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The Clinical Relevance of Microbiology in Acute and Chronic Wounds

McGuckin, Maryanne Dr ScEd, MT (ASCP); Goldman, Robert MD; Bolton, Laura PhD; Salcido, Richard MD

Clinical Management Extra: CME: CE

PURPOSE To improve clinical practice and the quality of patient care by providing a learning opportunity that enhances the participant’s understanding of how wound microbiology affects healing.

TARGET AUDIENCE This CME/CE activity is intended for physicians and nurses with an interest in interpreting the role of microorganisms in wound healing.

OBJECTIVES At the conclusion of this course, participants should be able to:

  1. Identify the microbiology of acute and chronic wounds, risk factors for infection, and advantages and disadvantages of wound culturing.
  2. Identify methods of debridement and wounds for which they are appropriate.
  3. Identify systemic antibiotic treatment options for acute and chronic wound infections.

Maryanne McGuckin, Dr ScEd, MT (ASCP) • Senior Research Investigator, Department of Rehabilitation Medicine • Senior Fellow, Leonard Davis Institute of Health Economics • University of Pennsylvania School of Medicine • Philadelphia, PA

Robert Goldman, MD • Assistant Professor, Department of Rehabilitation Medicine • University of Pennsylvania School of Medicine • Philadelphia, PA

Laura Bolton, PhD • Director of Scientific Affairs • ConvaTec, A Division of ER Squibb & Sons • Skillman, NJ • Adjunct Associate Professor • Division of Bioengineering, Department of Surgery • University of Medicine and Dentistry of New Jersey • Piscataway, NJ

Richard Salcido, MD • William Erdman Professor & Chair of Rehabilitation Medicine • University of Pennsylvania School of Medicine • Director of Rehabilitation Services • University of Pennsylvania Health System • Philadelphia, PA

Maryanne McGuckin, Dr ScEd, MT (ASCP) and Richard Salcido, MD, have disclosed that they have no significant relationships or financial interest in any commercial companies that pertain to this educational activity. Robert Goldman, MD, has disclosed that he is a consultant and stock shareholder of SensorPad Systems, Norristown, PA, and has received a grant from Chattanooga Group, Hixson, TN. Laura Bolton, PhD, has disclosed that she is an employee and stock shareholder of ConvaTec, A Division of ER Squibb & Sons, Princeton, NJ, and former employee and stockholder of Johnson & Johnson, Somerville, NJ.

Acknowledgments The authors wish to acknowledge the assistance of Lois Porten in the preparation of this manuscript. Submitted October 30, 2002; accepted December 10, 2002.

The role of microorganisms in wounds and their effect on healing is a debatable issue. When reviewing the clinical relevance of microorganisms in wounds, however, some general statements can be applied.

First, wounds can be classified as either acute or chronic. For this article, acute wounds are defined as those that follow the normal phases of healing; they are expected to show signs of healing in less than 4 weeks. 1,2 The most common acute wounds are postoperative wounds. Chronic wounds are defined as those that do not appear to follow the normal healing process in less than 4 weeks. 1,2 These wounds are most commonly located on the lower leg, foot, and pelvic region. 1,2

Second, in acute wounds, the risk of infection is greatest during the first 48 to 72 hours; microorganisms isolated during this period should be considered clinically relevant until proven otherwise. Chronic wounds—except for those in patients with diabetes or those with compromised immunity—are at low risk of infection; isolation of microorganisms from chronic wounds usually represents colonization, rather than infection.

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Chronic wounds have chronic causes; for example, reported pressure or trauma for pressure or diabetic neuropathic ulcers. After the cause of tissue deterioration has been alleviated and necrotic tissue has been removed, both acute and chronic wounds progress through the same phases of healing: hemostasis, inflammation, granulation, epithelization, and maturation (Table 1). In this article, each phase is addressed separately; readers should be aware that these processes occur simultaneously and interactively during healing. If the source of injury recurs, these processes may begin again in the presence of freshly damaged tissue, creating an appearance of disorder.

