CHAPTER 16 Wound infection: diagnosis and management
1. Compare and contrast the continuum of bacterial bioburden, including contamination, colonization, critical colonization, biofilm, and wound infection.
2. Identify risk factors for chronic wound infection.
3. Describe the processes used in obtaining a wound culture by biopsy, aspiration, and swab.
4. Interpret laboratory data indicative of a wound infection.
5. Identify situations appropriate for debridement, topical antimicrobials, and systemic antibiotics.
The body’s greatest defense against infection is intact skin. It is a mechanical barrier to microorganisms and its normal flora and acid pH control invasion of the skin by other microorganisms. When skin integrity is breached, the wound quickly becomes contaminated by body fluids and normal skin flora (Fonder et al, 2008). The effects of bacterial burden, called bioburden, on the wound are numerous and complex. Bacteria not only compete for the limited nutrients and oxygen present in the wound; they produce endotoxins and exotoxins that destroy or alter normal cellular activities, such as collagen deposition and cross-linking. Endotoxins are lipids and polysaccharides that are located in the cell wall of gram-negative organisms. When released, they activate the regulatory systems of the body (e.g., clotting, inflammation). Exotoxins are proteins released from bacteria that enzymatically inactivate or modify cells, causing them to die or disrupting their normal cellular functioning (Edwards and Harding, 2004). Excessive activity in these systems results in increased capillary permeability, leakage of fluid out of the vasculature, coagulopathies, and ultimately shock.
All chronic wounds contain some degree of bacterial bioburden and exhibit significantly elevated proinflammatory cytokines (interleukin-1, tumor necrosis factor-α, γ-interferon), matrix metalloproteinases (MMP-2, MMP-8, MMP-9), and neutrophils (Wolcott et al, 2009). In response to the proinflammatory proteins, neutrophils continue to arrive at the wound and release cytotoxic enzymes, free oxygen radicals, and inflammatory mediators triggering additional degradation of extracellular matrix and growth factors. Eventually protein lysis exceeds the synthesis of these proteins that are essential to wound repair so that the wound remains in the inflammatory phase and is unable to advance into the proliferative phase (Bjarnsholt et al, 2008; Woo and Sibbald, 2009).
The most common effect of this persistent chronic inflammatory state is delayed healing (Expert Working Group, 2008), which can deteriorate into infection, sepsis, multisystem organ failure, and death. Concomitantly, infection results in high cost, long hospitalization, as well as pain and suffering for patients and their families (Landis, 2008).
Continuum of bacterial bioburden
All wounds have some level of bacterial burden; few wounds are infected. The presence of organisms in the wound is an expectation. Recognizing the range of wound bioburden is helpful because it provides a framework from which to assess the significance of the situation and identify appropriate interventions. The continuum of bacterial bioburden can be subdivided into five microbial states: contamination, colonization, critical colonization, biofilm, and infection (Box 16-1).
BOX 16-1 Glossary of Terms
Antibacterial: Antiseptic that inhibits the growth of bacteria.
Antibiotic: Agent that can destroy or inhibit organisms. Has single target and therefore vulnerable to resistance.
Antimicrobial: General term for a substance that destroys or inhibits growth and replication of microorganisms.
Antiseptic /Antibacterial: Topical substance that inhibits growth and reproduction of organisms. Can be used on open wounds as well as intact skin. Strong biocidal agents and multiple pharmaceutical targets; little resistance developed to them; examples are iodine and silver. Duration of use limited to 2 weeks.
Bioburden: Presence of microorganisms on or in a wound. Continuum of bioburden ranges from contamination, colonization, critical colonization, biofilm, and infection. Bioburden includes the quantity of microorganisms present as well as their diversity, virulence, and interaction of the organisms with each other and with the body (synergism).
Biofilm: Complex community of aggregated bacteria embedded in a self-secreted extracellular polysaccharide matrix. Bacteria within biofilm respond to signals from other bacteria in the community to change their phenotype. Highly resistant to and poorly penetrated by antimicrobials. Can be removed with debridement. Reformation is prevented with antimicrobials and maintenance debridement (including autolysis).
Colonization: Replicating microorganisms adherent to the wound surface without a host reaction. Antimicrobials are not indicated.
Contamination: Nonreplicating microorganisms on the wound surface without a host reaction. All open wounds are contaminated by normal skin flora. Antimicrobials are not indicated.
