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Guideline for Prevention of Surgical Site Infection, 1999

C. Microbiology

According to data from the NNIS system, the distribution of pathogens isolated from SSIs has not changed markedly during the last decade (Table 3).[26,27] Staphylococcus aureus, coagulase-negative staphylococci, Enterococcus spp., and Escherichia coli remain the most frequently isolated pathogens. An increasing proportion of SSIs are caused by antimicrobial-resistant pathogens, such as methicillin-resistant S. aureus (MRSA),[28,29] or by Candida albicans.[30] From 1991 to 1995, the incidence of fungal SSIs among patients at NNIS hospitals increased from 0.1 to 0.3 per 1,000 discharges.[30] The increased proportion of SSIs caused by resistant pathogens and Candida spp. may reflect increasing numbers of severely ill and immunocompromised surgical patients and the impact of widespread use of broad-spectrum antimicrobial agents.

Outbreaks or clusters of SSIs have also been caused by unusual pathogens, such as Rhizopus oryzae, Clostridium perfringens, Rhodococcus bronchialis, Nocardia farcinica, Legionella pneumophila and Legionella dumoffii, and Pseudomonas multivorans. These rare outbreaks have been traced to contaminated adhesive dressings,[31] elastic bandages, [32] colonized surgical personnel,[33,34] tap water,[35] or contaminated disinfectant solutions.[36] When a cluster of SSIs involves an unusual organism, a formal epidemiologic investigation should be conducted.


D. Pathogenesis

Microbial contamination of the surgical site is a necessary precursor of SSI. The risk of SSI can be conceptualized according to the following relationship[37,38]:

Dose of bacterial contamination × virulence = Risk of surgical site infection
Resistance of the host patient

Quantitatively, it has been shown that if a surgical site is contaminated with >105 microorganisms per gram of tissue, the risk of SSI is markedly increased.39 However, the dose of contaminating microorganisms required to produce infection may be much lower when foreign material is present at the site (i.e., 100 staphylococci per gram of tissue introduced on silk sutures).[40-42]

Microorganisms may contain or produce toxins and other substances that increase their ability to invade a host, produce damage within the host, or survive on or in host tissue. For example, many gram-negative bacteria produce endotoxin, which stimulates cytokine production. In turn, cytokines can trigger the systemic inflammatory response syndrome that sometimes leads to multiple system organ failure.[43-45] One of the most common causes of multiple system organ failure in modern surgical care is intraabdominal infection.[46,47] Some bacterial surface components, notably polysaccharide capsules, inhibit phagocytosis, [48] a critical and early host defense response to microbial contamination. Certain strains of clostridia and streptococci produce potent exotoxins that disrupt cell membranes or alter cellular metabolism. [49] A variety of microorganisms, including gram-positive bacteria such as coagulasenegative staphylococci, produce glycocalyx and an associated component called "slime,"[50-55] which physically shields bacteria from phagocytes or inhibits the binding or penetration of antimicrobial agents.[56] Although these and other virulence factors are well defined, their mechanistic relationship to SSI development has not been fully determined.

For most SSIs, the source of pathogens is the endogenous flora of the patient’s skin, mucous membranes, or hollow viscera.[57] When mucous membranes or skin is incised, the exposed tissues are at risk for contamination with endogenous flora.[58] These organisms are usually aerobic gram-positive cocci (e.g., staphylococci), but may include fecal flora (e.g., anaerobic bacteria and gramnegative aerobes) when incisions are made near the perineum or groin. When a gastrointestinal organ is opened during an operation and is the source of pathogens, gramnegative bacilli (e.g., E. coli), gram-positive organisms (e.g., enterococci), and sometimes anaerobes (e.g., Bacillus fragilis) are the typical SSI isolates. Table 4 lists operations and the likely SSI pathogens associated with them. Seeding of the operative site from a distant focus of infection can be another source of SSI pathogens,[59-68] particularly in patients who have a prosthesis or other implant placed during the operation. Such devices provide a nidus for attachment of the organism.[50,69-73]

Exogenous sources of SSI pathogens include surgical personnel (especially members of the surgical team), [74-78] the operating room environment (including air), and all tools, instruments, and materials brought to the sterile field during an operation (refer to "Intraoperative Issues" section). Exogenous flora are primarily aerobes, especially gram-positive organisms (e.g., staphylococci and streptococci). Fungi from endogenous and exogenous sources rarely cause SSIs, and their pathogenesis is not well understood.[79]


E. Risk and Prevention

The term risk factor has a particular meaning in epidemiology and, in the context of SSI pathophysiology and prevention, strictly refers to a variable that has a significant, independent association with the development of SSI after a specific operation. Risk factors are identified by multivariate analyses in epidemiologic studies. Unfortunately, the term risk factor often is used in the surgical literature in a broad sense to include patient or operation features which, although associated with SSI development in univariate analysis, are not necessarily independent predictors. [80] The literature cited in the sections that follow includes risk factors identified by both univariate and multivariate analyses.

