Temporal patterns of hemodynamics, oxygen transport, cytokine activity, and complement activity in the development of adult respiratory distress syndrome after severe injury

J Trauma. 1994 May;36(5):651-7. doi: 10.1097/00005373-199405000-00009.

Abstract

The aim of this study was to search for early inflammatory mediators in severely traumatized patients that could predict the occurrence of adult respiratory distress syndrome (ARDS). We measured sequential plasma levels of tumor necrosis factor (TNF), interleukin 1 (IL-1), interleukin 6 (IL-6), interleukin 8 (IL-8), complement fragment C3a, and endotoxin. In addition, we measured sequentially the values of hemodynamics, oxygen transport, and pulmonary function. The temporal patterns seen 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 progressive 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 initial peaks, and there were no further increases in hemodynamic values. In 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 found to be predictive of posttraumatic ARDS. However, these and other mediators may augment or intensify the development of ARDS.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Complement C3a / analysis
  • Cytokines / blood*
  • Hemodynamics
  • Humans
  • Interleukins / blood
  • Middle Aged
  • Oxygen Consumption
  • Prospective Studies
  • Respiratory Distress Syndrome / blood
  • Respiratory Distress Syndrome / etiology
  • Respiratory Distress Syndrome / physiopathology*
  • Time Factors
  • Wounds and Injuries / blood
  • Wounds and Injuries / complications
  • Wounds and Injuries / physiopathology*

Substances

  • Cytokines
  • Interleukins
  • Complement C3a