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A proactive approach to wound infection

Kingsley, Andrew. Nursing Standard 15.30 (Apr 11-Apr 17, 2001): 50-4, 56, 58.

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Abstract
The management and treatment of infection is a complex and important area in tissue viability nursing. Andrew Kingsley discusses the value of microbiology to clinical practice and the importance of adopting a proactive approach to the management of infected wounds using an infection continuum and algorithm to help promote effective care.

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Headnote Kingsley A (2001) A proactive approach to wound infection. Nursing Standard. 15, 30, 50-58. Date of acceptance: February 28 2001. Headnote Summary Headnote The management and treatment of infection is a complex and important area in tissue viability nursing. Andrew Kingsley discusses the value of microbiology to clinical practice and the importance of adopting a proactive approach to the management of infected wounds using an infection continuum and algorithm to help promote effective care. Headnote Key words Headnote * Infection control * Wounds Headnote These key words are based on subject headings from the British Nursing Index. This article has been subject to double-blind review. THE DEVELOPMENT of wound infection is an ongoing problem for many patients. Infected wounds can cause great distress in terms of associated morbidity and mortality, increased length of hospital admission, delayed wound healing and increased discomfort, and have long been known to increase healthcare costs significantly (Green and Wenzel 1977, Plowman et al 2000). Healthcare professionals from all disciplines are involved in the

prevention and management of wound infection, but despite appropriate patient care and advances in treatment and prevention strategies, some wounds will become infected. It would be unrealistic to believe that all infections can be prevented as there are many variables involved in the development of wound infection. These include: general health status; underlying conditions that affect immunocompetency; the disease process or treatment given; tissue viability in the area surrounding the wound; the nature of the wound; time of access to health care; and species and quantities of microbes contaminating the site. In addition, there is a range of specific factors known to elevate risk of infection in surgical wounds (Table 1). It is a laudable objective to take appropriate measures to prevent infection where it is known that benefit can be gained, for example, through audit and feedback of surgical wound infection rates (Reilly et al 2001). However, it is equally important to limit the effects of infection once it has occurred. Early recognition of the signs of infection, local swelling, heat, pain and redness, followed by effective intervention, is necessary to achieve prompt resolution. Swelling, heat, pain and redness are also signs of inflammation but the degree of severity usually increases with infection. Infected wounds frequently have increased levels of exudate, pus and odour, and the patient might be pyrexial and/or have an elevated neutrophil count. Following the correct sequence of care using the infection continuum (Table 2) and algorithm for wound infection (Fig. 1) will help to promote wound healing, limit negative patient experiences and minimise additional costs to the healthcare system. Prevalence and cost of wound infection To the author's knowledge there have been no large-scale studies of the prevalence of all wound types present at any one time in the UK. Local audit data on pressure ulcer incidence in a district general hospital and associated community hospitals of approximately 600 beds in total for the year 2000 indicate an incidence of 2.5 per cent, which shows that 560 patients acquired sores during hospitalisation in North Devon (CAD Northern Devon 2000). In the UK, leg ulcer prevalence of individuals with active ulceration has been estimated at approximately 100,000 (Callam et al 1985). Two national prevalence studies of infection (all types) in hospital undertaken in 1980 (Meers et al 1981) and 1993/1994 (Emmerson et al 1996) provide some indication of the quantity of infected wounds. In the 1980 survey, 897 infected wounds were found in 43 participating centres, and 1,731 were found in 157 centres in 1993. In both surveys, surgical wounds and skin infections were two of the four largest categories of infection. Although the studies were carried out in hospital, infections were classified as hospital- or community-acquired infections. Of the skin infection groups, which included leg and pressure ulcers, 335 and 909 infections were classed as community-acquired in 1980 and 1993 respectively. Briggs (1996) tabulated six incidence figures from studies of surgical wound infection that ranged from 4.7 to 8.9 per cent. Plowman et al (2000) reported that the cost per case of hospitalacquired infections was on average 2 to 2.5 times greater than for non-infected skin or surgical wounds, which is equivalent to between f1,618 and L2,398 per person. This information indicates that a large number of wounds require healthcare interventions and that

