BASE DEFICIT AFTER MAJOR TRAUMA DIRECTLY RELATES TO NEUTROPHIL CD11-BEXPRESSION - A PROPOSED MECHANISM OF SHOCK-INDUCED ORGAN INJURY

Citation
Aj. Botha et al., BASE DEFICIT AFTER MAJOR TRAUMA DIRECTLY RELATES TO NEUTROPHIL CD11-BEXPRESSION - A PROPOSED MECHANISM OF SHOCK-INDUCED ORGAN INJURY, Intensive care medicine, 23(5), 1997, pp. 504-509
Citations number
27
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
03424642
Volume
23
Issue
5
Year of publication
1997
Pages
504 - 509
Database
ISI
SICI code
0342-4642(1997)23:5<504:BDAMTD>2.0.ZU;2-Z
Abstract
Objective: To determine whether expression of neutrophil integrin rece ptors is related to the degree of post-traumatic shock. Design: Data w ere collected prospectively on patients with major trauma admitted to the surgical intensive care unit. Setting: Denver General Hospital, Co lorado. Patients and participants: 17 severely injured adults. Measure ments and results: The mean fluorescence intensity and per cent positi ve of neutrophil integrin receptors CD11 b, CD18 and CD11 a, and systo lic blood pressure, blood transfusion, lactate and base deficit as ind ices of shock. CD11 b expression on circulating neutrophils was increa sed 6 and 12 h after trauma. After correcting for the other shock indi ces, base deficit predicted CD11 b expression at 12 h. CD11 b expressi on was negatively correlated with the circulating neutrophil count. Co nclusions: The degree of metabolic acidosis after trauma correlates di rectly with CD11 b receptor expression on circulating neutrophils. Thi s relation may be the mechanism whereby pest-traumatic shock results i n neutrophil sequestration and neutrophil-mediated organ injury and fa ilure.