Table 1

Table 1

Drawing conclusions from the research summarized in Table 1 about how microorganisms affect each stage of healing or the degree to which microbes invade healthy tissue during each stage is difficult because few sufficiently powered prospective clinical studies are available. However, several hypotheses can be generated from patterns reported in Table 1. Microorganisms appear to interact with acute and chronic wounds in similar but distinct ways during different stages of healing. Impaired hemostasis or inflammation reportedly favors infection, although microorganisms have mixed or beneficial effects on the granulation and epithelization stages of wound healing. Drawing conclusions from the literature is difficult because many variables affect the relationships between microorganisms and the wounds they populate, including wound attributes, patient or host characteristics, organism characteristics, and environmental variables.

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Pressure Ulcers, Venous Leg Ulcers, Ischemic Ulcers, and Neuropathic Ulcers

Chronic wounds offer special challenges in diagnosing and treating infections. Immunologic or vascular impairment may mask infection, while necrotic tissue or foreign matter may potentiate it.

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Evidence of infection


Because wound healing and clinical infection are inflammatory responses, differentiating between a wound resulting from injury and one resulting from invasive infection is essential. Colonizing microorganisms may be present in a wound resulting from injury. 3 For example, the presence of colonizing bacteria in leg ulcers has not been found to prevent healing. 4,5 In a wound resulting from infection, however, microorganisms are invading healthy tissue. 6 Histologically, infection is characterized by the invasion of viable tissue by pathogens and the presence of a polymorphonuclear (PMN) leukocyte response. 3 Adding to the confusion, PMNs are also early responders to chronic or acute tissue injury. Wound infection should be regarded as detrimental to healing. 7 Clinical infection in acute wounds has been correlated with tissue levels greater than 105 organisms per gram, but specificity and predictive value are poor. 4,8–10

To diagnose infection, microbiologic results must be evaluated in conjunction with local clinical findings, such as an increase in erythema, edema, pain, purulence, and lymphadenitis, or systemic factors, such as fever, leukocytosis, or glucose intolerance in patients with diabetes. 7,11–13 Organisms in wound fluid are not necessarily invading and may only be indicative, not diagnostic, of infection.

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Predisposing factors

Factors that predispose wounds to infection are well documented and influence the way colonized wounds respond. Patient-specific factors include advancing age, diabetes, steroid therapy and other immunosuppressants, extreme obesity, severe malnutrition, compromised circulation, and infection in remote sites. 11

Acute wounds are more susceptible to infection than chronic wounds. 12 Wounds that have not been debrided of necrotic tissue can predispose the patient to systemic infection; therefore, measures to prevent wound infection must include debridement of eschar or necrotic tissue and meticulous wound cleansing, along with measures to prevent wound dehydration. 7,12

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Debridement removes necrotic debris, which is a nidus for bacterial colonization. It also removes dying or senescent cells that could perpetuate the wound’s chronic nature. 14 Full-thickness wound contraction is significantly delayed if necrotic tissue is left in place. Debridement is supported by expert opinion, rather than controlled clinical trials. 15

Table 2 lists debridement options for various wound types. There are 5 basic types of debridement 16:

