Author(s) - International Wound Infection Institute



Introduction to The Wound Infection Evidence Matrix

The development of a structured survey of the evidence for wound infection was one of the principal outputs agreed by the International Wound Infection Institute at its inception. This process began with a simple listing of references (to be found in our “useful documents” section) and will conclude with a comprehensive list of reviewed, surveyed and abstracted papers on wound infection and its treatment. We see the provision of an evidence matrix as the next step along the route. The current version of the matrix is incomplete, but we believe that it is at an appropriate stage to be reviewed by our members. We welcome all of your comments.

One of the main features that we wanted to include was a rating system for the evidence. This is always problematic. The literature reveals multiple classifications and evidence hierarchies for ranking evidence 1,2,3,4,5. However, these evidence classifications and hierarchies contain many inconsistencies in interpretation and ranking. Although the gold standard for best evidence is generally considered to be a meta analysis or systematic review of double blinded randomised controlled trials, few, if any, such reviews are to be found in regards to the diagnosis or treatment of wound infection. Our rating system is focussed towards the levels of evidence as follows:

1. Meta analysis and systematic reviews

2. Randomised controlled trials

3. Non randomised controlled trials, case control trials, prospective cohort studies, animal studies, evidence summaries or evidence guidelines

4. Case reports, case series

5. Expert opinion, other literature reviews

Highly influential pieces have been published within all the above levels, some of which have contributed to changes in practice. Therefore we are considering the addition of an “impact” rating, separate to the evidence rating, based on the importance or significance of certain papers.

We hope that you find this draft of the evidence matrix to be useful. Equally importantly, please give us your opinion on how to improve and add to this document. In particular we would like your feedback on the following:

• How useful is the evidence matrix as provided?

• What other papers should be included?

• What impact score would you give to significant pieces?

Please let us know what you think. All comments will be gratefully received at wii@

Keryln Carville, Chair, Evidence sub-committee, April 2009

References:

1. Upshur, R. (2003). “Are all evidence-based practices alike? Problems in the ranking of evidence”. CMAJ, 169(7), downloaded

2. Brown JP, Josse RG; Scientific Advisory Council of the Osteoporosis Society of Canada. 2002 clinical practice guidelines for the diagnosis and management of osteoporosis in Canada. CMAJ 2002;167(Suppl 10):S1-34.

3. Centre for Evidence-Based Medicine. Levels of evidence and grades of recommendation. Oxford: The Centre. Available: levels_of_evidence.asp

4. Wright PJ, English PJ, Hungin AP, Marsden SN. Managing acute renal colic across the primary–secondary care interface: a pathway of care based on evidence and consensus. BMJ 2002;325:1408-12.

5. Evans, D. (2003). “Heirarchy of evidence: A framework for ranking evidence evaluating healthcare interventions.” Journal of clinical Nursing. 12(1), 77-84.

The Wound Infection Evidence Matrix – April 2009

|Author, date |Comment |Title |Key points |Grade |

|Bacteria, biofilms and wound healing |

|(Bowler, Duerden et al. 2001)| |Wound microbiology and |A thorough review of the literature on wound infection published up until 2001. Key points: all wounds are colonised and progression to | |

| | |associated approaches to |infection is as much due to host factors as to the type and number of bacteria present; most open wounds are polymicrobial, with |5 |

| | |wound management. |anaerobic bacteria constituting 50% of the species present in infected wounds; swab sampling is easy to carry out but results can be | |

| | | |misleading and this should only be carried out if there are clinical signs of infection, if the wound fails to heal or is deteriorating;| |

| | | |antibiotics induce bacterial resistance and antiseptics are preferred if topical treatment is required; debridement is an essential part| |

| | | |of infection control. In my opinion a literature review as is stated in the conclusion | |

|(Ceri, Olson et al. 1999) |Outlines new technology for |The Calgary biofilm device:|Biofilms have an inherent lack of susceptibility to antibiotics. Ceri et al describe the Calgary Biofilm Device (CBD) which is a method |3 |

| |selecting effective antibiotics |new technology for rapid |for the rapid and reproducible assay of biofilm susceptibility to antibiotics. | |

| |in the treatment of biofilms |determination of antibiotic|The paper describes the formation of biofilms and confirmation of their presence using quantitative microbiology and SEM, followed by | |

