-replacement of arterial prosthesis infected by bacterial biofilms: Long-term follow-up. J Vasc Surg 1994; 19: 226–235. [PubMed: 8114184]
72.: Robinson JA and Johansen K. Aortic sepsis: is there a role for in-situ graft reconstruction? J Vasc Surg 1991; 13: 677–684. [PubMed: 2027207]
73.: Schmitt DD, Bandyk DF, Pequet AJ, Malangoni MA and Towne JB. Mucin production by Staphylococcus epidermidis. Arch Surg 1986; 121: 89–95. [PubMed: 3942503]
74.: Vicaretti M, Hawthorne WJ, Ao PY and Fletcher JP. Does in-situ replacement of an infected vascular graft with a rifampicin soaked gelatin sealed dacron graft reduce the incidence of subsequent infection? Intl Angio 2000; 19: 158–65. [PubMed: 10905800]
75.: Torsello G, Sandmann W, Gehrt A and Jungblut RM. In-situ replacement of infected vascular prosthesis with rifampicin- soaked vascular grafts: Early results. J Vasc Surg 1993; 17: 768–773. [PubMed: 8464099]
76.: Naylor AR, Clark S, London NJ, Sayers RD, Macpherson DS, Barrie WW. Treatment of major aortic graft infection: preliminary experience with total graft excision and in situ replacement with a rifampicin bonded prosthesis. Eur J Endovasc Surg 1995; 9: 252–6. [PubMed: 7627664]

Bookshelf ID: NBK534262PMID: 30485017

Contents

< PrevNext >

PubReader
Print View
Cite this Page
Vicaretti M. Pathophysiology of Vascular Graft Infections. In: Fitridge R, Thompson M, editors. Mechanisms of Vascular Disease: A Reference Book for Vascular Specialists [Internet]. Adelaide (AU): University of Adelaide Press; 2011. 29.
PDF version of this title (177M)

In this Page

Introduction
Natural History of Prosthetic Vascular Graft Infections
Mechanisms of Graft Contamination at Operation
Pathogenesis of Graft Infections
Bacteriology of Vascular Graft Infections
Investigations for Detection of Prosthetic Graft Infections
Management of Prosthetic Graft Infections
Established Infection
Conclusion
References

Related information

PMC
PubMed Central citations
PubMed
Links to PubMed

Recent Activity

Clear Turn Off Turn On

Pathophysiology of Vascular Graft Infections - Mechanisms of Vascular Disease
Pathophysiology of Vascular Graft Infections - Mechanisms of Vascular Disease

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

Bookshelf