Depressed Mononuclear Leukocyte Chemotaxis in Thermally Injured Patients

Abstract

Microbial infection is the leading cause of morbidity and mortality in thermally injured patients. Since normal mononuclear leukocytes (MNL) function is essential in host defense, the chemotactic response of MNL from 25 thermally injured patients was evaluated in vitro. Patients with burns involving <20% total body surface had normal MNL chemotaxis, while MNL from patients with burns ≽20% had significantly depressed chemotaxis. This defect was most pronounced in patients with burns ≽40% and in those who died. Analysis of the data as a function of time revealed that patients who died generally had depressed chemotaxis immediately postburn and that their cells showed no functional improvement with time. In contrast, surviving patients with burns ≽40% initially had normal MNL chemotaxis which decreased significantly at approximately day 15 post burn, reached a nadir about day 45, and gradually returned to normal. Since the average burn size of these two groups was very similar, these data suggest that the early chemotactic response of MNL after a burn may be a predictive index of clinical outcome. Thirteen of the 25 patients developed infections and in all but one case depressed MNL chemotaxis preceded the septic event. Sera from patients with depressed MNL chemotaxis contained a cell-directed chemotactic inhibitor which was heat stable (56°C, 30 min), non-dialyzable and distinct from the sulfadiazine used for topical therapy. These studies document that depressed MNL chemotaxis occurs as a consequence of serious thermal trauma, that this defect may be due to a serum inhibitor and that abnormal MNL chemotaxis may contribute to septic morbidity and mortality in severely burned patients.