| | |susceptibilities of |the rigorous testing and assessment of the CBD assay using NCCLS reference strains of E coli, P aeruginosa and S aureus. Growth curves | |

| | |bacterial biofilms. |demonstrated that biofilms grew uniformly in each of the 96 wells. | |

| | | |Antibiotic susceptibility testing demonstrated that, compared to planktonic forms of the same bacteria, 100 to 1000 times the | |

| | | |concentration of an antibiotic was required to eradicate the biofilm. The authors claim that the CBD provides a method for the rational | |

| | | |selection of antibiotics effective against microbial biofilms. | |

|(Costerton, Stewart et al. |A good review of biofilms |Bacterial biofilms: a |A good and well-referenced review of biofilms. The review explains how biofilms form and develop, how they differ from planktonic |5 |

|1999) | |common cause of persistent |bacteria, the importance of quorum sensing as a possible target for interfering with their development. | |

| | |infections. | | |

|(Davies, Parsek et al. 1998) |The importance of signalling in |The involvement of |This study demonstrates that a cell-to-cell signal (quorum sensing) is required for the differentiation of individual cells of P |3 |

| |biofilms is described and it is |cell-to-cell signals in the|aeruginosa into complex biofilms. When differentiation is hindered by a mutation, the biofilm becomes abnormal and is sensitive to a | |

| |suggested this could be a way to |development of a bacterial |detergent biocide (SDS). Without the signalling device, the biofilms were not able to grow with the proper architecture and did not | |

| |control biofilms. |biofilm. |leave sufficient space between colonies. | |

| | | |The authors suggest that inhibition of the quorum sensing signals could be possible ways to control biofilms, given their resistance to | |

| | | |most antibiotics. | |

|(Dow, Browne et al. 1999) |Review |Infection in chronic |A thorough review that includes: definitions of contamination, colonization and infection; the pathogenesis of wound infection and how |5 |

| | |wounds: controversies in |the inflammatory response can delay wound healing; diagnosis of wound infection; quantification of bacterial burden. | |

| | |diagnosis and treatment. |Regarding bacterial burden, the authors caution that there is no hard cut-off figure above which colonization turns to infection and | |

| | | |that the level of microbial burden alone can not be used to define infection. They stress the importance of bacterial species and | |

| | | |variety, and the capacity of the host to tackle infection. They warn of the difficulties of quantitative biopsy and argue the case for | |

| | | |semi-quantitative assessment. | |

| | | |The paper also provides a detailed critique of specimen collection and culture techniques and concludes with a thorough overview of | |

| | | |treatment options including mechanical (debridement), antiseptics and the role of antibiotics. A useful table summarises the | |

| | | |antimicrobial options for empiric therapy. | |

| | | |A small number of the concepts have been challenged over the years since the publication of this review, but on the whole it is a | |

| | | |thorough and valuable resource on the subject of wound infection. | |

|(Dowd, Sun et al. 2008) |Highly significant study |Survey of bacterial |This study used specific techniques to identify the major populations of bacteria that occur in the biofilms found in three types of |3 |

| | |diversity in chronic wounds|chronic wound: diabetic foot ulcer, venous leg ulcer and pressure ulcer. The techniques were: three separate I 6S-based molecular | |

| | |using Pyrosequencing, DGGE |amplifications, followed by pyrosequencing, shotgun Sanger sequencing and denaturing gradient gel electrophoresis. | |

| | |and full ribosome shotgun |All chronic wound types contained certain specific major populations of bacteria: Staphylococcus, Pseudomonas, Peptoniphilus, | |

| | |sequencing. |Enterbacter, Stenotrophomonas, Finegoldia and Serratia species. However, each of the wound types showed marked differences in their | |

| | | |bacterial populations. | |

| | | |For example, in venous ulcers over 80% of the bacteria were facultative anaerobes, compared with 62% in diabetic foot ulcers, and just | |

| | | |over 20% in pressure ulcers. Pressure ulcers on the other hand comprised over 60% of strict anaerobes, compared with nearly 30% in | |

| | | |diabetic foot ulcers and virtually none in venous ulcers. | |

| | | |Different wound types also showed a different level of oxygen tolerance amongst their bacterial populations. The authors suggest that | |

| | | |this may imply each wound type has a distinct pathophysiology that affects the ecology of the wound environment determiging which | |

