Neuraxial anesthesia and surgical site infection.

Surgical site infections remain among the most common serious perioperative complications. The overall incidence is 1–3%, but the risk is 10% or more for colon resections. Deep-tissue and organ-space infections, and those involving implanted hardware, are especially serious. For example, the overall infection rate in a representative sample of patients undergoing hip and knee replacements in Taiwan is reported to be 1.8% in this issue of ANESTHESIOLOGY. Neither operating rooms nor patients are perfectly sterile. Thus, all surgical wounds become contaminated. Although the type and degree of contamination clearly matter, progression from contamination to clinical infection is largely determined by the adequacy of host defense. Oxidative killing by neutrophils is by far the most important defense. Oxidative killing is a function of local tissue oxygenation, which in turn is determined by arterial oxygen partial pressure, perfusion, and local rate of oxygen extraction. Tissue oxygenation is generally thought to be the best single predictor of infection risk. One strategy for preventing surgical site infections is to reduce contamination by timely administration of appropriate short-course or single-dose antibiotics, which should be repeated during prolonged procedures. Other well-established approaches include clipping rather than shaving the skin, topical decontamination in nasal carriers of Staphylococcus, and use of chlorhexidine–alcohol surgical scrub solutions. The other general approach for reducing infection risk is to use anesthetic strategies that maintain or even enhance host defense. For example, allowing surgical patients to become hypothermic both reduces tissue oxygenation and either impairs or enhances various immune functions. As might thus be expected, maintaining normothermia reduces infection risk by a factor of three. Erythrocyte transfusions—and especially transfusion of cells after prolonged storage—provoke a nonspecific inflammatory response, which may divert the immune system from a more appropriate focus on the very real threat posed by bacterial contamination. Minimizing erythrocyte transfusions, and transfusing cells stored less than 2 weeks, therefore reduces infection risk. Supplemental oxygen has the potential to enhance host defense against bacteria by augmenting tissue oxygenation to supernormal partial pressures. Increasing the fraction of inspired oxygen (i.e., 80% vs. 30%) doubles tissue oxygenation from !60 to !110 mmHg without causing atelectasis. Studies in 500 and 300 patients, respectively, reported that supplemental oxygen halves infection risk; however, a subsequent study in 1,400 patients found no benefit. The effect of supplemental oxygen on surgical site infection, thus, remains unclear. Chang et al. proposed another preventive approach: use of neuraxial rather than general anesthesia. At least three potential mechanisms make the strategy plausible. The first is that neuraxial anesthesia moderates the inflammatory response to surgery; as mentioned earlier, reducing nonspecific generalized responses may allow the immune system to focus better on the critical task of fighting bacteria. The clinical importance of this mechanism remains essentially unknown. A second mechanism by which neuraxial anesthesia might reduce infection is via vasodilation and consequent improvement in tissue oxygenation. Several studies document small (i.e., 10 mmHg) increases in tissue oxygen when epidural anesthesia was compared with the combination of epidural and general anesthesia, although another that compared epidural anesthesia with general anesthesia reported no effect on tissue oxygenation. Thus, available evidence suggests that neuraxial anesthesia at best only slightly increases tissue oxygenation. However, it remains possible that differences would be greater if tissue oxygenation during general anesthesia was compared with neuraxial anesthesia alone—rather than with combined neuraxial–general anesthesia as in the previous studies. The third mechanism by which neuraxial anesthesia, especially epidural anesthesia, could reduce infection risk is by providing excellent postoperative analgesia. Severe pain provokes an autonomic response, which, in turn, causes vasoconstriction and reduced peripheral perfusion. Unsurprisingly, severe surgical pain, therefore, reduces tissue oxygenation by !15 mmHg. Although none of these potential mechanisms is entirely convincing, some combination of the three may substantially reduce infection risk. Certainly, the factor-of-two reduction Chang et al. report is of considerable clinical importance. To put it in perspective, this reduction is similar to that produced by timely antibiotic administration.