Inflammatory mediators, infection, sepsis, and multiorgan failure after severe trauma

The relation of (multiple) organ failure (OF) to the release of
inflammatory mediators and the incidence of infection and sepsis
was studied prospectively in 100 patients with multiple trauma
(injury severity score=37). Sixteen patients died of OF, 47
patients survived OF, and 37 patients had no OF. Fifteen (24%) of
the patients with OF showed no signs of infection. In patients with
early onset of OF (n=45), infection followed with a lag of 2 or
more days. In 16 (44%) of these patients, infection led to a
deterioration in organ function. With late onset of OF (n=18),
infection preceded OF in nine patients. Polymorphonuclear
leukocyte—elastase, neopterin, C-reactive protein, lactate,
antithrombin III, and phospholipase A discriminated significantly
among the three outcome groups. Of all factors, only
polymorphonuclear leukocyte—elastase showed a difference between
patients with and without infection or sepsis, respectively. These
data indicate that infection might not play a crucial role in the
pathogenesis of posttraumatic OF in a substantial portion of
patients with trauma. Early OF, especially, seems to be mainly
influenced by the direct sequelae of tissue damage and shock (eg,
the release of inflammatory mediators). Since infection and sepsis
did not lead to an augmented release of mediators in patients with
trauma, the role of both entities remains unclear.