Surgical Site Infections and the Anesthesia Professionals' Microbiome: We've All Been Slimed! Now What Are We Going to Do About It? : Anesthesia & Analgesia

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Surgical Site Infections and the Anesthesia Professionals' Microbiome

We've All Been Slimed! Now What Are We Going to Do About It?

Roy, Raymond C. MD*; Brull, Sorin J. MD; Eichhorn, John H. MD

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doi: 10.1213/ANE.0b013e3181fe4942
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Dr. Peter Venkman: “Someone blows their nose and you want to keep it? …”

—Ghostbusters (1984)

We are grossly outnumbered! Each of us consists of approximately 10 trillion human cells, accompanied by our personal “microbiome” of 100 trillion microorganisms that live symbiotically inside and on our bodies. Surgical site infections are but one of the many complex features of this usually peaceful coexistence. These microorganisms have influenced our evolution. They are essential to our digestion, metabolism, and immunity. However, they also serve as the source of our infectivity. Since 2007, the National Institutes of Health has supported the international Human Microbiome Project in its effort to understand the extent to which our microbiomes are unique to each one of us as individuals and common to all of us as a species.1,2

Our microbiota are organized as biofilms, impressively structured communities within 3-dimensional matrices of extracellular polymeric substances, the “slime” attached to epithelial membranes.3 Chronic bacterial infections are now recognized as biofilms that limit access by host antibodies and macrophages and resist diffusion of antibiotics.36 Biofilms of the same species of bacteria may be nonpathogenic in one location and pathogenic in others. For example, the most common cause of surgical site infections, defined as infections occurring within 30 days postoperatively or within 1 year if the surgery involved an implant, is Staphylococcus aureus.7 Yet, 20% of us are persistent asymptomatic carriers of S aureus in our anterior nares; 30%, intermittent carriers.8 Because we are constantly shedding bacteria from our biofilms,6,9 we as patients and health care providers contaminate every operating room we enter.914

How should our personal microbiomic “slime” affect our efforts to reduce surgical site infections? A report in this issue of Anesthesia & Analgesia by Loftus et al.15 addresses bacterial transmission via the hands of anesthesia practitioners. This is part of the growing knowledge of the etiology of surgical site infections, and complements previous work by Loftus and his group,12 Koff et al.,16 Compère et al.,17 Call et al.,13 and Haessler et al.18

In 2005, the Centers for Disease Control and Prevention established the National Healthcare Safety Network by combining the National Nosocomial Surveillance System, the Dialysis Surveillance Network, and the National Surveillance System for Healthcare Workers to benchmark and study health care–associated infection surveillance data.19 The National Healthcare Safety Network provides national rates for 5 such health care–associated infections: central line–associated blood infection, urinary catheter–associated infection, ventilator-associated pneumonia, postprocedure pneumonia, and surgical site infection. Surgical site infection data are divided into risk groups. Each patient is graded by 3 criteria and assigned a 0- to 3-point score (Table 1): 1 point if the patient is an ASA physical status III or higher, 1 point if the surgical site is known to be contaminated before incision, and 1 point if the procedure duration is in the longest quartile for the specific operation being performed. In 2 recent studies of surgical site infections in older patients, S aureus was the responsible pathogen in 51% to 56% of cases, more than half of which were methicillin-resistant S aureus (MRSA). Other common pathogens included coagulase-negative staphylococci (in 8%–12% of cases), other Gram-positive bacteria (8%–13%), Escherichia coli (4%–5%), and other Gram-negative organisms (5%–13%).7,20

Table 1:
Percent Surgical Site Infections for Common Inpatient Surgical Procedures

Because of the enormous cost of surgical site infections,21 it is reasonable to ask if a change in practice can lower the national rate of infection seen in the data collected by the National Healthcare Safety Network. The report by Loftus et al. supports this assertion. Haessler et al.18 linked a systemic breakdown in operating room handwashing compliance caused by an institutional change in the hand antiseptic product to an increase in the rate of surgical site infections, exceeding both internal and national benchmarks. Koff et al.16 documented that increased handwashing frequency by anesthesia providers decreased the rate of health care–associated infections.

Because the responsible pathogen for most surgical site infections typically originates from the infected patient's own microbiota8,14 and contaminates through bacteremia, skin migration, or bacterial airborne dispersal (“cloud” formation), it is appropriate to wonder whether anesthesia providers could be directly implicated as the cause of a surgical site infection. Three case reports are particularly instructive. In 1969, an anesthesiologist was reported as the individual directly responsible for 2 clusters of group A Streptococcus pyogenes surgical site infections involving 20 patients.22 The route by which the bacteria arrived in the surgical wounds was not established, but it was clearly demonstrated that bacteria in the rectum of the carrier became airborne (as measured by the number of colony-forming units in operating room air samples) with physical activity, friction with clothing, or flatulence.9 Once airborne, the wound could be contaminated directly by the bacterial “cloud” or indirectly by transmission of bacteria lodged on surgical instruments or gloves.911 If this was the route of contamination, handwashing by the anesthesiologist would not have prevented infection. Alternatively, the anesthesiologist could have practiced poor personal hygiene and touched patients with his contaminated hands or contaminated endotracheal tubes, catheters, syringes, or IV injection ports such as stopcocks. In that bygone era (experienced by the 3 authors of this editorial), anesthesia providers generally did not wear gloves and washed their hands infrequently. Herpetic whitlow and paronychia were, at the time, occupational hazards for anesthesia professionals.

