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Stephanie Thomas Consultant Microbiologist Wythenshawe Hospital. Early & Late Onset Vascular Graft Infection Microbiology aspects. prosthetic vascular graft infection (PVGI). incidence 1 – 6 % (infra-inguinal 2-5%, aortofemoral 1-2%, aortic 1%) relative risk low

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Stephanie Thomas Consultant Microbiologist Wythenshawe Hospital

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Stephanie thomas consultant microbiologist wythenshawe hospital

Stephanie ThomasConsultant MicrobiologistWythenshawe Hospital

Early & Late Onset Vascular Graft Infection

Microbiology aspects

Prosthetic vascular graft infection pvgi

prosthetic vascular graft infection (PVGI)

  • incidence 1 – 6 %

    (infra-inguinal 2-5%, aortofemoral 1-2%, aortic 1%)

  • relative risk low

  • clinical consequences catastrophic!

  • recognized mortality 30-50%

    (up to 75% with intra-abdominal aortic grafts)

  • associated morbidity 40-70%

    (limb amputation rates up to 70% for lower extremity grafts)

    significant complication of arterial reconstruction

Risk factors for pvgi

risk factors for PVGI

  • groin incision

  • wound complications

  • immunosuppressive therapy

  • diabetes

  • cancer

  • immunologic disorders

Early pvgi classifications

early PVGI classifications

Last 10 years re classification

last 10 years: re-classification

early (acute) onset:< 4 months post operative

  • present as acute infection

    late onset:> 4 months post operative

  • up to 95 months post graft implantation *

  • insidous onset, systemic signs often missing

  • aetiology less certain

  • far more difficult to diagnose

    more pragmatic approach for diagnosis, predicting microbial aetiology and treatment regimes

*Seabrook et al, 1990, J Vasc Surg

Clinical presentation early v late

clinical presentation: early v late

Microbial aetiology early v late

microbial aetiology:early v late

Stephanie thomas consultant microbiologist wythenshawe hospital

HPA Surgical Site Infection Surveillance Service (SSISS)

National aggregated data on Surgical Site Infections (2004-09)

[33 hospitals (voluntary), 7,349 operations]

Staphylococcal predilection for implants

staphylococcal predilection for implants

Bandyk et al Arch Surg (1990)

S. epidermidis the infecting organism >60% of aortofemoral graft infections

Kaebnick HW et al, Surgery (1987)

S. epidermidis isolated from 75% of prostheses revised for

anastomotic pseudoaneurysm and 80% of aortofemoral prostheses

removed because of infection

Macbeth GS et al, J Vasc Surg (1984)

S. epidermidis cultured from diseased arterial walls and groin lymph

nodes in one third patients undergoing vascular prosthesis


Late onset infections

late onset infections


ubiquitous group, low virulence, significant pathogens in biomaterial-related infections

exopolysaccharide/ biofilm production (slime)

source of infection: contact with prosthetic surface during implantation (c.f.PJI, PVIE)

  • initial cryptic period

  • organisms colonise surfaces as bacteria-laden biofilm

  • protected by host defences glycocalix (slime)

  • lie dormant for years in biofilm growth mode

Stephanie thomas consultant microbiologist wythenshawe hospital

enlarging infection eventually recognised by the host

chronic inflammatory response adjacent to the graft

autolysis of peri-graft tissue and adjacent arterial wall

perigraft exudate, fluid collection

in time decreases the anastomotic tensile strength of anastomotic graft-artery interface

slime producing strain of S.epidermidis colonising fibres of a dacron vascular graft

Stephanie thomas consultant microbiologist wythenshawe hospital

  • prophylaxis efficacious BUT does not guarantee graft sterility

  • implanted prosthesis colonised with low virulence organisms

    • (skin, harboured in diseased arteries, breaks in surgical technique, bacteraemia)

      persistance – sinus formation - pseudoaneurysm

      late graft failure

Outcome by organism

outcome by organism

Zetrenne E, Bryan M, McIntosh B et al. (2007)

  • multi centre retrospective study to determine primary mode of therapy and rate of limb salvage for major PVGI

  • Samson Group 3-5

  • correlated grade, microbiology, outcomes

  • ??success of graft salvage determined by infective organism

Outcomes by group and organism

outcomes by group and organism

Principles of management for pvgi

principles of management for PVGI

evolved over 40 years

  • predominantly based on clinical experience

  • moderate amount of supportive lab evidence

  • no standardised methodology (sampling or processing)

  • current methods poorly sensitive

  • low density organisms, stationary growth mode

  • disrupt biofilm:

    • sonication techniques, Balotini bead technique

    • look for slime production

    • anti-staphylococcal antibody titres

Laboratory support

laboratory support

  • StandardOperating Procedure

  • standard sample set

  • national consensus treatment guidelines

    • re. choice & duration

    • ? dependant on

    • site of graft; e.g. aortic v peripheral

    • Intervention: salvage v excision

Legout l d elia pv sarraz bournet b et al 2012 med mal infect

Legout L, D’Elia PV, Sarraz-Bournet B, et al (2012). Med Mal Infect.

there is no correlation between the microbiological data and the location or type of vascular infection.

thus, the post operative intravenous antibiotherapy should be bactericidal with broad spectrum.

after obtaining intra-operative microbiological results, de-escalation therapy must include at least one anti-adherance agent, such as rifampicin in staphylococcal infections.

Summary pvgi

summary: PVGI

early onset:

  • acute presentation

  • post operative wound infection

  • microbiology representative

  • antibiotic choice narrow

    late onset:

  • insidious onset

  • low index of suspicion

  • microbiology variable

  • broad spectrum include Gram-negative & anti-biofilm agent

    • concern re changing patterns of resistance

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