Table 2

Table 2

Table 2

Table 2

  • Surgical debridement is performed with the patient under general or regional anesthesia. It is frequently used for deep tissue infection, drainage of abscess or involved tendon sheath, or debridement of bone. If deep or loculated infection is involved, urgent surgical debridement is required, along with administration of systemic antibiotics. These antibiotics, however, will not permeate eschar or kill bacteria within it.
  • Sharp debridement has traditionally been referred to as surgical debridement. However, sharp debridement is performed by many disciplines and has been recognized as a distinct debridement method in a recent clinical practice guideline. 17
  • Sharp debridement is performed in an office setting or at the patient’s bedside while the patient is under local anesthesia (local tissue infusion or topical gel). First, a local antiseptic is used, which is washed off before dressing the wound; then forceps, curette, and/or scalpel are used to perform the sharp debridement. Knowledge of local anatomy is essential. 18 Empirically, a series of local debridements is required to achieve the same result as 1 surgical debridement. Premedication with a narcotic analgesic can be useful in reducing pain from the procedure.
  • A vascular assessment 18 should be performed prior to sharp debridement if peripheral arterial disease is suspected. The patient may respond to debridement with further necrosis if oxygenation is not sufficient to sustain healing.
  • Pathergy is the tendency of some well-oxygenated wounds to increase in size after debridement. Pathergy occurs with pyoderma gangrenosum, which is an unusual type of leg wound in the differential diagnosis of venous ulceration. 19 If a chronic venous ulcer appears to become larger after debridement and compression therapy, a biopsy should be performed to determine if the wound has pyoderma gangrenosum or carcinoma.
  • Mechanical debridement is performed with wet-to-dry dressings. 16 For this type of debridement, gauze is moistened with a solution such as normal saline and wrung out until it is slightly moist. The gauze is fluffed completely and placed over the wound bed to bring it in contact with the maximum amount of wound surface to be debrided. The dressings are removed when the gauze is almost dry. Tissue debris and drainage will adhere to the gauze.
  • Although wet-to-dry dressings may be effective, they are overused, 20 nonspecific to necrotic tissue, 20 and may be associated with residual fibers in granulation tissue that may remain as foreign bodies and delay healing. 21,22 Because debridement with wet-to-dry dressings involves tearing debris from the viable surface, it can be painful. Attention should be paid to premedication if wet-to-dry dressings are used.
  • In addition, an antibiotic ointment with broad antimicrobial coverage, such as silver sulfadiazine, 23 can be used instead of wet-to-dry dressings. The ointment permeates eschar, making it softer and more easily debrided, and could be considered as having mechanical debridement effect. The argument for using silver sulfadiazine comes from the management of deep partial- and full-thickness burns. Burn eschar is similar to chronic wound eschar: It is nonviable, firmly adherent, denatured proteinacious material. When eschar interacts with silver sulfadiazine, this material is converted to yellow-grey “pseudoeschar” that, for burns, readily separates from the viable wound surface within several days. 23 A similar process empirically takes place with chronic, eschar-covered wounds, including ischemic wounds. Silver sulfadiazine has an excellent antimicrobial spectrum of activity, low toxicity, ease of application, and minimal pain. Silver sulfadiazine inhibits DNA replication and modification of the cell membrane of Staphylococcus aureus, Escherichia coli, Klebsiella species, Pseudomonas, Proteus, Enterobacteriaceae, and Candida albicans. It may cause a transient leukopenia (5% to 15% incidence) for large burn wounds. 23
  • Enzymatic debridement involves the use of natural proteases, such as papain, papain-urea, or collagenase, to facilitate removal of necrotic debris. 16 Enzymatic debridement may be more cost-effective than mechanical or autolytic debridement for uncomplicated, well-perfused pressure ulcers in the skilled care setting. 24,25 In this setting—where access to sharp debridement is limited—and for stagable nonischemic pressure ulcers, papain-urea may be an excellent practical choice. On the other hand, papain is a nonspecific, bulk debriding agent that attacks cysteine residues on any protein, including matrix proteins and growth factors. Because it is a nonselective agent that may also digest viable tissue, papain-urea promotes an inflammatory response and may increase pain. 26
  • Drainage may increase for some patients undergoing enzymatic debridement 27 and should be considered when planning dressing changes. Special care must also be taken for wounds with black or necrotic eschar, which are hypoxic. Hypoxic wounds may become more ischemic due to the inflammatory response engendered by nonselective debriding agents. In addition, certain enzymatic debridement agents depend on native wound proteases of the bulk debriding agent for deactivation 28; however, the presence of these inactivating enzymes cannot be assumed in the altered metabolic environment of ischemic wounds. Therefore, enzymatic agents should be applied only while necrotic tissue is present and with caution to wounds below the knee with necrotic eschar and suspected peripheral arterial disease. Vascular work-up is the highest priority for tissue at-risk for peripheral arterial disease. A lower-extremity black, expanding wound (even slowly expanding) should be considered ischemic until proven otherwise. If not, unexpected limb loss could result.
  • Autolytic debridement involves the action of natural enzymes in wound fluid to debride eschar and debris. This usually occurs under occlusive or semiocclusive dressings, such as hydrocolloids or film dressings. Autolytic debridement using a hydrocolloid gel has been reported to result in earlier restoration of a granulating venous ulcer bed than enzymatic debridement when both were applied under a semiocclusive film dressing. 29