the management of infected wounds costs a considerable amount of money, results in lost opportunities to provide care for other patients and, most importantly, can cause physical and psychological distress. Wounds and microbial contamination The presence of infection not only delays the healing process, but can also lead to necrosis, which increases the size of the wound. Rapid recognition of the signs and symptoms of infection and early instigation of treatment will ensure best patient outcomes and reduce the risk of cross-infection. Skin, body orifices and the gut lumen are covered in micro-organisms. Each site on the body will have a different micro-flora that will have adapted to varying conditions; not all bacteria are pathogenic. For example, the normal skin commensals such as micrococci and non-pathogenic Corynebacterium species might multiply in a wound without ill effect (Lawrence 1993a). Numbers of bacteria on the skin surface are sparse except in moist areas such as the axilla and groin (Cooper and Lawrence 1996a). Different types of wounds have different environments. Intact skin, acute and chronic wounds provide distinctly different environments for microflora (Mertz and Ovington 1993). Acute wound flora is similar to that of intact skin with aerobic and some anaerobic species, whereas traumatic tissue provides an environment suitable for microbe adherence, multiplication and point of entry to surrounding tissue (Mertz and Ovington 1993), making it more prone to infection. Cooper and Lawrence (1996b) suggest that almost all bacterial types have been implicated in the pathogenesis of wound infection at some time. This is not surprising as necrotic tissue and slough provide a good medium for bacterial multiplication (Haughton and Young 1995). Multiplication of anaerobes like bacteroides found in the colon, mouth, genital and upper respiratory tract can lead to odour. Clostridium perfringens produce an acrid smell and aerobic bacteria such as Proteus, Klebsiella and Pseudomonas have an equally foul-smelling odour (Haughton and Young 1995). A wound must become contaminated with the relevant species before bacteria can cause infection or odour. Cooper and Lawrence (1996a) describe three main routes of acquisition: * Self-contamination from surrounding skin or gastrointestinal tract. * Airborne contamination from dust (much of which is skin squamae) or water droplets. * Contact contamination from clothing, equipment or carers' hands. Factors that affect the risk of wound infection include size, shape, age, and site of the wound, presence of foreign bodies and necrotic tissue, local vascularity and immunocompetency (Cooper and Lawrence 1996a). Wounds with necrotic tissue and large amounts of exudate will encourage microbial proliferation, while a dry wound environment hinders tissue repair. Infection involves cellulitis, which is the development of peri-wound erythema and pus formation, often with little systemic disturbance. However, if cellulitis is not treated, it can delay wound healing and might lead to septicaemia (Grey 1998). The most common cause of wound sepsis is Staphylococcus aureus (Cooper and Lawrence 1996b) and Beta-haemolytic streptococci (Lancefield group A). Treatment of these infections is empirical, partly because the bacteriology of ulcers with extensive surrounding cellulitis is

similar to that of chronic non-infected ulcers (Grey 1998). Lawrence (1993a) reports that Group A streptococcus is so pathogenic it almost inevitably leads to infection. Potentially pathogenic bacteria commonly found in wounds are mostly aerobic (Cooper and Lawrence 1996b). This is supported by Lawrence (1993a) who recorded the percentage incidence of bacteria in 58 venous ulcers. A review of leg ulcer bacteriology concluded that although streptococcal invasion was unlikely to initiate ulceration, it resulted in ulcer deterioration or delayed healing (Hayes 1997).