In 2000, 2 pediatric intensive care unit nurses were identified as nasal carriers of MRSA and were treated.23 Hygienic measures in the unit were tightened, closely monitored, and reinforced frequently. Two months later, a blood culture positive for MRSA prompted a reexamination of the hospital environment. MRSA recolonization of the anterior nares was documented in 1 nurse, but she was not involved in the care of the index patient. The other nurse was the source of contamination, but her nasal cultures were negative for MRSA. However, cultures from her hands, forearms, elbows, axillae, neck, perineum, and anus were all positive, because she had extensive eczema. Despite apparently demonstrating excellent hygienic practice, she contaminated the sample of blood she collected from the patient. Skin typically resists S aureus colonization.24 When there is loss of skin integrity, however, as occurs with eczema, atopic dermatitis, psoriasis, furunculosis, or a wound, colonization readily occurs, especially in patients who are known nasal carriers.25,26

There is also the case of an orthopedic surgeon with chronic hepatitis C virus infection who did not infect any of his patients with the hepatitis C virus. However, during the year in which he was treated with interferon-α, his surgical site infection rate increased from 1% to 9%. After his hepatitis C therapy was completed, his surgical site infection rates returned to 1%.27 Interferon-α produces flu-like symptoms. Fatigue could have caused lapses in adherence to operating room asepsis protocol. Such lapses have been associated with an increase in the rate of surgical site infections.14,28 Alternatively, the flu-like symptoms he exhibited could have been premonitory of an increase in airborne dispersal of bacteria (the “cloud”). When healthy asymptomatic nasal carriers of S aureus were deliberately infected with a rhinovirus, a 2-fold increase in airborne dispersal of coagulase-negative staphylococci was observed.29 Histamine-induced sneezing caused almost a 5-fold increase in airborne dispersal of S aureus from healthy nasal carriers.30

Much of the airborne cloud associated with cloud-forming patients was reduced by having the patients change from street clothes to surgical scrubs. Adding surgical masks did not provide any additional reduction in the number of colony-forming units collected.31,32 The primary value in wearing surgical facemasks is to protect health care workers from splashes of body fluids from patients, rather than reduce the risk of airborne dispersal of bacteria by the health care worker. Evidence supporting the effectiveness of surgical masks in decreasing surgical site infections is equivocal at this time.33 To date, most of the effectiveness research regarding the use of high-efficiency particulate air filters as surgical masks has focused on prevention of health care–associated infections related to viral transmission and not on reduction of surgical site infections related to the airborne dispersal of bacteria.

If we accept that we are “slimed” by our personal bacteria, constantly contaminate our environment, and cause some surgical site infections, then we must also accept responsibility for reducing our personal contributions to surgical site infections. The obvious answer is “as simple as washing your hands.”34 Sadly, our documented compliance with handwashing guidelines is abysmal.35 There are multiple explanations for the wildly variable rates in our compliance with one of the most basic (and effective) procedures to decrease surgical site infection: hand hygiene. Self-protection of health care workers is a major subliminal driver for performance of hand hygiene, such that the rates of handwashing are significantly lower before patient contact than after.36 Lack of a positive role model leads medical students, residents, and nurses to copy the (negative) behavior of their supervisors.37 The length of professional education seems to be inversely correlated with the rate of hand hygiene compliance, with nurses having a higher rate of compliance than physicians.38 Knowledge of being observed (Hawthorne effect) doubles the rate of compliance with handwashing requirements,39 but the effect is transient. Translation of community handwashing behavior (i.e., inherent behavior learned in the community) to hospital settings seems to be the predominant driver of all handwashing behavior.40 Implementation of a Six Sigma process to increase compliance was effective and sustained for a 9-month observation period,41 although a significant incidence of unintentional noncompliance remained. Finally, there are nihilistic data to suggest that although many health care–associated infections may be prevented by improved handwashing compliance, they will not be completely eradicated42 because health care providers also contaminate the perioperative environment in ways not involving their hands, and because the patient's own microbiota are a prominent source of pathogenic bacteria.

Based on these data, we suggest it is time for us as individuals, and as a profession, to address the following questions: Should we obtain and monitor anesthesia provider–specific data regarding surgical site infections? What should we do with such data? How would we apply them? Equally importantly, is it reasonable to assume, if the occurrence of surgical site infections and care from a specific health care provider are temporally related, that this evidence is causative? Should all operating room personnel (surgeons, nurses, and anesthesiologists) be routinely cultured (anterior nares, skin lesions) for S aureus and MRSA? Would such cultures suffice, or should more invasive cultures, such as those obtained from the axillae, perineum, and rectum be required? Should known nasal carriers of S aureus be required to wear high-efficiency particulate air masks routinely or when they are sneezing frequently from respiratory allergens or have an upper respiratory infection? Should anesthesia providers with active eczema, atopic dermatitis, or furunculosis be restricted from administering (or even from directing or supervising) anesthesia to patients receiving implants or from placing central lines? Focusing on the data in this current article from Loftus et al., should we eliminate the routine use of stopcocks in our IV lines? Likewise, should we be developing better disinfecting protocols for our anesthesia equipment, including pagers, stethoscopes, and operating room–based computer keyboards? And should we ban all other equipment and accessories (such as personal bags and purses, portable radios, cell phones, lab coats, iPods, and speakers) from the operating rooms?

The cost of surgical site infections to patients and to all health care delivery systems is very high. We assume that the increased cost of implementing effective processes, however significant, will be more than offset by the reduced cost of treating surgical site infections, but this remains an unproven hypothesis. Lastly, we must avoid the trap of treating only surrogate end points, such as making expensive decisions to reduce bacterial contamination, without also documenting that these decisions lead to a reduction in surgical site infections and improve patient outcome.


We thank P. Samuel Pegram, Jr., MD, and Robert J. Sherertz, MD, Section on Infectious Disease, Department of Internal Medicine, Wake Forest University School of Medicine, for their thoughtful discussions during the preparation of this editorial.


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