[Prostanoid release and lipid peroxidation in patients with thoracic trauma]. / Prostanoidfreisetzung und Lipidperoxidation bei Patienten mit Thoraxverletzungen.

UNLABELLED: There is compelling data from recent clinical studies on the impact of damage to the lung on the fate of traumatized patients. The lung reacts with a tremendous release of inflammatory mediators, but, on the other hand, this organ's ability in inactivating those factors is simultaneously attenuated. What is more, it is well known, that there often are no clinical signs of pulmonary dysfunction despite severe lung injury in the early posttraumatic phase. Therefore, in this prospective clinical study the following questions were addressed: (i) Is there any difference of the patients' lung response whether or not the (poly)trauma is associated with damage to the chest, (ii) either in the early or the late posttraumatic phase, and (iii) is there any marker that may prove to be a (significant) predictor of poor overall outcome? METHODS: Upon approval of the local IRB/EC, 35 patients (pts) were enrolled who suffered from multiple injuries. The first blood samples were drawn at admission, then every two hours and in daily intervals. The plasma concentrations of following mediators were analyzed: prostanoids (PGI2, TxA2, PGE2, PGF2 alpha) and products of O2-radicals (malondialdehyde, conjugated dienes). All values were calculated on the basis of the actual plasma protein content to eliminate fluid-induced dilution effects. Subsets of pts were performed according to the different injury pattern: (i) pre-dominantly thoracic trauma (TX, n = 9); (ii) polytrauma with (PTX, n = 19), and (iii) without (PT, n = 7) damage to the lung. RESULTS: As early as at admission, all pts revealed a severity-independent increase (p < 0.01) in most mediators' plasma levels. The pattern-related inflammatory response was most pronounced in casualties who had experienced thoracic trauma irrespective of whether it was combined with polytrauma. Within 1 to 3 days, the plasma levels of most mediators but PGE2 and MDA (all pts) as well as PGF2 alpha (PTX-group) normalized. The reactions of the lipid peroxidation products admitted of no group-differences. CONCLUSIONS: Although there was a pattern-related release of (most) prostanoids which was rather pronounced in polytrauma associated with damage to the lung, we failed in proving any predictive marker to specifically estimate outcome, so far.

Chest trauma and its impact on the release of vasoactive mediators.

Every year, major chest injury is involved in 56% of deaths in trauma victims. Blunt chest trauma apparently plays a crucial role in trauma-induced death of multiply injured patients. Therefore, the aim of this study was to evaluate the impact of different types of injuries, including lung tissue damage, on the release of various prostanoids. In a prospective study, the release of arachidonic acid (AA) metabolites was estimated in patients suffering blunt chest trauma alone, i.e., single thoracic injury, and in multiple injured patients including blunt chest trauma. The results were compared with those of patients suffering from single long bone fractures of the leg without additional injury. The plasma concentrations of the AA metabolites, prostacyclin, thromboxane, prostaglandin F2 alpha, and prostaglandin M were determined immediately after admission and in hourly and daily intervals thereafter. Despite clearly different injury scores, elevated levels of circulating AA metabolites were found in the plasma in all patients. This study reveals that any trauma increases significantly the release of prostanoids into the peripheral blood without regard to the impact of tissue damage. This phenomenon is, however, most pronounced following lung injury. On the basis of these results we suggest that there is a specific impact of those mediators in blunt chest trauma. The prostanoids apparently are suitable to describe and even to monitor the extent of thoracic trauma, thus giving additional information in some respect to the individual outcome.