• H H Simms and R D'Amico.
• Department of Surgery, Rhode Island Hospital/Brown University School of Medicine, Providence, USA.
• Arch Surg Chicago. 1997 Feb 1;132(2):171-7.

ObjectiveTo determine the mechanisms and prevalence of posttraumatic auto-oxidative receptor injury and immune suppression to subsequent nosocomial infections.DesignPurified 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 1125 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.SettingSurgical intensive care unit in a university-affiliated hospital.ResultsTwenty-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.ConclusionsCritically 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.

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