Cytokine, complement, and endotoxin profiles associated with the development of the adult respiratory distress syndrome after severe injury.
OBJECTIVE
The adult respiratory distress syndrome (ARDS) is a frequent complication after severe accidental trauma. This study examines the hypothesis that increased systemic concentrations of proinflammatory cytokines, endotoxin, or complement fragments may predict the development of ARDS.


METHODS
Prospective, observational study.


METHODS
Two Level I university trauma centers.


METHODS
Fifteen severely injured patients (Injury Severity Score of > or = 25).


METHODS
Standard emergency department, operating room, and intensive care unit management.


RESULTS
Plasma samples were obtained at 4-hr intervals from the time of injury and were assayed for concentrations of endotoxin, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, IL-8, and complement fragments C3a and C4a. Hemodynamic and oxygen metabolism variables also were measured at 4-hr intervals after injury. Seven patients developed ARDS and eight patients did not. The PaO2/FIO2 ratio was significantly decreased in the patients with ARDS compared with non-ARDS patients as early as 4 hrs postinjury, and remained significantly decreased throughout the initial 24 hrs after severe accidental injury. Plasma IL-8, IL-6, C3a, and C4a concentrations were markedly increased starting in the immediate postinjury period in both ARDS and non-ARDS patients, but no significant differences were found between the two groups until 16 hrs after injury when plasma IL-8, C3a, and C4a concentrations became significantly higher in the ARDS group. Neither the ARDS nor non-ARDS patients showed the presence of circulating IL-1 beta, TNF-alpha, or endotoxin at any postinjury time point.


CONCLUSIONS
These results demonstrate that measurements of plasma concentrations of proinflammatory cytokines, endotoxin, or complement fragments are not helpful in predicting the development of ARDS after severe accidental injury.
Donnelly
T J
TJ
Department of Medicine, UCLA Medical Center.
Meade
P
P
Jagels
M
M
Cryer
H G
HG
Law
M M
MM
Hugli
T E
TE
Shoemaker
W C
WC
Abraham
E
E
D000328:Adult; D001784:Blood Gas Analysis; D015926:Complement C3a / Q000032:analysis*; D015934:Complement C4a / Q000032:analysis*; D006259:Craniocerebral Trauma / Q000145:classification / Q000150:complications*; D004731:Endotoxins / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006439:Hemodynamics; D006801:Humans; D015601:Injury Severity Score; D007375:Interleukin-1 / Q000097:blood*; D053583:Interleukin-1beta; D015850:Interleukin-6 / Q000097:blood*; D016209:Interleukin-8 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption; D010446:Peptide Fragments / Q000097:blood*; D011237:Predictive Value of Tests; D011379:Prognosis; D011446:Prospective Studies; D011863:Radioimmunoassay; D012128:Respiratory Distress Syndrome / Q000097:blood* / Q000453:epidemiology* / Q000209:etiology / Q000503:physiopathology; D012307:Risk Factors; D015996:Survival Rate; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*
D004731:Endotoxins; D007375:Interleukin-1; D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D010446:Peptide Fragments; D014409:Tumor Necrosis Factor-alpha; C052994:interleukin-1beta (163-171); D015926:Complement C3a; D015934:Complement C4a