Surgical Site Infections
Sarah Y. Won
Edward S. Wong
Despite advances in operative techniques, better understanding of the pathogenesis of surgical site infections (SSIs), and widespread use of prophylactic antibiotics, SSIs continue to be a major source of morbidity and mortality for patients undergoing operative procedures. It is estimated that SSIs develop in 2% to 5% of the 27 million patients undergoing surgical procedures each year, resulting in 300,000 to 500,000 infections (1, 2, 3). They account for approximately 20% of all healthcare-associated infections (HAIs), making the surgical site the second most common site of HAIs, second only to infections of the urinary tract (3). Compared to surgical patients without SSIs, patients with SSIs have a 2 to >12 times increased risk of death, with 77% of deaths in SSI patients related to the infection (4, 5, 6, 7). SSIs add, on average, 7.4 additional hospital days, but can add up to an additional 18 inpatient days, at a cost of between $3,000 and $60,000 per SSI (1, 2,4, 5, 6, 7, 8, 9, 10, 11).
In addition, the rising incidence of methicillin-resistant Stapylococcus aureus (MRSA), which is responsible for 7.5% of all SSIs, adds considerable morbidity and mortality in the United States (12). MRSA SSIs may triple rates of death and add an additional $14,000 per infection, compared to patients with methicillin-sensitive S. aureus (MSSA) SSIs (4). Total cost of SSIs, including indirect expenses related to SSIs, likely exceeds $10 billion annually in the United States (5).
As a consequence of the significant morbidity, mortality, and cost of SSIs, prevention of SSIs has been receiving increased regulatory, third-party payer, and public attention. SSI prevention has become part of a major quality improvement initiative called Surgical Care Improvement Projects (SCIPs) (13). The Centers for Medicare and Medicaid Services (CMS), the primary payer for Medicare and Medicaid patients, are no longer paying additional reimbursements for certain SSIs, like mediastinitis and select orthopedic infections, and require reporting on two SSI prevention process measures advocated by SCIP (14) (see Table 21-1). Public reporting of SSI rates is mandated in an increasing number of states. As a result, understanding the epidemiology, implementing evidence-based prevention measures, and surveillance of SSIs have become all the more important for infection preventionists, surgical teams, and hospitals.
DEFINITION OF SURGICAL SITE INFECTIONS
Clinically, a surgical site can be considered infected when purulent drainage is present at the incision site. This may be associated with local swelling, erythema, tenderness, wound dehiscence, or abscess formation. However, local signs and symptoms may not always be present, nor are they necessarily due to infection when they are present. Therefore, the clinical definition of SSI that has been the most widely adopted is the simplest one—that of a surgical site draining a purulent exudate. Clinicians are encouraged to culture all purulent exudates, but neither culture nor a positive microbiologic result is required for diagnosis of an SSI.
However, the definition of an SSI that is to be used for surveillance and epidemiologic purposes must meet additional needs. Such a definition must be simple to use but also unambiguous so that hospitals with varying surveillance resources will be able to apply it and obtain consistent results so that comparisons between hospitals are meaningful. The Centers for Disease Control and Prevention (CDC) has developed and published definitions for the surveillance of SSIs—see below (15), and they are now widely adopted for surveillance and are the de facto national standard.
SSIs are classified as incisional or organ/space. Incisional SSIs are divided further into superficial incisional SSI (when they involve the skin and or subcutaneous tissue—see below) or deep superficial SSI (involvement of the fascia and/or muscle—see definitions below). An organ/space SSI involves structures or organs beneath the area of the incision (15). The anatomic location of each site is depicted in Figure 21-1.
Superficial incisional SSIs are the most common, accounting for more than 50% of all SSIs. However, while only one third of all SSIs are organ/space infections, these infections account for over 90% of deaths related to SSIs (16).
Operative sites are followed for 30 days for the development of SSI, unless an implant is involved, in which case the period of surveillance is extended to a year (15).
TABLE 21-1 Six Performance Measures of the CMS’ SCIP | ||||||||||||||
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Superficial Incisional Surgical Site Infections: Superficial Incisional Primary/Superficial Incisional Secondary
Superficial incisional SSIs (superficial incisional primary [SIP] or superficial incisional secondary [SIS]) must occur within 30 days after the operative procedure and must involve only skin and/or subcutaneous tissue of the incision, and at least one of the following must be present:
Purulent drainage from the superficial incision
Microorganisms isolated from an aseptically obtained culture of fluid or tissue from the superficial incision
At least one of the following signs or symptoms of infection—pain or tenderness, localized swelling, redness, or heat—and the superficial incision is deliberately opened by the surgeon and is culture positive or not cultured. A culture-negative finding does not meet this criterion.