Critical Colonization: Replicating microorganisms present on the wound and attached to the cells and structures in the wound. Level of bacteria inhibits wound healing but host does not exhibit classic signs of infection. Topical antimicrobials are indicated.
Disinfectant: Chemical that destroys, neutralizes, or inhibits growth of microorganisms. Usually used on inanimate objects and intact skin; harmful to open tissue. Examples includes alcohol and hydrogen peroxide.
Infection: Microorganisms invade tissue and yield a local or systemic response. Cultures are obtained to direct antibiotic selection.
Osteomyelitis: Bone infection characterized by a mixture of inflammatory cells, fibrosis, bone necrosis, and new bone formation.
Planktonic Bacteria: Free-floating (not anchored) bacteria, such as occurs with contamination and colonization.
Contamination
Contamination is the presence of nonreplicating microorganisms on the wound surface (Sibbald et al, 2006). Because all open wounds are inevitably contaminated by normal skin flora, the body is continually challenged to defend itself against invasion (Basu et al, 2009). Contaminating microorganisms may be endogenous (e.g., normal skin and gastrointestinal flora) or exogenous, present in the external environment (e.g., bed linen, devices, hospital personnel) (Woo and Sibbald, 2009). Early contaminants usually are gram-positive organisms (Staphylococcus aureus, Corynebacterium, Streptococcus, coagulase-negative staphylococcus), followed by gram-negative organisms (Escherichia coli, Klebsiella, Proteus.) Later anaerobic organisms, such as Prevotella, Bacteroides, and Peptostreptococcus, and fungi are present and are difficult to isolate with routine culture techniques because they typically lodge deep in the wound (Landis, 2008). Local or systemic antibiotics are not required for the contaminated wound.
Colonization
With colonization, the microorganisms adhere to the surface of the wound and replicate. Colonization does not impair healing (Edwards and Harding, 2004). The bacteria are not pathogenic and do not require treatment with local or systemic antibiotics. Inappropriate use of antibiotics during this phase has contributed to the prevalence of antibiotic-resistant organisms (Landis, 2008).
Critical colonization
Critical colonization describes a level of bacterial presence that affects skin cell proliferation and tissue repair; however, there is no systemic response (i.e., fever or leukocytosis) (Landis, 2008). Microorganisms are present on the surface of the wound and are attached to the wound surface but there is no invasion of the tissues by the bacteria. The key characteristic associated with critical colonization are presented in Box 16-2 and include nonhealing (wound size fails to decrease over 2 or more weeks) (Sibbald et al, 2006). In addition to nonhealing, subtle indicators of critical colonization may include friable, unhealthy granulation tissue (dull dark red or overly bright red), exuberant granulation tissue, increased exudate, odor, and a change or increase in pain. Necrotic material or debris may be present and serve as a nutrient source for the invading organism(s) but is not an indicator of critical colonization (Sibbald et al, 2006; Woo and Sibbald, 2009). When critical colonization is suspected, topical antimicrobials should be implemented (Table 16-1) for a time-limited period (usually 2 weeks) and the situation reevaluated (EWMA, 2005).