Table 5 lists patient and operation characteristics that may influence the risk of SSI development. These characteristics are useful in two ways: (1) they allow stratification of operations, making surveillance data more comprehensible; and, (2) knowledge of risk factors before certain operations may allow for targeted prevention measures. For example, if it is known that a patient has a remote site infection, the surgical team may reduce SSI risk by scheduling an operation after the infection has resolved.

An SSI prevention measure can be defined as an action or set of actions intentionally taken to reduce the risk of an SSI. Many such techniques are directed at reducing opportunities for microbial contamination of the patient’s tissues or sterile surgical instruments; others are adjunctive, such as using antimicrobial prophylaxis or avoiding unnecessary traumatic tissue dissection. Optimum application of SSI prevention measures requires that a variety of patient and operation characteristics be carefully considered.


1. Patient characteristics

In certain kinds of operations, patient characteristics possibly associated with an increased risk of an SSI include coincident remote site infections [59-68] or colonization,[81-83] diabetes, [84-87] cigarette smoking,[85,88-92] systemic steroid use,[84,87,93] obesity (>20% ideal body weight),[85-87,94-97] extremes of age,[92,98-102] poor nutritional status,[85,94,98,103-105] and perioperative transfusion of certain blood products.[106-109]


a. Diabetes

The contribution of diabetes to SSI risk is controversial, [84-86,98,110] because the independent contribution of diabetes to SSI risk has not typically been assessed after controlling for potential confounding factors. Recent preliminary findings from a study of patients who underwent coronary artery bypass graft showed a significant relationship between increasing levels of HgA1c and SSI rates.[111] Also, increased glucose levels (>200 mg/dL) in the immediate postoperative period (<48 hours) were associated with increased SSI risk.[112,113] More studies are needed to assess the efficacy of perioperative blood glucose control as a prevention measure.


b. Nicotine use

Nicotine use delays primary wound healing and may increase the risk of SSI.[85] In a large prospective study, current cigarette smoking was an independent risk factor for sternal and/or mediastinal SSI following cardiac surgery.[85] Other studies have corroborated cigarette smoking as an important SSI risk factor.[88-92] The limitation of these studies, however, is that terms like current cigarette smoking and active smokers are not always defined. To appropriately determine the contribution of tobacco use to SSI risk, standardized definitions of smoking history must be adopted and used in studies designed to control for confounding variables.


c. Steroid use

Patients who are receiving steroids or other immuno-suppressive drugs preoperatively may be predisposed to developing SSI,[84,87] but the data supporting this relationship are contradictory. In a study of long-term steroid use in patients with Crohn’s disease, SSI developed significantly more often in patients receiving preoperative steroids (12.5%) than in patients without steroid use (6.7%).[93] In contrast, other investigations have not found a relationship between steroid use and SSI risk.[98,114,115]


d. Malnutrition

For some types of operations, severe protein-calorie malnutrition is crudely associated with postoperative nosocomial infections, impaired wound healing dynamics, or death.[116-124] The National Academy of Sciences/National Research Council (NAS/NRC),94 Study on the Efficacy of Infection Control (SENIC),[125] and NNIS[126] schemes for SSI risk stratification do not explicitly incorporate nutritional status as a predictor variable, although it may be represented indirectly in the latter two. In a widely quoted 1987 study of 404 high-risk general surgery operations, Christou and coworkers derived an SSI probability index in which final predictor variables were patient age, operation duration, serum albumin level, delayed hypersensitivity test score, and intrinsic wound contamination level.[117] Although this index predicted SSI risk satisfactorily for 404 subsequent patients and was generally received as a significant advance in SSI risk stratification, it is not widely used in SSI surveillance data analysis, surgical infection research, or analytic epidemiology.