Diagnosis of superficial incisional SSI by the surgeon or attending physician
There are two specific types of superficial incisional SSI:
Superficial incisional primary (SIP): a superficial incisional SSI that is identified in the primary incision in a patient who has had an operation with one or more incisions (e.g., C-section incision or chest incision for coronary artery bypass graft [CAGB] with a donor site)
Superficial incisional secondary (SIS): a superficial incisional SSI that is identified in the secondary incision in a patient who has had an operation with more than one incision (e.g., donor site [leg] incision for CABG)
 FIGURE 21-1 The anatomy of SSIs and their appropriate classifications. |
The following should not be reported as superficial incisional SSIs: (a) stitch abscess (minimal inflammation and discharge confined to the points of suture penetration), (b) localized stab wound infection, (c) infection of a circumcision site in newborns, (d) infected burn wound, (e) incisional SSI that involves or extends into the fascial and muscle layers (should be reported as deep incisional SSI), and (f) involves both superficial and deep incision sites (report as deep incisional SSI).
Deep Incisional Surgical Site Infections: Deep Incisional Primary/Deep Incisional Secondary
Deep incisional SSIs (deep incisional primary [DIP] or deep incisional secondary [DIS]) must occur within 30 days after the operative procedure if no implant is left in place or within 1 year if implant is in place; the infection must appear to be related to the operative procedure; and the infection must involve deep soft tissues (fascial and muscle layers) of the incision; and at least one of the following must be present:
Purulent drainage from the deep incision but not from the organ/space component of the surgical site.
A deep incision that spontaneously dehisces or is deliberately opened by a surgeon and is culture positive or not cultured when the patient has at least one of the following signs or symptoms: fever (>38°C), or localized pain or tenderness. A culture-negative finding does not meet this criteria.
An abscess or other evidence of infection involving the deep incision that is found on direct examination, during reoperation, or by histopathologic or radiologic examination.
Diagnosis of a deep incisional SSI by a surgeon or attending physician.
There are two specific types of deep incisional SSI:
Deep incisional primary (DIP): a deep incisional SSI that is identified in the primary incision in a patient
who has had an operation with one or more incisions (e.g., C-section incision or chest incision for CAGB with a donor site)
Deep incisional secondary (DIS): a deep incisional SSI that is identified in the secondary incision in a patient who has had an operation with more than one incision (e.g., donor site [leg] incision for CABG)
Infection that involves both superficial and deep incision sites should be classified as a deep incisional SSI.
Organ/Space Surgical Site Infections
Organ/space SSIs involve any part of the body, excluding the skin incision, fascia, or muscle layers, that is opened or manipulated during the operative procedure. Specific sites are assigned to organ/space SSIs to identify the location of the infection (e.g., intra-abdominal site).
Organ/space SSIs must occur within 30 days after the operative procedure if no implant is left in place or within 1 year if implant is in place and the infection appears related to the operative procedure; and the infection involves any part of the body, excluding the skin incision, fascia, or muscle layers, that is opened or manipulated during the operative procedure; and at least one of the following must be present:
Purulent drainage from a drain that is placed through a stab wound into the organ/space
Microorganisms isolated from an aseptically obtained culture of fluid or tissue in the organ/space
An abscess or other evidence of infection involving the organ/space that is found on direct examination, during reoperation, or by histopathologic or radiologic examination
Diagnosis of an organ/space SSI by a surgeon or attending physician
Occasionally, an organ/space infection drains through the incision. Such infection generally does not involve reoperation and is considered a complication of the incision; therefore, it should be classified as a deep incisional SSI.
INCIDENCE OF SURGICAL SITE INFECTIONS
The true incidence of SSIs across the United States has traditionally been difficult to measure for several reasons: (a) much of the earlier incident data came from the CDC’s National Nosocomial Infections Surveillance System (NNIS), which was a voluntary network of 200 larger acute care hospitals that reported HAIs to the CDC, and was not representative of all hospitals; (b) the increasing number of outpatient surgical procedures that were not included in SSI surveillance; (c) and with shorter inpatient stays, SSIs occurring postdischarge with unclear if any or how much postdischarge surveillance was performed.