BOX 16-2 Criteria for Colonization and Infection*
TABLE 16-1 Commonly Prescribed Topical Antimicrobials
| Topical Agent | Action | Comments |
|---|---|---|
| Acetic acid 0.25%–0.5% | Bactericidal | Effective against Pseudomonas aeruginosa Used as irrigant or soak Protect periwound skin, changes pH |
| Cadexomer iodine | Broad spectrum | Effective against Methicillin-resistant Staphylococcus aureus (MRSA) Slow release of iodine from beads Concentrations are nontoxic to fibroblasts Microspheres absorb bacteria and exudate while slowly releasing iodine to remove inhibitory cytokines Confirm patient is not allergic to iodine prior to use |
| Chlorhexidine 0.02% | Broad spectrum | Effective against Staphylococcus aureus and Escherichia coli Consider use in patients allergic to iodine Use as irrigant solution |
| Honey | Produces H2O2, contains antioxidants | Releases antiinflammatory products Reduces odor through bacterial metabolism that yields lactic acid instead of ammonia or sulfur Confirm patient is not allergic to honey, bee products, or bee stings prior to use |
| Hydrofera blue | Methylene blue and gentian violet | Effective against Methicillin-resistant Staphylococcus epidermidis (MRSE), Vancomycin-resistant enterococcus (VRE), S. aureus, S. epidermidis, Serratia, E. Coli |
| Hydrogen peroxide | Oxidative debridement when necrotic tissue/debris present in wound | Not effective in reducing organisms Useful in removing debris because of its effervescent effects Use with care in closed cavities because of gas release |
| Mupirocin 2% ointment | Blocks activity of enzyme in bacteria responsible for making proteins | Effective against Methicillin-resistant Staphylococcus aureus (MRSA), β-hemolytic streptococcus, Streptococcus pyogenes Contraindicated for large burns Contains polyethylene glycol, which may damage kidneys if absorbed through skin |
| Povidone-iodine 1%–10% | Broad spectrum | No reported resistance Do not use scrub in open wound Confirm patient is not allergic to iodine prior to use |
| Silver dressings and creams | Broad spectrum | Concentration, rate of release, method of delivery vary by type of dressing (e.g., Acticoat provides rapid and sustained release when activated by water; Contreet hydrocolloid/foam provides sustained release as long as dressing absorbs exudate) Incorporated into cream, mesh, transparent, hydrogel, hydrocolloid, foam, alginate dressings, with selection based on wound characteristic and patient’s needs (see Chapter 18) Effective against Methicillin-resistant Staphylococcus aureus (MRSA), Vancomycin-resistant enterococcus (VRE) Minimal allergic response Potential for tissue staining (see Plate 43) |
| Sodium hypochlorite (Dakin’s solution) | Chlorine action kills organisms | Not usually recommended unless other alternatives are unavailable |
Bacitracin zinc-neomycin, gentamycin sulfate, Polymyxin B, Garamycin for topical wound care are not commonly prescribed due to frequent development of sensitization.
Biofilms
Once microorganisms begin to adhere to the surface of the wound, they begin to develop biofilm (Pupp and Williams, 2008). A biofilm is a complex structure of microorganisms embedded in an extracellular matrix of hydrated polysaccharide that is permanently attached to the biologic or nonbiologic surface. Almost 70% of chronic wounds have a biofilm present, whereas only 6% of acute wounds have documented biofilm (Bjarnsholt et al, 2008). The biofilm comprises various types of organisms living together in symbiotic relationships and a harmonious community. Proteus aeruginosa and S. aureus are the most common microorganisms forming chronic biofilm (Bjarnsholt et al, 2008). The number of organisms is limited by nutrient availability. Bacteria within the biofilm respond to signals from other bacteria in the community to change their phenotype, increasing the difficulty of identifying an antibiotic that is effective in eradicating the biofilm. The polysaccharide matrix protects the organism from invasion by other organisms, the phagocytic activity of polymorphonuclear neutrophils, oral or topical antibiotics, and topical antiseptics (silver, chlorhexidine, Dakin solution, povidone-iodine). Biofilms form on other moist surfaces, such as prosthetic implants and biomaterials (e.g., stainless steel pits in orthopedic surgery) (Pupp and Williams, 2008). As the biofilm progresses, the risk of difficult-to-treat infection rises.
Treatment of biofilm requires a two-pronged approach or a biofilm-based wound care plan. First the wound is surgically débrided. Sharp debridement may be adequate when it can be conducted aggressively and with minimal pain. Following debridement, topical therapy with moisture-retentive dressings and wound irrigation techniques provide continued debridement through autolysis. This approach is essential to prevent re-formation of the biofilm. Some investigators advocate weekly surgical or sharp redebridement, referred to as continued maintenance debridement, to keep wound biofilm in a weakened and susceptible state (Wolcott et al, 2009).
Two agents that appear promising for removing biofilm are topical doxycycline and cadexomer iodine. Doxycycline, a tetracycline, acts as a competitive inhibitor of MMPs and in studies has been applied once per day. This application of doxycycline remains under investigation and is not approved by the Food and Drug Administration. Cadexomer iodine is a topical broad-spectrum antiseptic that has been used in wound care for a number of years. The product slowly releases iodine beads into the wound and removes inhibitory cytokines while absorbing wound exudate. One study showed cadexomer iodine destroyed Pseudomonas biofilms after 24 hours of exposure to an in vitro biofilm model of skin wounds (Thorn et al, 2009).
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
