The anesthesia provider’s role in the prevention of surgical site infections

Published on 07/02/2015 by admin

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The anesthesia provider’s role in the prevention of surgical site infections

William J. Mauermann, MD

Surgical site infections (SSIs) continue to be a substantial source of patient morbidity and fatality after surgical procedures. They are the second most common cause of nosocomial infections, lead to increased length of stay in the hospital and increased mortality rate, and contribute significantly to health care costs. More recently, SSIs have become a marker of quality of care in the United States. Regulatory agencies have deemed that some SSIs are avoidable; in the United States, Medicare will no longer reimburse institutions for certain SSIs, including mediastinitis after cardiac surgery and SSIs following bariatric surgery and some orthopedic operations. This chapter will focus on the pathophysiology of SSIs as well as the anesthesia provider’s role in the prevention of these complications.

Pathophysiology of surgical site infections

Even with strict aseptic technique and a clean surgical wound, some degree of bacterial contamination undoubtedly occurs in every operation. It has been well documented that the first 4 to 6 h after contamination determine whether the body will clear the bacteria or an established infection will occur. Thus, preventing SSIs relies in large part on optimizing the immune system during the perioperative period.

The body’s first defense against bacterial contamination is the neutrophil. Neutrophils are critically dependent on adequate O2 stores to maintain their oxidative killing capacity. In one study, subcutaneous O2 tension was measured in operative patients considered at elevated risk for developing SSI. In patients with subcutaneous O2 tensions greater than 90 mm Hg, no SSIs developed, whereas patients with a subcutaneous O2 tension of 40 to 50 mm Hg had an infection rate of 43%. As will be detailed in the following discussion, anesthesiologists may play an important role in the maintenance of immune and, in particular, neutrophil function.

Hypothermia

Without active efforts to warm patients, mild perioperative hypothermia (core body temperature 34° C-36° C) is commonly observed. In a landmark study, 200 patients undergoing colorectal operations were randomly assigned to a mild hypothermia group (34.4° C ± 0.4° C) or a normothermia group (37° C ± 0.3° C). This trial was stopped early because of the high rates of SSIs in the hypothermia group; the incidence of SSIs in the hypothermia group was 18.8%, versus 5.8% in the normothermia group. Patients who developed SSIs stayed nearly 1 week longer in the hospital. In addition, patients who were maintained at normothermia had evidence of increased wound healing and tolerated oral intake sooner. In a subgroup analysis, 74% of the hypothermic patients had evidence of intraoperative vasoconstriction, versus 6% of the normothermic patients.

The effect of hypothermia on SSIs is multifactorial. In the aforementioned study, the high incidence of vasoconstriction in the hypothermic group likely means a decrease in blood flow and O2 delivery to the surgical site and, thus, impairment in the oxidative killing capacity of neutrophils. In addition, animal models have shown that hypothermia induces an anti inflammatory T-cell cytokine profile similar to that seen in patients with thermal injuries. Lastly, irrespective of the effect on blood flow and O2 delivery to the surgical wound, hypothermia decreases the neutrophils’ production of superoxide radicals for any given O2 tension. Indeed, bacterial killing by neutrophils is reduced in the face of hypothermia. With all that is known regarding the complications from mild perioperative hypothermia, including an increased risk of SSIs, it should be every clinician’s goal to maintain patients’ normothermia unless contraindicated.

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