Since 2005, the National Health Safety Network (NHSN) superseded the NNIS, and unlike the NNIS, the NHSN allows for surveillance of healthcare infections outside the intensive care units, and at other types of healthcare facilities, including ambulatory surgery centers (14). In addition, the NHSN currently includes data from more than 2,000 hospitals across the United States due to two main reasons (a) 21 states’ legislative mandates to report surveillance data through the NHSN, and (b) the opening of the NHSN to all hospitals, regardless of size (16, 17, 18, 19). Therefore, these SSI rates may be more representative of the true incidence of SSIs. In the most recent NHSN report 2006 to 2008, which includes data from 1,545 hospitals, SSI rates were reported by operative procedure and NNIS risk index (an index used to predict risk of SSIs; see further description below), with lowest risk of SSI designated by NNIS risk index = 0, and highest risk designated by NNIS risk index = 3. Between 2006 and 2008, the pooled mean number of SSI per 100 inpatient operations was as low as 0.2 for gallbladder surgery (NNIS risk index = 0, lowest SSI risk group) and as high as 26.7 for rectal surgery (risk index = 3, highest SSI risk group) (17).
In general, the highest rates of infection occur after abdominal surgeries (reported per 100 surgeries): rectal (3.5-26.7), liver transplant (11.6-20.1), bile/liver/pancreas (8.1-13.7), colon (4.0-9.5), small bowel (3.4-6.8), and kidney transplant (3.7-6.6); however, rates for appendix (1.1-3.5), gallbladder (0.23-1.72), and exploratory abdominal surgery (1.7-2.8) were fairly low. Neck surgeries (NNIS risk index = 2 and 3) also had a high rate of 11.4 SSIs per 100 surgeries. Rates of other high-volume surgeries, therefore with a high absolute number of infections, include all coronary bypass surgery (0.4-8.5), cardiac surgery (1.1-1.8), hip prosthesis (0.7-2.4), knee prosthesis (0.6-1.6), laminectomies (0.7-2.3), spinal fusion (0.7-4.2), cesarean section (1.5-3.8), vaginal hysterectomy (0.7-1.2), and abdominal hysterectomy (1.1-4.0).
For eight outpatient procedures, the rates were between 0.0 and 1.31 per 100 surgeries, but again, it is unclear if any or how postdischarge surveillance was performed (18).
In contrast to SSIs among adults, the rate of SSIs among children has not been studied as extensively. However, medical centers with large pediatric surgical services have published their infection rates. Among these centers, the rate of pediatric SSIs varied from 3.4 per 1,000 admissions at the Children’s Hospital in Buffalo (18) to 5.5 per 1,000 admissions at the University of Virginia (20). Horwitz reported a rate of 4.4% of all surgeries at three institutions (21). Duque-Estrada reported an overall infection rate of 575 pediatric surgeries to be 6.7%, ranging from 2.7% of clean surgeries to 14.6% of dirty/infected surgeries (20). Both the Horwitz and the Duque-Estrada studies showed increased risk due to the amount of contamination at surgery and duration of surgery, with no difference in risk due to patient-specific factors, length of prior hospitalization, location of operation, or other coexisting diseases, raising the concern that factors at operation, rather than overall physiologic status, contribute to SSIs in children. Another study examining risk factors for sternal wound infection in children undergoing cardiac surgery with sternotomy showed overall SSI rate of 2.7%, with 62% of the infections defined as superficial infections and 38% deep infections. Younger age, cyanotic heart disease, and central venous catheter dwell time increased risk (22). According to CDC estimates based on NNIS, National Health Discharge Service (NHDS), and the American Hospital Association survey, the SSI rates from well-baby nurseries, high-risk nurseries, and intensive care units (both children and adults) were 0.003, 0.2, and 0.95 per 1,000 admission-days, respectively (3).
MICROBIOLOGY
Table 21-2 depicts the most common SSI pathogens and their antibiotic resistance as reported to the NHSN from January 2006 to October 2007 (14). Over the past several decades, the species of microorganisms, and their relative importance, in causing SSI still have not changed considerably. S. aureus and coagulase-negative staphylococci continue to be the two most common pathogens isolated largely from clean surgical procedures. When surgery involves entry of the respiratory, gastrointestinal, or gynecologic tracts, pathogens are often polymicrobic, involving aerobic and anaerobic microorganisms endogenous to the organ resected or entered.
