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Wound infection prevention

All skin wounds are vulnerable to infection, so recognising and intervening when infection appears to be setting in can improve healing time 

Identification of the four principal signs of inflammation and the use of 'antiseptic' solutions for infected wounds dates back to as early as 14-37AD, according to documented evidence by Celsus, a Roman physician. However, the subsequent suggestion that wounds should be encouraged to suppurate (Claudius Galen [130-200 AD]) was misplaced and, as we now know, dangerous. 

Florence Nightingale recognised the need for infection prevention through hand-washing, and gradually theories and terminology relating to wound infection developed. It is essential that healthcare practitioners have at least a basic understanding of microbiology, normal healing mechanisms and the ability to recognise the signs and symptoms of infection in a wound. Successful interventions at an early stage may facilitate healing and avoid infection and its potentially life-threatening complications. This article will make evidence-based recommendations for managing patients with infected wounds.

Wound infection

All wounds, whether acute or chronic, are contaminated with the presence of organisms on the surface of a wound.1 Normal bodily flora live harmlessly without causing any active disease or ill-health and often offer protection from more harmful or pathogenic organisms, for example Staphylococcus aureus and Staphylococcus epidermidis, on the skin.2 The natural physical barrier of intact skin prevents contamination from micro-organisms.3 A wound is created when this barrier is breached, either through surgical procedures or trauma, allowing the movement or ingress of organisms from different body sites and the environment. Direct contact and poor hand washing technique pre- and post-operatively have been cited as significant factors for wound infection.4

The presence of multiplying organisms on the surface of a wound is defined as wound colonisation in the absence of a host immune response5 or associated clinical signs and symptoms. On the wound infection continuum, colonisation may escalate to critical colonisation6 when the body's immune system can no longer control the multiplying organisms, resulting in wound infection.7 Therefore, wound infection is defined as the presence 

of multiplying organisms which overwhelm the body's immune system, resulting in spreading cellulitis (inflammation of the tissues).7 This implies systemic disease that is likely to impede healing and potentially lead to blood stream infection or septicaemia. 

Wound pathogens

Skin harbours at least 200 species of bacteria (equating to 1,012 organisms on the skin of the body) that are considered to be normal flora.8 The normal flora are specific to the individual and may be influenced by various factors, including genetics, age, sex, stress, nutrition and diet. Wounds can be infected by bacteria, fungi, protozoa or viruses but, particularly in chronic wounds, different micro-organisms may co-exist in polymicrobial communities, especially at the wound margins.9 

The concept of biofilms has attracted interest over the last few years and comprises complex, continuously changing microbial communities, containing bacteria and fungi which synthesise and secrete a protective matrix that attaches the biofilm firmly to a living or non-living surface.10 Following attachment, the organisms are protected from external threats, such as antimicrobial agents and the immune system, by being encased in a gelatinous, thick, slimy barrier of sugars and proteins. The presence of biofilm may be suspected in chronic inflammation and/or non-healing wounds. It is difficult to identify but is needed to direct treatment.11

Sampling techniques include wound swabbing, needle aspiration and wound biopsy. One drawback of wound swabbing is that it may only identify surface colonising pathogens, not the deep-seated infecting pathogens. The most accurate information about the type and quantity of pathogenic bacteria is provided by wound biopsy, but it is an invasive procedure, not taught as a nursing skill, and will be reserved for non-healing wounds despite treatment for infection.12 It has been suggested that routine swabbing, such as at weekly intervals or at the time of frequent dressing changes, is neither helpful nor cost-effective.13 The usual practice of taking wound swabs for culture augments the process of clinical decision-making and should not be undertaken without good clinical rationale. The diagnosis of infection in chronic wounds should be made on the clinical signs and symptoms and supported by the results of laboratory tests.14 

Patient risk factors for wound infection

It is not clear why some patients and not others succumb to wound infection; ultimately, this is determined by the virulence (pathogenicity and invasiveness) of the organism and immunological status of the patient.15 More specifically, it depends upon host resistance, number and type of bacteria (disease-producing ability) and transference to other body parts. The risk of wound infection is increased by the patient's health status - any condition that debilitates or destabilises the patient, age, nutritional status, medication (eg, corticosteroids, cytotoxics, immunosuppressants), poor tissue perfusion due to anaemia, cardiac, respiratory, renal disease, plus psychosocial lifestyle factors are all attributable. 

