Abstract

OBJECTIVE:

To examine cellular and immunologic mechanisms by which intraoperative hypothermia affects surgical patients.

SUMMARY BACKGROUND DATA:

Avoidance of perioperative hypothermia has recently become a focus of attention as an important quality performance measure, aimed at optimizing the care of surgical patients. Anesthetized surgical patients are particularly at risk for hypothermia, which has been directly linked to the development of sequelae, such as coagulopathy, infection, morbid myocardial events, and death after surgery. However, many of the underlying immunologic mechanisms remain unclear.

METHODS:

Venous blood samples from healthy volunteers were exposed for up to 4 hours to various temperatures following the addition of a 1 ng/mL lipopolysaccharide challenge. Innate immune function, assessed by the ability of monocytes to present antigen and coordinate cytokine release, was determined by qualitative and quantitative measurements of HLA-DR surface expression 2 hours following incubation, and proinflammatory tumor necrosis factor-alpha (TNF-alpha) and anti-inflammatory (IL-10) cytokine release in the first 4 hours.

RESULTS:

Monocyte incubation at hypothermic temperatures (34 degrees C) reduced HLA-DR surface expression, delayed TNF-alpha clearance, and increased IL-10 release. Conversely, hyperthermia (40 degrees C) increased monocyte antigen presentation and resulted in rapid decay of TNF-alpha. However, IL-10 release was also increased. Normothermia (37 degrees C) attenuated IL-10 release following the initial proinflammatory surge.

CONCLUSION:

Hypothermia exerts multiple effects at the cellular level, which impair innate immune function, and are associated with increased septic complications and mortality. These findings provide a physiological basis for perioperative temperature monitoring, which is a valid surgical performance measure that can be used to reduce surgical complications associated with avoidable hypothermia.