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April 1992

Inflammatory Mediators, Infection, Sepsis, and Multiple Organ Failure After Severe Trauma

Author Affiliations

From the Departments of Surgery (Drs Waydhas, Nast-Kolb, Duswald, and Schweiberer, Mr Trupka, and Ms Lenk) and Clinical Chemistry and Clinical Biochemistry (Drs Jochum and Fritz), Klinikum Innenstadt, Ludwig Maximilians-University, Munich, Germany.

Arch Surg. 1992;127(4):460-467. doi:10.1001/archsurg.1992.01420040106019

• 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.

(Arch Surg. 1992;127:460-467)