In relation to surgical wound infection, the potential for wound infection risk is increased by contamination perioperatively, long procedure length, large/deep wounds, trauma with delayed treatment, the presence of a foreign body and location in a site of possible high contamination, eg, perineum. The duration and presence of necrotic tissue in a chronic wound will attract bacteria and increase the risk of infection. A comprehensive summary of the signs and symptoms of infection in acute and chronic wounds can be found by the World Union of Wound Healing Society (WUWHS).12

Bacterial load has a direct impact on wound healing, and experimental evidence suggests that a bacterial load of between 105 and 106 organisms per gram in a wound bed, irrespective of the organism, will adversely affect wound healing.16 Harding17 states that 'Work cited as long ago as 1970 suggests that optimal wound healing cannot be achieved unless bacteria are eliminated from wounds'. However, Hampton18 believes that, in reality, complete removal of bacteria from a wound is unlikely to be achieved, but a reduction in bacterial load and an increase in healing rates might well be achieved through the use of appropriate dressings.

Treatment of the infected wound should not be based on culture results alone but should reflect the clinical status (bleeding, tissue fragility, increasing pain, exudate and/or odour) which should be readily recognised as possible signs and symptoms of infection and treated symptomatically.

Management of wound infection

Once diagnosed and antibiotic sensitivities identified, an appropriate management plan should be decided upon with priority aims being to optimise the patient's general health status, reduce the bacterial burden, facilitate healing and reduce the risk of cross-contamination. A holistic patient assessment should inform and guide the process. In some cases broad-spectrum antibiotics may be used in non-healing wounds or those at high risk of infection, which is justified on the grounds that they provide a high local concentration and avoid systemic allergic reactions.19 However, their effect may be reduced by the presence of ischaemic and necrotic tissue9 and the growing concerns about antibiotic resistance must also be considered. 

Despite past concerns about the use of topical antiseptics, the discriminate, short-term use of, for example cadexomer iodine and the newer silver formulations, may be beneficial20 but more research is needed. The three main generic groups of wound dressing products that have the potential to reduce the bacterial burden in infected wounds are those containing silver, honey and iodine. Larval therapy has grown in popularity due to its perceived beneficial effects of reducing the bacterial burden, odour and exudate. 

The following list considers the various antiseptics that may be used to treat wound infection:

- Acetic acid solution: effective against Pseudomonas aeruginosa - the surrounding skin must be protected.

- Chlorhexidine solution/powder, impregnated dressings: as an alternative in patients allergic to iodine preparations.

- Honey: available for direct application, impregnated dressings - antimicrobial effects have been attributed to some components and physical properties but its activity is variable.

- Hydrogen peroxide solution, cream: caution needed due to reports of gas embolism.

- Iodine PVP-I solution, cream, ointment, spray, impregnated dressings, Cadexomer iodine ointment, paste, powder, impregnated dressings: modern products slowly release relatively low levels of iodine, reducing the likelihood of toxicity and staining. 

- Povidone iodine (polyvinylpyrrolidone iodine - PVP-I): an iodine-surfactant complex.

- Cadexomer iodine: releases iodine from highly absorbent beads.

- Potassium permanganate solution, tablets for dissolving in water: used as a soak to reduce wound bacterial load - has astringent effect; may be useful in 'weepy' wounds.

- Polyhexamethyl biguanide (PHMB) - solution, impregnated dressings: also known as polyhexanide and polyaminopropyl biguanide; related to chlorhexidine. Currently used mainly for burns.

