Immune disorders after severe injury

Septic complications are still the major cause of death in patients with severe injuries, whether due to polytrauma, large burns, or difficult surgical operations. The very high incidence of such infectious episodes in spite of the continuous development of new broad spectrum antibiotics and appropriate intensive care managements, may suggest that any kind of severe injury leads to a state of acquired immunologic deficiencies. Thus an intensive relation has been demonstrated between the extend of body burned surfaces and the neutrophil chemotaxis whose dramatic decline could originate either from an intraleukocytic defect, or from inhibitory factors released by the damaged tissues. Furthermore, any important tissular destruction has been shown to stimulate the clonal proliferation of T suppressor lymphocytes which could be considered as a physiological protective mechanism against the development of an autoimmunization towards self-structures released by the wound in the blood stream. Factors able to activate T suppressor lymphocytes after injury are multiple and among them most important are: HLA-bearing cell wall components, histamine released by tissue mast cells, soluble factors produced at the level of the wound, bacterial endotoxins, arachidonic acid metabolites, etc. Finally, it has been mentioned that this state of immune deficiency after injury may still be exacerbated by iatrogenic measured like catheters, antibiotherapy, corticotherapy, and mainly by malnutrition.