The relative paucity of reference to anaerobic infection in wounds might be partly explained by the difficulties in isolating them in comparison to aerobes, requiring time, patience and specialised techniques (Bowler 1998). In a series of investigations of 44 infected and 30 uninfected leg ulcers, aerobic species colonised both groups 100 per cent of the time, whereas the presence of anaerobic species increased from 73 per cent in the uninfected ulcers to 82 per cent in the infected group (Bowler and Davies 1999). In Bowler's (1998) review of 62 studies, bacteroides and peptostreptococcus (anaerobic species) were isolated in 33 studies, making them among the most frequent isolates. Disappearance of these anaerobic species has been associated with improved wound healing, which demonstrates the significance of anaerobes in wound infection. Grey (1998) notes that anaerobic cellulitis caused by bacteroides or clostridium species is a rare condition in diabetic foot ulcers and usually occurs as a result of synergism between aerobes and anaerobes. Sacral pressure ulcers are prone to mixed aerobe-anaerobe infection because of proximity to the source of gut flora. Bowler and Davies (1999) suggest that because of the variety of mixed flora in ulcers and the increase in anaerobic species in infected ulcers, aerobicanaerobic synergism might be of greater importance than any specific pathogen in the development of wound infection. Hayes (1997) stated that little more was needed to determine the flora of leg ulcers and that the next step was to determine the interaction of the bacteria with the host.

On investigating wound healing, Trengove et al (1996) found that bacterial groups in ulcers change over time, but that with the exception of skin flora, these changes were not related to changes in wound healing. According to Cooper and Lawrence (1996a), quantities as much as 106 colony-forming units (CFU) per gram tissue or millilitre of exudate persist for long periods, but decline as wound healing progresses. Trengove et al (1996) found that there was a significantly greater chance of failure to heal if four or more groups of bacteria were present in the wound. They concluded that because changes in wound flora occur independently of healing progress, qualitative bacteriology is of little benefit in predicting the effect of contaminating bacteria on healing. In the absence of clinical infection, wound swabs are not necessary in routine treatment. The value of microbiology The value of microbiology is linked to the activity being undertaken. Research is aimed at generating information for the formulation of treatment modalities for clinical practice, for example, attempting to understand the relevance to practice of the aerobe-anaerobe presence in open wounds. Reviews of the research literature on wound infection and occlusive dressings (Hutchinson and Lawrence 1991, Hutchinson and McGuckin 1990) help to determine whether important concepts in wound care, such as the predominant use of occlusive dressings, are safe and beneficial for patients. Clinical practice is based on principles derived from research that can be used empirically.

Microbiological techniques rely on growing organisms for identification and take 48 to 72 hours, which allows time for infection to develop if first-line/best-guess treatment is not employed immediately. For practical purposes, infection is a clinical diagnosis and not a microbiological one. However, microbiology is clinically valuable for determining that the firstline choice of antibiotics is correct for the sensitivity patterns of the causative organisms. This checking process aimed at the increasing problem of antibioticresistant strains of bacteria, such as methicillinresistant Staphylococcus aureus (MRSA), helps to ensure the resolution of infection as rapidly as possible.

Early resolution of wound infection promotes best patient outcomes, reducing the ill effects they might otherwise experience from the infection. Quantification of bacteria can aid research definitions of infection - 10^sup 5^ and 10^sup 6^ per gram tissue or millilitre of exudate - and is commonly used (Miller 1996). The 'plus' system (+/-) is used to quantify the amount of bacteria present in light, moderate or heavy growths (Lawrence 1993b). This information, which is sometimes recorded on microbiology report forms, should not influence whether treatment is given or not, or the antibiotic dosages - swabs should only be sent for culture because the clinical signs of infection that warrant treatment are present. Antibiotic dosages are maintained within therapeutic levels and discontinuation should be titrated to the absence of clinical signs. The microbiology result should be interpreted with the patient's clinical condition. Providing detailed information on the clinical situation including the signs and symptoms and antibiotic use means the microbiologist's assessment will focus on the patient's situation and, therefore, be more relevant to the clinician. Tissue biopsy provides the most accurate results, but this is an invasive procedure that is difficult to achieve for the mass of specimens required and, therefore, wound swabbing is the technique of choice. Few nurses are taught how to swab a wound (Donovan 1998), there is no consensus on swabbing methodology (Gilchrist 1996), absorbency of swab tips varies (Lawrence and Ameen 1998), and incorrect storage and transportation time can affect the final result.

