Antisepsis in the Time of Antibiotics

Abstract

If John Snow, a founding father of both anesthesiology and epidemiology, were alive today, undoubtedly he would attack the problem of health care–associated infections (HCAIs) as doggedly as he approached the 1854 cholera epidemic in London.1 Although Snow did not know that Vibrio cholerae was the causative organism, he clearly demonstrated that cholera was communicated by drinking contaminated water from the Broad Street pump. Conversely, in the case of HCAIs associated with surgery, the causative organisms are readily determined, yet the source and mechanism of transmission are frequently unclear. Following in the footsteps of Snow are Koff, Loftus, and their Dartmouth colleagues. They are exploring whether anesthesia providers are the source, or vectors for the transmission, of bacteria that cause surgical site infections (SSIs). In earlier publications, they documented transmission of pathogenic bacteria to the anesthesia operating room work area and established an association between contamination of this area and contamination of IV stopcocks, between contaminated stopcocks and nosocomial infections, and between contamination, nosocomial infection, and hand hygiene by anesthesia providers.2,3 If Joseph Lister, founding father of antiseptic surgery, were alive today, he would be pleased with the low SSI rate today compared with 1867.4 Undoubtedly he would have applied his antiseptic protocols, including carbolic acid, not only to the surgical field and instruments but also to the anesthesia work area and equipment if they had existed in his day. However, in his era, there were no laryngoscopes, bronchoscopes, or endotracheal tubes to pass through bacteria-rich oral and nasal cavities, no spinal or epidural needles or central venous catheters to disrupt the integument, and no anesthesia machines to contaminate. Following in the footsteps of Lister, the Dartmouth group demonstrated that improved hand hygiene by anesthesia providers reduced HCAIs at their institution in their study patients.3 In this issue of Anesthesia & Analgesia, this group goes on to document anesthesia work area and IV stopcock contamination by anesthesia providers in and between operating rooms and between the first and second case in the same operating room, despite application of hand hygiene and anesthesia work area antisepsis protocols typical in modern operating rooms.5 Most anesthesiologists and their quality of care arbiters currently believe that the major contribution of the anesthesia team to the reduction of HCAIs relates to antimicrobial prophylaxis. Unfortunately, approximately 5% of surgical patients continue to experience SSIs despite timely administration of the appropriate antibiotic. In one recent study, intensifying the already rigorous intraoperative antisepsis protocol for surgeons did not reduce SSIs.6 In another, surgical glove perforation did not increase SSIs in patients who received antibiotics.7 If we have reached a plateau in our attempts to lower the SSI rate because we have gone as far as we reasonably can with surgical antisepsis and antimicrobial prophylaxis, then the remaining targets are the patient and the anesthesia provider. Does the work of Koff, Loftus, and others suggest that anesthesia providers have become the typhoid Marys and Johns of the 21st century?8,9 We think these monikers are premature until 4 issues are addressed and resolved: contamination as a surrogate marker versus cause of infection, reproducibility of data, completeness of the data, and consequences of proposed changes in protocols. Contamination of surgical gloves, instruments, and anesthesia equipment has been demonstrated many times as a function of time from the last cleansing or opening to air and exposure to activity by health care personnel or patients.10–12 However, contamination is not equivalent to infection. It is reasonable to assume that the level of contamination is a reliable marker for the effectiveness of cleaning protocols and that above a certain level contamination may spread to sites where bacteria can be introduced or reintroduced to the patient, such as stopcocks.2 If the bacteria causing the SSI comes from colonizing sites within the patient's own microbiome, as is currently believed to be occurring most frequently,13 and the source of the bacteria contaminating the anesthesia site is also the patient, then the level of contamination is a reasonable surrogate marker for HCAI. In this situation, however, it is difficult to understand how more frequent handwashing and more effective decontamination will reduce the incidence of SSI, unless the primary route of bacterial migration is from the patient to the surgical site via the anesthesia field, stopcock in the IV line, and the blood. Similarly, decontamination of the anesthesia work area seems unlikely to reduce the incidence of postoperative pneumonia if the causative bacteria are transmitted from the patient's own oropharynx or nasopharynx by the endotracheal tube.14 Better patient preparation may be where efforts are best focused. Identifying patients who are nasal carriers of Staphylococcus aureus, treating their infection with antibiotic ointment and antiseptic wash preoperatively, and providing antiseptic mouthwash to intubated patients have proven to be effective measures to reduce HCAI.15,16 If the origin of the bacterial contamination of anesthesia equipment and IV stopcocks is the anesthesia provider, and the bacteria causing the SSI is identical to that carried by the anesthesia provider, then the level of contamination may identify him or her as the cause of SSI. Koff and Loftus et al. have documented this potential but not the actual occurrence. However, an editorial in this issue of the journal provides 2 examples whereby a specific anesthesiologist and a surgeon were clearly identified either as the cause of or the vector for several SSIs.17 The studies by Loftus et al. need to be reproduced at other institutions to confirm their observations of a reduction of HCAIs from 17.2% to 3.8%.3 If similar results are obtained, then the contribution of bacteria from the microbiome of anesthesia providers has been significantly underestimated as a cause of HCAI. A logical next step would then be to collect contamination and SSI data for each anesthesia provider. If an association is established, most likely he or she is shedding bacteria above the norm because of a treatable condition, such as eczema, an upper respiratory infection superimposed on nasal colonization of S aureus, or carbunculosis.17 Two major defense mechanisms for skeptics are challenging the data or declaring the cure as worse than the disease. But even supporters of improved hand hygiene call for better data in 2 areas. One is that many HCAIs manifest after the patient has left the hospital or outpatient surgery center and are frequently not included in outcomes data.18,19 Thus, the current data underestimate the problem. Finally, we must remember we are trying to eliminate SSIs. Measures that reduce contamination must also reduce the SSI rate. Instituting policies and procedures without subjecting them to evidence-based scrutiny may increase the cost and decrease the convenience of providing care, or even worse, increase the infection rate.20 Two examples support the need for testing protocol changes for effectiveness. First, when a needleless IV access device replaced a conventional needle access device, HCAIs increased.21 Second, protocol-driven handwashing and glove wearing did not reduce bacterial colonization and contamination in nurses with dermatitis.22 This is not an argument against washing hands or wearing gloves, but evidence that we need to develop multiple strategies to reduce contamination and infection. We have not yet found the solution to the problem of HCAI in general or SSI in particular. It needs more attention from the anesthesia community than it has historically provided despite the interest of our founding fathers. At the very minimum we should do 3 things: (1) determine the effectiveness of our local anesthesia work area decontamination protocols, (2) continue to administer the proper antibiotic in a timely manner, and (3) continue to wash our hands between cases. However, we also plead that the study by Koff et al.3 demonstrating decreased SSIs with increased handwashing by anesthesia providers be repeated at several other institutions.