Autolytic debridement is contraindicated for an infected wound, 16 although some dressings may be used for autolytic debridement at the discretion of the clinician if appropriate medical treatment is initiated.

Clinicians should read the package inserts for enzymatic debridement products and dressings used for autolytic debridement prior to use.

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Wound cleansing

Wound cleansing removes bacteria and debris from a wound. The goal is to use as little chemical and mechanical force as possible and protect healthy granulation tissue. In general, wounds are cleansed initially and before a new dressing is applied.

Research during the last several decades has shown that many agents commonly used to cleanse wounds (eg, Dakin solution, hydrogen peroxide, acetic acid, and some concentrations of povidone-iodine) are cytotoxic to fibroblasts. Normal saline delivered at 8 pounds per square inch (psi) via a 35-mL syringe and a 19-gauge angiocatheter is usually sufficient to dislodge debris from a wound bed. 30,31

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Wound culture methods and the defining characteristics of wound infection are the subjects of considerable controversy. 32 In the absence of clinical symptoms of infection, wound culturing is generally agreed to have little meaning 6,33 and, at least for surgical wounds, daily direct wound observation yields the highest sensitivity and specificity of infection diagnosis. 6

If one holds bacterial culturing to scientific standards of validity, sensitivity, specificity, and positive or negative predictive validity, the evidence base for culturing wounds is in its infancy. 34 It is growing, however. Further research is needed to clarify and improve validity of wound culturing as a predictor of wound infection.

Available evidence on clinical validity, as well as clinical benefits and disadvantages of known methods of wound culturing, are presented in Table 3.

Table 3

Table 3

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In 1860, Louis Pasteur said, “The germ is nothing. It is the terrain in which it is found that is everything.”35 More than 150 years later, pathogens and wound care can still be discussed in this same way. There are, however, some basic facts about microorganisms 33:

  • Gram-negative organisms are not always equal to Gram-positive organisms in terms of invasiveness and pathogenicity.
  • The number of organisms in a wound cannot be used as an indication of invasiveness.
  • Breaking the stratum corneum is an important multiplier of “organism” virulence.
  • Acute wounds react differently to microbes than chronic wounds. For example, normal skin flora, if present in large numbers, can lead to sepsis in a patient with a graft/flap; a chronic leg ulcer can continue to harbor these organisms for years with little threat to a patient.

In 1999, Bowler et al 36 extensively studied the microbiology of acute and chronic wounds. They examined 45 chronic wounds—primarily leg ulcers, but also pressure and foot ulcers—and reported 195 isolates. Aerobic microorganisms were isolated from most chronic wounds (98%). The predominant isolates were coagulase-negative Staphylococcus, S aureus, ß-hemolytic Streptococci, Streptococcus viridans, Corynebacterium species, E coli, K pneumoniae, and Enterobacter aerogenes. Propionibacterium acnes and Bacteroides g enus were the most frequent anaerobic isolates.