Because of these difficulties microbes might not be sampled or could die on route to processing. Specimens might grow commensals, without growing pathogens that are responsible for causing the infection. Specimens taken from clinically infected wounds that yield no growth should not be considered proof of absence of infection, but suggest the possibility of a false-negative result. Microbiological results can provide a valuable interpretation of the patient's condition, but only when considered in combination with clinical signs and symptoms and general health status. Infection continuum and treatment algorithm An infection continuum can be used to provide a framework for clinical practice. This framework relies on an understanding of some commonly used terms plotted along a line that represents an ever increasing quantity of microbes in proportion to the host's immune response. The potential for a wound to become infected is determined by two main factors: the micro-organic contamination of the wound; and the person's resistance to that contamination (Kingsley 1992). The ability of the immune system to maintain a healthy defence against infection is unique to each person and depends on a number of factors (Box 1). The infection continuum is presented in Table 2 and uses the term 'critical colonisation' (Davis 1998). Figures 2 and 3 describe the mid-point between colonisation, which is a point of healthy balance between microbes and host, and infection (Figs. 4 and 5) where the host defences have been overwhelmed and the signs of cellulitis are evident. Further description of the signs of infection and critical colonisation are outlined in the treatment algorithm (Fig. 1), which incorporates the classic signs of infection plus those outlined by Cutting and Harding (1994), and personal observation from clinical practice. Conclusion In clinical practice, a diagnosis of infection is based on the presence of signs and symptoms, although Cutting (1994) suggests that definitive identification is achieved by culturing microorganisms. He also reports that clinical indicators, such as inflammation and discharge, have a low predictive value of infection in wounds. As with microbiological results, interpreting the clinical indicators of infection in the context of each patient will enhance diagnosis. In patients with a suspected wound infection, this means observing the wound site for change, usually an increase in each of the signs of inflammation greater than would normally be expected for that type of wound at that stage in the healing cascade. By comparing actual clinical signs with expected norms, practitioners could improve the predictive value considerably, initiate antiseptic dressings and/or antibiotic therapy early, thus maximising patient outcomes. A lack of knowledge about what constitutes infection, coupled with delays in initiating firstline treatment, because practitioners are awaiting swab results to diagnose or confirm infection, leads to poor patient outcomes, increased costs associated with unnecessary swabbing and unnecessary or prolonged courses of antibiotics, in turn increasing the likelihood of the development of resistance to antibiotics from ineffective prescribing.

To improve care in patients with wound infection, nurses need to feel confident in their ability to diagnose and treat infected wounds, which can be aided by the use of clear frameworks and algorithms. Nurses who have a good knowledge of the principles of infection control in tissue viability will be more assertive when negotiating the initiation of medically prescribed therapy for patients with wound infections.

Sidebar Online archive Sidebar For related articles visit our online archive at: www.nursing-standard.co.uk and search using the key words below. Sidebar Box 1. Factors affecting immune response to infection Sidebar * Underlying health * Any treatment he or she might be undergoing * Wound aetiology * Shape of the wound * Whether the wound can discharge pus adequately * Presence of foreign bodies or necrotic tissue * Level of skin health in the immediate peri-wound area * Size of the innoculum of microbes at initiation of wound or the proximity to ongoing contamination sources * Species of pathogens present * Number of species present * Ability of the species present to work synergistically References