In recent years, however, there has been noted in SSIs, as in other sites of HAIs, a shift toward infections with antibioticresistant strains of both gram-positive and gram-negative microorganisms. In the NHSN report, from 2006 to 2007, about half of S. aureus SSI isolates were methicillin resistant, and 20% of enterococcal infections were vancomycin resistant. Almost a quarter of all E. coli were resistant to quinolones, almost 15% of K. pneumoniae resistant to third-generation cephalasporins, more than 30% of A. baumanii were resistant to carbapenems, and 2% to 5% of E. coli and K. pneumoniae were carbapenem resistant (12). Infections involving fungi, especially Candida albicans and non-albicans Candida species, are becoming more common because of the increasing number of immunocompromised patients undergoing operative procedures and use of broad-spectrum antibiotics.
TABLE 21-2 SSI Pathogens (NHSN) 2006-2007, n = 7,025 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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In addition, SSIs caused by unusual microorganisms are also increasingly being recognized; for example, SSIs caused by Rhizopus rhizopodiformis due to contaminated adhesive dressings (23,24), multiple outbreaks of infections with rapid growing Mycobacterium species (25, 26, 27, 28, 29), Nocardia, and Rhodococcus bronchialis after coronary artery bypass surgery have been reported (30,31). Healthcare-associated SSIs and prosthetic valve endocarditis due to Legionella pneumophila after contamination by tap water have been described (32, 33, 34). Clusters of infections by such unusual microorganisms clearly warrant investigation to rule out common source exposures.
PATHOPHYSIOLOGY AND RISK FACTORS OF SURGICAL SITE INFECTION
In 1965, Altemeier and Culbertson (35) stated that the risk of an infection varies (a) directly in proportion to the dose of bacterial contamination, (b) directly in proportion
to the virulence of the microorganism, and (c) inversely in proportion to the resistance of the host, that is, the patient’s ability to control the microbial contamination.
to the virulence of the microorganism, and (c) inversely in proportion to the resistance of the host, that is, the patient’s ability to control the microbial contamination.
The host’s ability to control the inevitable bacterial contamination of a surgical wound is a complex interaction between overall host characteristics (i.e., age, immunosuppression, obesity, diabetes), appropriate antimicrobial prophylaxis, surgical site conditions during and at the end of the operation (i.e., blood flow, damaged or necrotic tissue, foreign material, including drains and sutures), and operative characteristics (i.e., use of razors for shaving, skill of surgeon, type of surgery). Practically, the surgical site condition may be influenced by perioperative homeostasis, which includes blood glucose levels, normovolemia, oxygenation, and temperature. The condition of the surgical site is also determined by the underlying disease process at the surgical site, that is, severity of trauma or prior radiation.
MICROBIAL RISK FACTORS
Surgical Site Classification
The risk of developing an SSI is affected by the degree of microbial contamination of the operative site. A widely accepted system of classifying operative site contamination was developed by the National Research Council for its cooperative study of the effects of ultraviolet irradiation of operating rooms on SSIs (36), with the least contamination in clean sites and the most in dirty-infected sites. This classification scheme, in a modified form, is as follows:
Clean sites (wounds): These are surgical sites in which no inflammation is encountered and the respiratory, alimentary, genital, and urinary tracts are not entered. In addition, clean wounds are primarily closed and, if necessary, drained with closed drainage. Surgical sites for operations that follow nonpenetrating (blunt) trauma should be included in this category if they meet these criteria.
Clean-contaminated sites (wounds): These are operative sites in which the respiratory, alimentary, genital, or urinary tract is entered under controlled conditions and without unusual contamination. Specifically, operations involving the biliary tract, appendix, vagina, and oropharynx are included in this category, provided no evidence of infection or major break in technique is encountered.
Contaminated sites (wounds): These include open, fresh accidental wounds or operations with major breaks in sterile technique or gross spillage from the gastrointestinal tract. Surgical sites through which there is entry into the genitourinary tract with infected urine or biliary tract with infected bile, and surgical sites in which acute, nonpurulent inflammation is encountered, fall into this category.
Dirty and infected sites (wounds): These include old traumatic wounds with retained devitalized tissue, foreign bodies, or fecal contamination. Surgical sites where a perforated viscus or pus is encountered during the operation fall into this category.
Early studies showed that this surgical site (wound) classification scheme did predict the risk of subsequent SSIs. In Cruse and Foord’s (37) study, surgery involving clean, clean-contaminated, contaminated, and dirty surgical sites had infection rates of 1.5%, 7.7%, 15.2%, and 40%, respectively. The SSI rates in the National Research Council cooperative study were 3.3% for refined clean sites, 7.4% for other clean sites, 16.4% for contaminated sites, and 28.6% for dirty sites (36).