Bacteria are often classified as pathogenic or nonpathogenic; however, this classification may not be as definitive when discussing the role of bacteria in wounds. Variables, such as the number of bacteria, nature of bacteria, multiple isolates, and antagonistic effects, and patient variables (wound type, general health, and clinical signs of infection) should be addressed before bacteria are considered pathogenic or nonpathogenic.

In Bowler et al, 36 the mean number of anaerobic and aerobic bacteria was 2.0 and 2.3, respectively. In chronic infected wounds, mixed anaerobes were the predominant isolates. This contradicts several studies 37–39 that have reported aerobic pathogens (including facultative), such as S aureus and Pseudomonas aeruginosa, as being associated with delayed healing and infection in acute and chronic wounds.

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Antibiotics and antisepsis

An algorithmic approach is important when evaluating a patient with an infected wound. First, the practitioner must decide whether the patient has a local or a systemic infection. Local signs of infection in a wound include rubor, dolor, and calor; systemic signs of infection include fever, tachycardia, hypotension, delirium, and alterations in mental status in older patients. 40 Then the practitioner must decide which antibiotic is most appropriate for the patient. Systemic antibiotics administered to combat wound infection can be divided into 5 main groups: penicillins, cephalosporins, aminoglycosides, fluoroquinolines, and sulfonamides (Table 4). Other antibiotics include clindamycin, metronidazole, and trimethoprim.

Table 4

Table 4

When considering antibiotic therapy for a patient with a wound, most practitioners make their selection based on the spectrum of coverage the antibiotic will provide. Before making a final selection, however, practitioners should consider parameters beyond the wound and targeted pathogen. Many important questions must be answered before prescribing an antibiotic to a patient with a wound, including:

  • Does the patient have known allergies?
  • Does the patient have any metabolic impairments that would alter the pharmacokinetics or the pharmacodynamics of the drug (ie, impaired renal or liver function)?
  • What are the effects of the drug on the hemopoietic system?
  • What attributes does the drug possess for effective tissue penetration (ie, how much of the drug actually ends up in the tissue of interest)? This is especially important in patients with osteomyelitis. 41
  • How is the drug metabolized?
  • What is the patient’s total weight and lean body and fat mass? These compartmentalized components of body mass affect the antibiotic’s delivery to the targeted site.

The adverse effects of antibiotics are well known and those that impede wound healing should be considered and counteracted. By their very nature, antibiotics wipe out normal flora (especially in the gastrointestinal tract), predisposing a patient to Clostridium difficile infection 42 and diarrhea. This scenario makes a pelvic wound hard to keep dry and predisposes a patient to dehydration.

Antibiotic resistance is a major concern, specifically methicillin-resistant S aureus (MRSA), penicillin-resistant Streptococcus pneumoniae, vancomycin-resistant Enterococcus, and multidrugresistant Gram-negative bacilli. 42,43 Therefore, when antibiotic therapy is ordered, the wound care specialist must be alert for signs of antibiotic resistance and attentive to the results of the laboratory data, especially culture and sensitivity. Patients who are immunocompromised or have impaired chemotaxis, resulting in bacterial overgrowth or candidiasis, will need concomitant treatment with selected antimycotic or antifungal agents. Consider establishing a relationship with an infectious disease specialist who can participate as an active member of the wound care team.

Other considerations when prescribing an antibiotic include the patient’s length of hospital stay, the availability of home health services and infusion services, the influence of the pharmacy and therapeutics committee, the hospital’s formulary, and the influence of the payer’s approval of prescription benefits.

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Surgical Site Infections

Considerable research has been devoted to identifying risk factors for surgical site infection and to classifying acute wounds by factors identified with risk of infection.