| | | |bacteria can develop. | |

| | | |Results were compared with those from traditional culture-based analyses. In only one wound type did the culture methods correctly | |

| | | |identify the primary bacterial population. Standard culturing techniques are inherently flawed as they only examine the 1% of | |

| | | |microorganisms that are able to grow rapidly in pure culture. Also, certain populations may never be cultured in the laboratory due to | |

| | | |reduced metabolic activity, obligate cooperation with other bacteria, need for specialized nutrients or environmental conditions. | |

| | | |The paper gives full details of the bacteria identified. | |

|(Hill, Davies et al. 2003) |Molecular analysis reveals a much|Molecular analysis of the |Culture analyses of CVLU generally reveal staphylococci, streptococci, enterococci and facultative Gram-negative bacilli. However, |3 |

| |greater diversity of microflora |microflora in chronic |anaerobic isolation techniques and prolonged incubation reveal the presence of fastidious and slow-growing anaerobic species such as | |

| |in chronic wounds than do culture|venous leg ulceration. |Fusobacterium and peptostreptococci. Cultivation-dependent methods for characterising the microflora of chronic wounds are limited. | |

| |techniques. | |The authors describe the analysis using 16S rDNA sequences of tissue from a CVLU which demonstrated significantly greater bacterial | |

| | | |diversity than culture methods. Sequences even suggested novel species of bacteria. This technique can clearly not be used routinely so | |

| | | |the clinical application is limited but may inform treatment in deteriorating or long-lasting wounds. | |

| | | |The study states that this was one patient and one wound that was analysed? Would that make it a 4? | |

|(James, Swogger et al. 2008) |Well-designed and highly |Biofilms in chronic wounds.|Chronic wound specimens were taken from 77 subjects and acute wound specimens from 16. All specimens were cultured using standard |3 |

| |significant study revealing that | |techniques and in addition, light and scanning electron microscopy were used to analyse 50 chronic and 17 acute specimens. Molecular | |

| |biofilms may be present in at | |analyses were performed on the other 27 chronic specimens. | |

| |least 60% of chronic non-healing | |There was a statistically significant difference between the chronic and acute specimens in terms of presence of biofilm: 60% of the | |

| |wounds | |chronic but only 6% of the acute (p 10(5) organisms per gram of tissue) was less in Acticoat-treated wounds than in those treated with | |

| | | |silver nitrate (5 vs 16). Secondary bacteremias arising from infected burn wounds were also less frequent with Acticoat than with silver| |

| | | |nitrate-treated wounds (1 vs 5). Acticoat dressing offers a new form of dressing for the burn wound, but it requires further | |

| | | |investigation with greater numbers of patients in a larger number of centers and in different phases of burn wound care (Published | |

| | | |abstract). | |

|(Wright, Lam et al. 1999) | |Efficacy of topical silver |BACKGROUND: Fungal infections of burn wounds have become an important cause of burn-associated morbidity and mortality. The nature of |3 |

| | |against fungal burn wound |fungal infections dictates aggressive treatment to minimize the morbidity associated with these infections. Persons with large total | |

| | |pathogens. |body surface area burns are particularly susceptible to fungal infections and are treated in such a manner as to minimize their risk of | |

| | | |infection. METHODS: This study examined the in vitro fungicidal efficacy of a variety of different topical agents. By placing fungal | |

| | | |inocula in contact with mafenide acetate, silver nitrate, silver sulfadiazine, and a nanocrystalline silver-coated dressing, we | |

| | | |determined the kill kinetics of these topical agents against a spectrum of common burn wound fungal pathogens. RESULTS: The topical | |

| | | |antimicrobials that were tested demonstrated varying degrees of efficacy against these pathogens. CONCLUSION: The nanocrystalline | |

| | | |silver-based dressing provided the fastest and broadest-spectrum fungicidal activity and may make it a good candidate for use to | |

| | | |minimize the potential of fungal infection, thereby reducing complications that delay wound healing (Published abstract). | |

| | | | | |

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Acknowledgements:

The IWII is very grateful to the following members for the development of this matrix:

Dr Keryln Carville, Curtin University of Technology, Australia

Terry Swanson, South West Healthcare, Warrnambool, Victoria, South Australia

Dr Marc Despatis, Cape Breton Health Care Complex, Canada

Jude Douglass, IWII Member, UK

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