Theoretical arguments can be made for a belief that severe preoperative malnutrition should increase the risk of both incisional and organ/space SSI. However, an epidemiologic association between incisional SSI and malnutrition is difficult to demonstrate consistently for all surgical subspecialties.[118-120,124,127-131] Multivariate logistic regression modeling has shown that preoperative proteincalorie malnutrition is not an independent predictor of mediastinitis after cardiac bypass operations.[85,132]

In the modern era, total parenteral nutrition (TPN) and total enteral alimentation (TEA) have enthusiastic acceptance by surgeons and critical care specialists.[118,133-137] However, the benefits of preoperative nutritional repletion of malnourished patients in reducing SSI risk are unproven. In two randomized clinical trials, preoperative "nutritional therapy" did not reduce incisional and organ/space SSI risk.[138-141] In a recent study of high-risk pancreatectomy patients with cancer, the provision of TPN preoperatively had no beneficial effect on SSI risk.[142] A randomized prospective trial involving 395 general and thoracic surgery patients compared outcomes for malnourished patients preoperatively receiving either a 7- to 15-day TPN regimen or a regular preoperative hospital diet. All patients were followed for 90 days postoperatively. There was no detectable benefit of TPN administration on the incidence of incisional or organ/space SSI.[143] Administering TPN or TEA may be indicated in a number of circumstances, but such repletion cannot be viewed narrowly as a prevention measure for organ/space or incisional SSI risk. When a major elective operation is necessary in a severely malnourished patient, experienced surgeons often use both pre- and postoperative nutritional support in consideration of the major morbidity associated with numerous potential complications, only one of which is organ/space SSI.[118,124,130,133,137,138,144-149] In addition, postoperative nutritional support is important for certain major oncologic operations,[135,136] after many operations on major trauma victims, [134] or in patients suffering a variety of catastrophic surgical complications that preclude eating or that trigger a hypermetabolic state. Randomized clinical trials will be necessary to determine if nutritional support alters SSI risk in specific patient-operation combinations.


e. Prolonged preoperative hospital stay

Prolonged preoperative hospital stay is frequently suggested as a patient characteristic associated with increased SSI risk. However, length of preoperative stay is likely a surrogate for severity of illness and co-morbid conditions requiring inpatient work-up and/or therapy before the operation.[16,26,65,85,94,100,150,151]


f. Preoperative nares colonization with Staphylococcus aureus

S. aureus is a frequent SSI isolate. This pathogen is carried in the nares of 20% to 30% of healthy humans.[81] It has been known for years that the development of SSI involving S. aureus is definitely associated with preoperative nares carriage of the organism in surgical patients.[81] A recent multivariate analysis demonstrated that such carriage was the most powerful independent risk factor for SSI following cardiothoracic operations.[82]

Mupirocin ointment is effective as a topical agent for eradicating S. aureus from the nares of colonized patients or healthcare workers. A recent report by Kluytmans and coworkers suggested that SSI risk was reduced in patients who had cardiothoracic operations when mupirocin was applied preoperatively to their nares, regardless of carrier status.[152] In this study, SSI rates for 752 mupirocin-treated patients were compared with those previously observed for an untreated group of 928 historical control patients, and the significant SSI rate reduction was attributed to the mupirocin treatment. Concerns have been raised regarding the comparability of the two patient groups.[153] Additionally, there is concern that mupirocin resistance may emerge, although this seems unlikely when treatment courses are brief.[81] A prospective, randomized clinical trial will be necessary to establish definitively that eradication of nasal carriage of S. aureus is an effective SSI prevention method in cardiac surgery. Such a trial has recently been completed on 3,909 patients in Iowa.[83] Five types of operations in two facilities were observed. Preliminary analysis showed a significant association between nasal carriage of S. aureus and subsequent SSI development. The effect of mupirocin on reducing SSI risk is yet to be determined.


g. Perioperative transfusion

It has been reported that perioperative transfusion of leukocyte-containing allogeneic blood components is an apparent risk factor for the development of postoperative bacterial infections, including SSI.[106] In three of five randomized trials conducted in patients undergoing elective colon resection for cancer, the risk of SSI was at least doubled in patients receiving blood transfusions.[107-109] However, on the basis of detailed epidemiologic reconsiderations, as many as 12 confounding variables may have influenced the reported association, and any effect of transfusion on SSI risk may be either small or nonexistent.106 Because of methodologic problems, including the timing of transfusion, and use of nonstandardized SSI definitions, interpretation of the available data is limited. A metaanalysis of published trials will probably be required for resolution of the controversy.[154] There is currently no scientific basis for withholding necessary blood products from surgical patients as a means of either incisional or organ/space SSI risk reduction.


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