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Surgical wounds are stratified into 4 categories, according to wound class and anatomic location 44:

  • Class I, clean wounds: uninfected operative wounds in which no inflammation is encountered and the respiratory, alimentary, genital, or urinary tract is not entered. Examples include surgical repair of a hernia or breast therapy.
  • Class II, clean-contaminated wounds: operative wounds in which the respiratory, alimentary, genital, or urinary tract is entered under controlled conditions and without unusual contamination. Examples include gynecologic procedures or a gastrectomy.
  • Class III, contaminated wounds: open, fresh, accidental wounds; operations with major breaks in sterile technique or gross spillage from the gastrointestinal tract; and incisions in which acute, nonpurulent inflammation is encountered. Examples include a ruptured appendix or a perforated bowel.
  • Class IV, dirty/infected wounds: old traumatic wounds with retained devitalized tissue and those with existing clinical infection or perforated viscera. One example is debridement of a pressure ulcer.
  • This classification has been recognized since 1964. 44 In 1992, it was modified to add definitions of surgical site infections (SSI) 45:
  • Superficial incisional SSI: involves only skin and subcutaneous tissue of the incision; occurs less than 30 days postoperatively.
  • Deep incisional SSI: involves deep soft tissues (ie, fascial and muscle layers) of the incision; occurs less than 30 days postoperatively if no implant is involved and less than 1 year postoperatively if an implant is involved.
  • Organ/space SSI: involves any part of the anatomy, other than the incision, opened and manipulated during the operative procedure; occurs less than 30 days postoperatively if no implant is involved and less than 1 year postoperatively if an implant is involved.
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Risk factors

In 1999, the Centers for Disease Control and Prevention (CDC) published a guideline on prevention of SSIs based on the need to correct for intrinsic patient risk factors, 46 such as diabetes, nicotine use, steroid use, malnutrition, prolonged preoperative hospital stay, preoperative nares colonization with S aureus, and preoperative transfusion. For each risk factor, recommendations are identified, ranging from strongly recommended to unresolved. The guideline also lists additional risk factors that should be considered, including obesity, age, and the American Society of Anesthesiologists (ASA) score.

Although no single risk factor will consistently lead to infection, studies have shown that the likelihood of developing an SSI increases when multiple risk factors are present. 47 Identifying a patient’s risk during the preoperative stage is critical, rather than assuming the risk is based on the type of surgical procedure.

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Table 3 presents the advantages and disadvantages of the most common culturing methods for acute surgical wounds. In 1982, Hardin and colleagues 48 reported on the survival of anaerobics in surgical wounds and found no selective suppression of anaerobic bacteria by atmospheric air. Aerobic and anaerobic bacteria may increase or decrease in number during the course of a surgical procedure and are probably related to the degree of initial contamination, mechanical debridement, and amount of irrigation. 49 It has also been reported that aerobic and anaerobic bacteria can survive on swabs for 24 hours when exposed to room air. 49 From this, one can assume that clinically significant anaerobic bacteria are relatively aerotolerant when present in a mild infection.

When collecting specimens from operative sites, the swab should be saturated to minimize drying during transfer to the microbiology laboratory. The best procedure for specimen collection in terms of sensitivity, specificity, and predictive value is needle aspiration. If a delay of more than 24 hours is expected, the specimens should be transferred to an anaerobic collection vial, which will allow for growth of anaerobic and facultative aerobic bacteria. 49

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The pathogens present in an acute wound can be directly correlated to the surgical procedure. For example, the usual cause of infection in a clean surgical procedure is S aureus from an exogenous source or from the patient’s own flora. In a clean-contaminated, contaminated, or dirty/infected SSI, polymicrobial aerobic and anaerobic flora, resembling the endogenous flora of the resected organ, are the most frequently isolated pathogens. 50

According to data from the National Nosocomial Infections Surveillance System (NNIS), 51 the incidence and distribution of pathogens isolated from infections during the last decade have not changed. An increase in multiple-resistant bacteria, such as MRSA, has been noted, however. 52 In addition, several studies have reported SSI rates after discharge ranging from 20% to 84%. 53,54

To understand the increase of SSIs and the quantitative nature of pathogens, identification of risk factors for an SSI must be extended to the postdischarge period. Although the focus has always been on the isolated pathogen, the increase in SSIs should direct future activities to identification of postdischarge SSIs through standardized surveillance methods and surgeon-specific infection rates.