The correlation of site (wound) class to the risk of SSIs would suggest that intraoperative site contamination should also be linked to the risk of subsequent infections. However, conflicting results were obtained when the microbiology of intraoperative site contamination was examined and attempts were made to correlate microorganisms isolated intraoperatively with pathogens responsible for the SSIs. Barlett et al. (38) isolated bacteria from 43 of 91 (47%) intraoperative surgical site irrigation cultures. However, they found no significant difference in the rate of subsequent SSIs between those patients with and those without positive cultures. Further, there was no relationship between the concentration of bacteria in the sites and the subsequent development of infection. A more recent prospective study of neurosurgical patients found no association between total colony-forming unit (CFU) counts of skin flora, either before or after skin preparation, at the operative site and SSIs (39). Therefore, it is clear that degree of microbial contamination is only one risk factor for development of SSIs.
Sources for Pathogens Causing Surgical Site Infections
Pathogens that cause SSIs are predominately acquired endogenously from the patient’s own flora or potentially from exogenous contact with operating room personnel or the environment. It is believed that, within 24 hours of an operative procedure, most surgical sites are sufficiently sealed, unless the site was closed secondarily or involved drain placement, making the surgical site resistant to inoculation and infection. Thus, most pathogens, whether endogenously or exogenously acquired, are believed to be implanted at the time of surgery (40). Theoretically, the operative site can be seeded postoperatively by the hematogenous or lymphatic route or by direct inoculation of the closed operative site, but such mechanisms of acquisition are thought to occur infrequently (40). Ehrenkranz and Pfaff (41), however, described a cluster of sternal infections occurring postoperatively that were preceded by infections caused by the same microorganisms at remote sites (pneumonias and bacteremias). In the outbreak of Legionella sternal infections reported by Lowry et al. (34), patients were not exposed to contaminated tap water containing Legionella during bathing and dressing changes until well after cardiac surgery. Thus, there is evidence to suggest that inoculation (and infection) may occasionally occur postoperatively. Nonetheless, the period of greatest risk for infection remains the time between opening and closing the operative site.
Endogenous Sources of Pathogens The patient’s own flora at or contiguous to the site of operation accounts for the majority of SSIs (42). S. aureus and coagulase-negative staphylococci, the first and second most frequent causative microorganisms, are residents of skin and mucous membranes, and presumably they are directly inoculated
into the operative site during incision or subsequent manipulations. Between 2006 and 2007, 44% of all SSIs reported to the NHSN were either due to coagulase-negative Staphylococcus or S. aureus; over 56% of SSIs were due to gram-positive microorganisms and yeast, common skin commensals (12). Unsurprisingly, colonization of the nares and skin with S. aureus is a risk factor for developing SSI due to S. aureus, and may quadruple the odds of a S. aureus SSI compared to those who are not colonized (43). Recently, in a double-blind randomized trial, rapid identification of S. aureus colonization by PCR, and subsequent decolonization of the skin and nares of colonized individuals with chlorhexidine showed a 60% reduction in cardiac surgery SSIs due to S. aureus (44). However, in order to prevent one S. aureus SSI, the number needed to screen and treat was 250 and 23, respectively, making screening and decolonization not cost-effective.
into the operative site during incision or subsequent manipulations. Between 2006 and 2007, 44% of all SSIs reported to the NHSN were either due to coagulase-negative Staphylococcus or S. aureus; over 56% of SSIs were due to gram-positive microorganisms and yeast, common skin commensals (12). Unsurprisingly, colonization of the nares and skin with S. aureus is a risk factor for developing SSI due to S. aureus, and may quadruple the odds of a S. aureus SSI compared to those who are not colonized (43). Recently, in a double-blind randomized trial, rapid identification of S. aureus colonization by PCR, and subsequent decolonization of the skin and nares of colonized individuals with chlorhexidine showed a 60% reduction in cardiac surgery SSIs due to S. aureus (44). However, in order to prevent one S. aureus SSI, the number needed to screen and treat was 250 and 23, respectively, making screening and decolonization not cost-effective.
Skin antisepsis during preparation of the operative site for surgery is routinely performed and reduces the surface population of all skin microorganisms, therefore reducing risk of SSIs. Darouiche et al. (45) recently published a prospective randomized study of patients undergoing clean-contaminated surgery (70% abdominal, 30% nonabdominal), which demonstrated a >40% reduction in total SSIs among patients randomized to preoperative chlorhexidine-alcohol skin preparation compared to providine-iodine scrub. This decrease was due to a significant decline in incidence of superficial and deep incision infections caused by gram-positive bacteria and Candida, demonstrating the importance of skin flora on incisional SSI pathogenesis, even among clean-contaminated surgeries.
