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H. Hank Simms, MD; Ronald D'Amico

Arch Surg. 1997;132(2):171-177.

Abstract
Objective
To determine the mechanisms and prevalence of posttraumatic auto-oxidative receptor injury and immune suppression to subsequent nosocomial infections.

Design
Purified polymorphonuclear neutrophils from 30 critically ill trauma patients (mean [±SD] Injury Severity Scores, 21.5±7.3) were incubated with glucose and glucose-oxidase to generate superoxide anion. Subcellular fractionations were performed with iodine I 125 monoclonal antibodies against the Fc receptors CD32w and CD16 and complement receptors CD35 and CD11b/CD18. Plasma membrane expression of these receptors was then determined during the first week of hospitalization.

Setting
Surgical intensive care unit in a university-affiliated hospital.

Results
Twenty-three (77%) of 30 patients had persistent auto-oxidative reduction in Fc and complement receptors induced by glucose and glucose-oxidase. Nosocomial infections occurred in 20 (87%) of 23 patients with auto-oxidative injury vs 1 (14%) of 7 patients without auto-oxidative receptor injury (P<.01, unpaired t test). Patients without auto-oxidative injury had expression for each receptor no different from buffer control.

Conclusions
Critically ill trauma patients have auto-oxidative receptor injury, which is closely linked with the development of nosocomial infections. These results provide a biological basis for the early use of auto-oxidants in critically ill trauma patients.

Arch Surg. 1997;132:171-177

Author Affiliations
From the Department of Surgery, Rhode Island Hospital/Brown University School of Medicine, Providence.

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