REFERENCES Akca O et al (1999) Post-operative pain and subcutaneous oxygen tension. Lancet. 354, 9172, 41-42. Ayliffe G et al (Eds) (2000) Control of Hospital Infection: A Practical Handbook. Fourth edition. London, Arnold. Bowler P (1998) The anaerobic and aerobic microbiology of wounds: a review. Wounds. 10, 6, 170-178. Bowler P, Davies B (1999) The microbiology of infected and non-infected leg ulcers. International Journal of Dermatology. 38, 8, 573-578. References Briggs M (1996) Epidemiological methods in the study of surgical wound infection. Journal of Wound Care. 5, 4, 186-191. Callam M et al (1985) Chronic ulceration of the leg: extent of the problem and provision of care. British Medical Journal. 290, 6485, 1855-1856. Clinical Audit Department Northern Devon Trust (2000) Quarterly Pressure Ulcer Incidence Reports (Unpublished data). Devon, Northern Devon Trust. Cooper R, Lawrence J (1996a) The prevalence of bacteria and implications for infection control. Journal of Wound Care. 5, 6, 291-295. Cooper R, Lawrence J (1996b) Micro-organisms and wounds. Journal of Wound Care. 5, 5, 233-236. Cruse P, Foord R (1980) The epidemiology of wound infection: a 10-year prospective study of 62,939 wounds. Surgical Clinics of North America. 60, 1, 27-40. References Cutting K (1994) Detecting infection. Nursing Times. 90, 50, 60-62. Cutting K, Harding K (1994) Criteria for identifying wound infection. Journal of Wound Care. 3, 4, 198-201. Davis E (1998) Education, microbiology and chronic wounds. Journal of Wound Care. 7, 6, 272-274. Donovan S (1998) Wound infection and wound swabbing. Professional Nurse. 13, 11, 757759. Emmerson A et al (1996) The second national prevalence survey of infection in hospitals: overview of the results. Journal of Hospital Infection. 32, 3, 175-190. References Gilchrist B (1996) Sampling bacterial flora: a review of the literature. Journal of Wound Care. 5, 8, 386-388. Green J, Wenzel R (1977) Post-operative wound infection: a controlled study of the increased duration of hospital stay and direct cost of hosp talization. Annals of Surgery 185, 3, 264-268. Greif R et al (2000) Supplemental perioperative oxygen to reduce the incidence of surgical wound infection. New England Journal of Medicine. 342, 3, 161-166.

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Reilly J et al (2001) The importance of definitions and methods in surgical wound infection audit. Journal of Hospital Infection. 47, 1, 64-66. Seropian R, Reynolds B (1971) Wound infection after pre-operative depilatory versus razor preparation. American Journal of Surgery. 121, 3, 251-254. References Sizer T (Ed) (1996) Standards and Guidelines for the Nutritional Support of Patients in Hospitals, British Association for Parenteral and Enteral Nutrition. London, BAPEN. Thomas C (1988) Medical Microbiology Sixth edition. London, Balliere Tindall. Trengove N et al (1996) Qualitative bacte riology and leg ulcer healing. Journal of Wound Care. 5, 6, 277-280. Watt-Watson J et al (2000) The impact of nurses' empathic responses on patients' pain management in acute care. Nursing Research, 49, 4, 191-200. AuthorAffiliation Andrew Kingsley RGN, is Infection Control Tissue Viability Nurse Specialist, Northern Devon Healthcare Trust, North Devon District Hospital, Barnstaple. Email: andrew.kingsley@ ndevon.swest.nhs.uk

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Indexing (details)
MeSH Algorithms, Bandages, Cost of Illness, Debridement, Decision Trees, Great Britain -- epidemiology, Humans, Microbiological Techniques -standards, Prevalence, Risk Factors, Wound Healing, Wound Infection -- economics, Wound Infection -- epidemiology, Wound Infection -- microbiology, Infection Control -- methods (major), Skin Care -- methods (major), Skin Care -- nursing (major),Wound Infection -- nursing (major), Wound Infection -- prevention&control (major) A proactive approach to wound infection Kingsley, Andrew Nursing Standard 15 30 50-4, 56, 58 6 2001 Apr 11-Apr 17, 2001 2001 Harrow-on-the-Hill RCN Publishing Company Harrow-on-the-Hill

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