However, if the skin became heavily colonized—for example, as a result of dermatitis—resident flora may persist and be carried into the operative site. In addition, even optimal skin antisepsis may not be able to eradicate all skin bacteria, as up to 20% of these bacteria live beneath the skin’s surface along the hair follicles and sebaceous glands (40).
During nonclean surgery, besides the significant role of skin flora that can contaminate the incision, normal flora of the gastrointestinal, respiratory, genital, and urinary tracts can directly contaminate the operative site when these tracts are opened or when injury has occurred to one of these tracts prior to surgery.
The patient’s endogenous flora at distant sites may also be a source of SSI. Wiley and Ha’eri (46) noted that human albumin microspheres (HAMs) were like human skin squames and could be used as tracer particles. When they applied HAM to the patient’s skin outside the area of the incision, they demonstrated that the tracer particles could be easily recovered from the operative site (in 40 of 40 orthopedic operations), suggesting that surface microflora can migrate from distant sites and gain entrance to the operative site despite distance and the use of cloth and adhesive drapes as barriers. Finally, microorganisms causing infections at remote sites may gain access to operative sites by hematogenous or lymphogenous seeding, which is most commonly associated with bacteremia after implantation of prosthetic material (47). Untreated urinary tract, skin, and respiratory tract infections have also been associated with an increase in the rate of SSIs (48,49).
Exogenous Sources of Pathogens Personnel The hands and nails of the operative team harbor microorganisms that can contaminate the surgical site by direct inoculation during the operative procedure (50, 51, 52). This has led to the use of surgical gloves as a barrier to the transfer of microorganisms and to the surgical hand scrub to reduce the microbial population on the skin of the hands. Initially introduced as a way of protecting operating room personnel against dermatitis from Listerian antisepsis, surgical gloving has became a standard of practice as a method to prevent the passage of microorganisms from the surgeon’s hands to the patient’s surgical site. Whether surgical gloves are an effective barrier has been questioned, since studies have demonstrated that glove perforations occur frequently; this occurs in up to a third or more of operations (37,52). Nonetheless, with appropriate preoperative scrubbing to reduce the burden of microorganisms on the surgeon’s hands, there is no evidence that such perforations of surgical gloves are of any clinical significance. Dodds et al. (53) found no difference in the rate of SSIs among 100 hernia repairs that were or were not associated with glove perforations.
However, despite standard hand hygiene and gloving, outbreaks due to artificial nails have been reported, due to sequestered microorganisms trapped between the natural and artificial nail (54).
In addition to the hands, other body sites in the operative team may be sources for exogenous contamination of the operative site. The hair and scalp of hospital staff (as well as of patients themselves), nares and oropharynges have been shown to harbor potentially pathogenic bacteria, including S. aureus and gram-negative bacteria (55). Despite those observations, however, only a few outbreaks of SSIs have been traced to the hair/scalp or nasopharynx of the operative team (50,56). However, outbreaks of group A Streptococcus SSI have been traced to anal or vaginal carriage by operating room personnel (57, 58, 59, 60).
Environment The microorganisms that are isolated from the operating room environment are usually considered nonpathogens or commensals that are rarely associated with infections (61). Atypical mycobacteria are ubiquitous and can be recovered from hospital dust but are rarely incriminated in SSIs. In the clusters of infections due to Mycobacterium fortuitum and M. chelonae that followed valve replacement surgery and augmentation mammoplasty (27, 28, 29), it was bone wax or gentian violet marking solution that was incriminated rather than the general operating room environment. Spores of Clostridium perfringens have been isolated from the ventilation system and floors of operating rooms (62), but when investigators looked for potential sources for these microorganisms that cause devastating SSIs, they concluded that C. perfringens was either endogenously acquired from the patient’s own gastrointestinal flora (63) or acquired from contaminated surgical instruments that had been inadequately sterilized between cases (64).
In those rare instances when inanimate sources in the operating room have been incriminated, the sources have been contaminated solutions, antiseptics, or dressings. Contaminated elastic dressings have been implicated
in SSIs caused by Rhizopus (24,25,65) and C. perfringens (66). Contaminated solutions have been the source for SSIs caused by P. aeruginosa, P. multivorans, and Serratia marcescens (67, 68, 69).
in SSIs caused by Rhizopus (24,25,65) and C. perfringens (66). Contaminated solutions have been the source for SSIs caused by P. aeruginosa, P. multivorans, and Serratia marcescens (67, 68, 69).
