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

Abstract

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.

Cytokine-induced venodilatation in humans in vivo: eNOS masquerading as iNOS

“…Indeed, plasma levels of neopterin have The study was performed in human beings in vivo. This been used as a marker of the severity of inflammation in has obvious advantages, including clinical relevance, and clinical practice [33][34][35]. It would be interesting to dein this study it was possible to detect cytokine-induced NO termine whether induction of GTP cyclohydrolase 1 in generation which has not been seen when cytokine-exother cells also increases NO generation from constitutive posed human veins were studied in vitro [5].…”

Enhanced Release of Elastase Is Not Concomitant With Increased Secretion of Granulocyte-Activating Cytokines in Whole Blood From Patients With Sepsis

“…20 " 24 Elevated plasma levels of elastase have been described in patients with sepsis and correlated with morbidity and mortality of these patients. 25 " 30 Although in vitro studies suggest an upregulation and activation of PMN by TNF-α, IL-lß, and IL-8, the interactions between altered release of these cytokines and elevated elastase secretion by PMN during sepsis remain to be determined. Therefore, it was the objective of this study to investigate whether PMN activation determined by the release of elastase is dependent on increased synthesis and secretion of inflammatory cytokines in whole blood from patients with sepsis.…”

Pathophysiology of Shock, Sepsis, and Organ Failure

“…Moreover, the studies showed without doubt that, in patients who have incurred severe infection followed major surgery or trauma, the underlying cellular and humoral biochemical events are quite similar regardless of the etiology of the insult. The clinical outcome seems to be only due to the magnitude of the inflammatory response, which is of course highest when trauma is superimposed by infection (Waydhas et al 1992).…”