TEMPORAL PATTERNS OF HEMODYNAMICS, OXYGEN-TRANSPORT, CYTOKINE ACTIVITY, AND COMPLEMENT ACTIVITY IN THE DEVELOPMENT OF ADULT-RESPIRATORY-DISTRESS-SYNDROME AFTER SEVERE INJURY

Citation
P. Meade et al., TEMPORAL PATTERNS OF HEMODYNAMICS, OXYGEN-TRANSPORT, CYTOKINE ACTIVITY, AND COMPLEMENT ACTIVITY IN THE DEVELOPMENT OF ADULT-RESPIRATORY-DISTRESS-SYNDROME AFTER SEVERE INJURY, The journal of trauma, injury, infection, and critical care, 36(5), 1994, pp. 651-657
Citations number
36
Categorie Soggetti
Emergency Medicine & Critical Care
Volume
36
Issue
5
Year of publication
1994
Pages
651 - 657
Database
ISI
SICI code
Abstract
The aim of this study was to search for early inflammatory mediators i n severely traumatized patients that could predict the occurrence of a dult respiratory distress syndrome (ARDS). We measured sequential plas ma levels of tumor necrosis factor (TNF), interleukin 1 (IL-1), interl eukin 6 (IL-6), interleukin 8 (IL-8), complement fragment C3a, and end otoxin. In addition, we measured sequentially the values of hemodynami cs, oxygen transport, and pulmonary function. The temporal patterns se en in the patients who developed ARDS were compared with those who did not. In the patients who developed ARDS, the first observed findings were low cardiac index (CI) and oxygen delivery (DO2) followed by prog ressive increases in IL-6, IL-8 and C3a levels, worsening of pulmonary function, and increases in hemodynamic values. The maximum values of IL-6, IL-8, and C3a occurred after the onset of ARDS. In the patients who did not develop ARDS, initial oxygen transport values were not low , the levels of IL-6, IL-8, and C3a decreased rapidly from their initi al peaks, and there were no further increases in hemodynamic values. I n both ARDS and nonARDS patients, no measurable quantities of TNF, IL- 1, or endotoxin were found. We concluded that none of the mediators we measured reached their peaks before the onset of ARDS and none were f ound to be predictive of posttraumatic ARDS. However, these and other mediators may augment or intensify the development of ARDS.