It is currently standard practice to wet mop the floor of the operating room with a disinfectant between cases. Coupled with a more thorough wet vacuuming of the rooms and corridors at night, this routine is believed to provide a sufficiently clean environment that minimizes the risk of the operating room environmental surfaces and floors as a source of infection.
Air The role of the operating room air as a source of infection and the need for special ventilation systems in the operating room have long been subjects of debate. The largest source of airborne microbial contamination is the staff in the operating room (61,62). It is presumed that microorganisms become airborne as a result of conversation, which creates droplet nuclei from the respiratory tract, or as a result of shedding from hair or exposed skin. Tracer particle studies using HAMs suggest that airborne microorganisms from the respiratory tract or the head and neck area of operating room personnel can settle on the operative site (46,70,71). Despite this possibility, there is little evidence that the airborne route of transmission contributes significantly to SSIs. Evidence that SSI resulting from airborne contamination occurs at all is based on outbreaks of group A b-hemolytic streptococcal infections that have been reported in the literature (57, 58, 59, 60). In these outbreaks, the evidence for airborne transmission was as follows. First, streptococci with the same serotype as the isolates from infected surgical sites were isolated from sites of colonization (anal, vaginal, or pharyngeal) in operating room personnel. Second, the sites of carriage (anal or vaginal) had no possibility of direct contact with the operative site. Moreover, some of these carriers were ancillary personnel who, while they were in the same room, did not work directly in the operative field. Finally, when settling plates were used during these investigations, the epidemic microorganism could be recovered from the air of a room during exercise by the carrier.
Additional evidence for the role of airborne transmission comes from studies on the use of laminar flow air systems and ultraviolet irradiation to provide ultraclean air. Early studies appeared to show a reduction in SSIs when special air-handling systems were used to reduce airborne microbial contamination (72, 73, 74, 75). However, many of these studies were flawed, because they were not comparative, had inadequate sample sizes, were not randomized or blinded, or included other interventions that could affect the rate of SSIs. A well-designed multicenter European study compared infection rates among total hip and knee replacement procedures that were performed in rooms with ultraclean air provided by special ventilation systems, antimicrobial prophylaxis alone, or ultraclean air plus antimicrobial prophylaxis (76). In rooms with ultraclean air, the frequency of SSIs decreased from 3.6% to 1.6%; however, when antimicrobial prophylaxis alone was used, the rates dropped from 3.4% to 0.8%. The combination of interventions decreased rates from 3.4% to 0.7%. These results helped demonstrate antimicrobial prophylaxis to be more beneficial in prevention of SSIs than ultraclean air, with no additional benefit of ultraclean air when antibiotics were used.
HOST RISK FACTORS
It is clear that degree of microbial contamination is only one of several variables that determine SSI outcome. Intuitively, host susceptibility, that is, the host’s intrinsic ability to defend itself against microbial invasion, should be an important determinant of the risk of infection following surgery. Over the years, studies have demonstrated that such factors as age, obesity, current smoking, prior irradiation at the site of the procedure, malignancy, immunosuppressives, the presence of certain underlying diseases such as diabetes (and hyperglycemia), and S. aureus nasal colonization can all increase risk of SSI (36,43,77, 78, 79, 80, 81, 82).
Age
Of these host factors, advanced age has consistently been found to be a risk factor for SSIs, likely due to increased comorbidities, decreased immune function, increasing frailty, and malnutrition (36,37,77,83, 84, 85). In contrast, others, like Garibaldi and Cushing (86), did not find age to be a risk factor. In their study, it was suggested that age is a marker for increased comorbidities. In the national nosocomial infection study by Haley et al. (87), the percentage of SSIs after 75 years decreased. Recently, Kaye, using a large cohort of over 70,000 procedures, demonstrated that the risk of SSI increased by 1.1% per year between ages of 17 and 65; however, at ≥65 years, the risk of SSI decreased by 1.2% per year (88). Though unclear why rates of SSI should decrease after 65 years of age, lower rates may be a reflection of a surgical selection bias, that only healthier older patients are taken for surgery, or that very old patients are “hardy survivors,” with better genetics that enable them to better handle the stressors of surgery. Nevertheless, other studies have shown that elderly patients with SSIs are at increased risk for death compared to younger patients with SSIs. For instance, elderly patients with S. aureus SSI were greater than three times more likely to die than younger patients with S. aureus SSIs (89).