- Silver (silver sulfadiazine cream, impregnated dressings; ionic silver, impregnated dressings; nanocrystalline silver): available in several forms including silver sulphadiazine (silver-antibiotic combination) dressings. More recently, dressings have become available that release charged silver atoms (ionic silver - Ag+) on contact with wound fluid. The amount/rate of ionic silver released from different dressings is variable. Initial release of high levels followed by sustained release appears to aid reduction in bacterial numbers and a wide spectrum of activity. Staining of the wound bed and surrounding skin may occur but is reversible. 

- Sodium hypochlorite solution: not usually recommended unless suitable alternatives are unavailable.

- Triclosan solution - impregnated dressings: mainly used as a skin disinfectant or surgical scrub.

[List adapted from WUWHS (2008).12]

Conclusion

Correct diagnosis is vital to reduce the ever-increasing costs and reduced quality of life associated with wound management in general, and to prevent and manage wound infection effectively, as well as the growth in antibiotic-resistant organisms. Indiscriminate use of antibiotics is a significant contributory factor in bacterial resistance and often unnecessary for treating wound infection successfully.

 

References

1. Stotts NA. Wound infection: diagnosis and management. In: Morison MJ. Ovington LG. Wilkie K. (eds) Chronic Wound Care. A Problem-Based Learning Approach. London: Mosby Elsevier Limited; 101-16; 2004. 

2. Wilson J. Infection control in clinical practice. (2nd ed). London: Bailliere Tindall; 2001.

3. White RJ, Cooper R, Kingsley A. Wound colonisation and infection: the role of topical antimicrobials. Br J Nurs 2001;10(9):563-78.

4. Collier M. Recognition and management of wound infections. Worlwidewounds. 2004. 

5. Ayton M. Wounds that won't heal. Nurs Times 1985;81(46):16-9. 

6. White RJ. The wound infection continuum. In: White R J, ed. (2003) Trends in Wound Care. Wiltshire: MA Healthcare Limited; 12-17, 2003.

7. Kingsley A. A proactive approach to wound infection. Nurs Stand 2001;15(30):50-8.

8. Todar K. Todar's online textbook of bacteriology. 2008. 

9. Bowler P, Duerden B, Armstrong D. Wound microbiology and associated approaches to wound management. Clin Microbiol Rev 2001;14(2):

244-69.

10. Stoodley P, Sauer K, Davies DG, Costerton JW. Biofilms as complex differentiated communities. Rev Microbiol 2002;56:187-209.

11. Phillips PL. Wolcott RD. Fletcher J. & Shultz GS. Biofilms made easy. Wounds International 2010;1(3):1-6.

12. World Union of Wound Healing Society. Wound infection in clinical practice. An international consensus. London: MEP Ltd; 2008. Available at: www.mepltd.co.uk.

13. Gilchrist B. Taking a wound swab. Nurs Times 2000;96(4 Suppl):2.

14. Benbow M. Wound swabs and chronic wounds. Practice Nurse 2010;39(9):27-30.

15. Flanagan M. Wound management: ACE Series. Edinburgh: Churchill Livingstone; 1997.

16. Dow G, Browne A, Sibbald RG. Infection in chronic wounds: controversies in diagnosis and treatment. Ostomy Wound Manage 1999;45(8):23-7:29-40;41-2.

17. Harding K. The use of antiseptics in wound care. Journal of Wound Care 1996;5(1):44-7. 

18. Hampton S. Actisorb Silver 220: a unique antibacterial dressing'. British Journal of Nursing 2002;Silver Supplement;17-9. 

19. Bikowski J. Secondarily infected wounds and dermatoses: a diagnosis and treatment guide. J Emerg Surg 1999;17:197-206.

20. Drosou A, Falabella A, Kirsner RS. Antiseptics on wounds: an area of controversy. Wounds 2003;15(5):149-66.