Early & Late Onset Vascular Graft Infection
Microbiology aspects
Stephanie Thomas
Consultant Microbiologist
Wythenshawe Hospital
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
– groin incision
– wound complications
–
–
–
–
immunosuppressive therapy
diabetes
cancer
immunologic disorders
early PVGI classifications
Szilagyi
Definition of infection
Samson
Definition of infection
Group 1 dermis only
Group 1
no deeper than dermis
Group 2 extends to subcut
tissues, does not
invade implant
Group 2
involves subcut tissue,
does not come into
contact with graft
Group 3 arterial implant involved Group 3
based on level of:
• anatomic invasion
• graft involvement
involve body of graft but
not anastomosis
Group 4
surrounds exposed
anastomosis, no
bacteramia/bleeding
Group 5
involve graft-to-artery
anastomosis, associated
with septicaemia/bleeding
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
time of onset clinical presentation
early-acute
• post surgical wound infection
(<4 mo)
traditional SSI
presence of graft
exacerbates
clinical severity
late
(> 4 mo)
can be many
months/yrs
•wound complications:
anastomotic dehiscence, hematoma, seroma,
incisional necrosis
• sepsis (blood cultures!)
• occult/few or no overt sx
• anastmotic pseudoaneurysm
• peri-graft exudation with sinus formation
• graft thrombosis and failure
• graft-enteric erosion, fistula formation, hemorrhage
microbial aetiology:
early v late
time of microbial aetiology
onset
early• Staphylococcus aureus
acute
(<4 mo)
• Streptococci
?? treatment
• Augmentin
• Flucloxacillin &
Gentamicin
Incision site contamination:
• E.coli, Klebsiella, Pseudomonas
late
(>4 mo)
•E.coli, Klebsiella, Bacteroides,
Candida
• Coagulase negative staph
(Staph.epidermidis)
• ??????
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
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
implantation
late onset infections
CoNS:
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
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
– 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
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
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
– Standard Operating 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.
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 antiadherance agent, such as rifampicin in
staphylococcal infections.
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