Diabetes and Hyperglycemia
One risk factor associated with SSIs is elevated blood glucose levels perioperatively or a history of diabetes. Pathophysiologically, diabetes impairs leukocyte adherence, phagocytosis, and overall ability to kill bacteria. In addition, the extracellular glycosylation of proteins due to high blood glucose levels impairs wound healing (90). Cruse and Foord (37) reported higher rates of SSIs in their patients with diabetes, as did Nagachinta et al. (91) in their prospective study of 1,009 cardiac surgery patients. In the latter study’s regression analysis, diabetes mellitus and obesity were the two host factors that remained independently associated with sternal or mediastinal SSIs. Since these early studies, diabetes has most consistently been associated with increased SSI, especially deep sternal wound infections, in cardiovascular patients (90,92,93,94), but has also been a documented risk factor in patients undergoing mastectomy and hepatobiliary-pancreatic cancer surgeries as well (95,96).
More important than a history of diabetes may be the level of postoperative hyperglycemia. Latham et al. (93)
observed that in cardiac surgery patients, the risk of SSIs after cardiovascular surgery correlated with the level of postoperative hyperglycemia. The odds of developing an SSI was >2.5 when blood glucose was 200 or more within 48 hours after surgery, compared to those with levels <200 (93). Other cohort studies (90,94) have also demonstrated improved deep sternal SSI rates with improving blood glucose levels to <200 in the 48 hours postoperatively, most effectively achieved with continuous insulin infusion.
observed that in cardiac surgery patients, the risk of SSIs after cardiovascular surgery correlated with the level of postoperative hyperglycemia. The odds of developing an SSI was >2.5 when blood glucose was 200 or more within 48 hours after surgery, compared to those with levels <200 (93). Other cohort studies (90,94) have also demonstrated improved deep sternal SSI rates with improving blood glucose levels to <200 in the 48 hours postoperatively, most effectively achieved with continuous insulin infusion.
However, it is unclear if more aggressive hyperglycemia management, below glucose levels of 200, is associated with decreases in cardiovascular SSI. The Diabetic Portland Project, which was an observational cohort study of diabetic cardiovascular surgery patients, demonstrated, over time, the progressive reduction in sternal wound infections, mortality, and length of stay with the use of progressive lowering of target blood glucose ranges by using continuous insulin pump protocols (97). The lowest rates of deep sternal wound infections were found by targeting blood glucose levels of 100 to 150. However, a meta-analysis of five randomized controlled trials comparing conventional blood glucose control (blood glucose <200, which is the current recommendation by IDSA/CDC) versus strict glucose control did not show any SSI, mortality, or length of stay, benefits to strict glycemic control; however, the studies had multiple limitations of sample size and methodologic quality (98).
In addition to postoperative hyperglycemia, long-term hyperglycemia may be a risk factor for SSIs as well. Dronge et al. (99) demonstrated in a retrospective study that patients with good long-term control of blood glucose (hemoglobin A1c <7%) had decreased infectious complications (SSIs, pneumonia, urinary tract infection, or sepsis) across a broad range of surgeries, specifically excluding cardiac cases. In Latham’s study (93) of cardiac patients, patients with good long-term control of diabetes (hemoglobin A1C <8%) were at less risk of developing postoperative hyperglycemia.
Nutrition
The association between malnutrition and SSIs is not well proven. The National Research Council study showed that the crude rate of SSIs was 22% in severely malnourished patients compared to 7% in well-nourished patients (36). However, subsequent studies have not demonstrated an increased risk of SSIs with malnutrition, after adjusting for other risk factors (91,100). Multiple trials have not demonstrated any benefit of preoperative total parenteral nutrition (TPN) or other “nutritional therapies” in prevention of SSIs (101).
On the contrary, studies have repeatedly demonstrated the increased risk of SSIs with obesity (36,91,102,103). This increased risk is likely multifactorial, including increased amount of tissue necrosis, compromised blood flow, but also may be due to inadequate dosing of prophylactic antibiotics (104). Forse et al. (104) demonstrated a decrease in wound infections in morbidly obese patients undergoing gastroplasty surgery from 16.5% to 5.6% (2.5% in normal weight patients) by administration of 2 g of cefazolin, rather than 1 g normally administered perioperatively.
Smoking
Nicotine may increase rates of SSI by reducing blood flow, therefore delaying primary wound healing. Nagachinta et al. (91) demonstrated in a large prospective trial that patients who are current smokers have twice the increased odds of SSI compared to ex-smokers or nonsmokers. Other studies have supported these findings.
PROCEDURAL RISK FACTORS
Prolonged Preoperative Stay
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