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Preoperative antibiotics

Classification of the 4 major antibiotics and their spectrum of activity are presented in Table 4. Readers should also refer to current guidelines for antibiotic prophylaxis of surgical wounds. 55

The use of antimicrobial prophylaxis has greatly changed surgical procedures in the past 20 years and now represents one of the most frequent uses of antimicrobial agents in hospitals, accounting for as many as one-half of all antimicrobial use. 56–59

Approximately 80% to 90% of surgical patients receive antibiotic prophylaxis, although several reports have shown that the choice of regimen, timing of administration, and duration is inappropriate in approximately 25% to 50% of cases. 60 Meta-analysis and literature reviews have concluded that (1) antibiotic prophylaxis reduces the odds or relative risk of SSI, (2) broad-spectrum antibiotics may be superior to limited-spectrum antibiotics for certain procedures, and (3) single-dose antibiotics appear to be as effective as multiple-dose antibiotics in terms of adverse events (C difficile colitis) and microbial resistance. 60–65

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Perioperative oxygen

Low oxygen content can predispose devitalized tissue to bacterial colonization, which is believed to be a key phase in the development of an SSI. 66 Administration of high concentrations of oxygen increases wound oxygen tension, allowing for more effective neutrophil function and reduced infection rates. 67

Although oxygen is part of standard perioperative care, the use of high oxygen concentrations intraoperatively and during recovery has not been well studied. One randomized controlled trial using wound infection within 15 postoperative days as the primary outcome found a 5% infection rate in the study group versus 11% in the control group. 68 Although these results are promising, additional controlled studies are needed to address the many variables associated with oxygen delivery and its effect on SSIs.

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Multidrug-resistant bacteria

Microbiologically, multidrug-resistant bacteria (MDRB) occur as a result of small lengths of DNA, called transposons (which carry a variety of antibiotic-resistant genes), moving from the bacterial chromosome to plasmid or viral DNA that can then be freely exchanged between bacteria. 69 The increase in MDRB has resulted from widespread, often inappropriate, use of antibiotics in medicine and in farming. In 1992, the CDC estimated that approximately 13,300 Americans died of health care–acquired infections caused by MDRB. 70 From this data, it can be inferred that 130,000 to 150,000 patients have died of these infections in US hospitals in the last decade. Efforts focused on reducing MDRB have included guidelines, physician education, and inpatient strategies. However, the most important preventive strategy to reduce the risk of transmitting MDRB is good hand hygiene. A recently released guideline from the CDC 71 provides recommendations and rationales for improving compliance with hand hygiene and reducing nosocomial infections.

The 2 most common MDRB are MRSA and vancomycin-resistant Enterococcus (Table 5). Other MDRB include C albicans, Mycobacterium tuberculosis, and the first case of vancomycin-resistant S aureus in the United States, identified in July 2002. 72 There is a distinct difference between MRSA infection and MRSA colonization. MRSA infection is marked by clinical consequences, such as fever, elevated white blood cell count, and evidence of wound separation and/or tissue destruction. MRSA colonization is defined as the presence of the organism but without the clinical manifestations of infection.

Table 5

Table 5

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Because we do not live in a sterile environment, there will always be clinical decisions to be made relevant to microorganisms. Although all colonization and infection are not preventable, there is sufficient evidence to show that colonization and infection can be prevented in at least 30% of situations if good infection control programs are in place and health care workers practice the single most important function in preventing infection: hand hygiene. In the course of clinical practice, constant vigilance can help limit cross-contamination. Awareness of the risk factors for chronic and acute wound infection and of strengths and limitations of wound culture methods can add valuable perspective for interpreting microbial diagnostic results and for prescribing and intervening effectively for contamined wounds.

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