Abstract
Trauma, shock, and sepsis are accompanied by profound immunosuppression. This immunosuppression is evidenced by abnormalities in cellular immunity, humoral immunity, macrophage function, and neutrophil function [1, 2]. The resultant immunodeficiency is not merely of academic interest, but rather expresses itself in the form of increased susceptibility of severely injured patients to infections caused not only by organisms usually considered pathogenic, but also by so-called nonpathogenic microbes. A major difficulty encountered in studying this immunosuppression in vivo is the multiplicity of factors causing it. It is often impossible to sort out the interrelating effects of trauma, sepsis, surgery, and anesthesia on the patient’s immune system. An additional confounding issue is often the emergent appearance of clinical problems in severely injured patients. The rapidity with which clinical events occur usually makes it impossible to establish a baseline with which subsequent measurements may be prospectively compared.
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