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The initial transfusion therapy after trauma has been identified as an independent risk factor for the incidence of multiple organ failure (MOF). Late occurrence of MOF in severely injured patients may be a clinical consequence of disturbed mediator homeostasis. For this reason, levels of interleukin (IL)-6, IL-10, and soluble tumor necrosis factor receptors (sTNFR) p55 and p75 were analyzed in the plasma of patients with comparable injury severity but with a different supply of packed red blood cells (PRBC). Thirty-eight multiple trauma patients with an injury severity score range of 25-54 points were separated into two groups according to their PRBC supply within the first 24 h after trauma. Patients who received at least 15 units of PRBC were analyzed in group 2 (n = 11); the remaining patients (n = 27) were assigned to group 1. The incidence of MOF was higher (P < 0.05) in group 2 patients. Correspondingly, levels of all assayed mediators were found significantly elevated at several time points in this patient group. We conclude that increases in mediator concentrations may be causally related to the extent of blood transfusion therapy itself or to the conditions for which it was needed.

Clinical and experimental evidence suggests that traumatic brain injury (TBI) leads to a systemic immune response. To examine whether TBI causes a release of procalcitonin (PCT) or neopterin (NT) into the circulation, we compared plasmatic mediator levels among multiple injured patients with or without TBI. In total, 98 trauma patients (24 with TBI only, 39 with extracranial injuries excluding TBI, and 35 with combined injuries) and 35 healthy volunteers were studied. Blood was sampled at 15 predefined time points within 132 h after injury and analysed for NT and PCT. Multivariate statistical comparisons were adjusted for different severity of head, thorax, abdomen and extremity injuries, as quantified by the Abbreviated Injury Scale (AIS). PCT was normal 3 h after trauma, but 24 h after extracranial injuries a massive release (median 3 ng/mL) was observed. Significant positive associations between injury severity and posttraumatic PCT levels were found for abdominal and extremity, but not for cranial or thoracic injuries. Only modest changes of marginal statistical significance were detected for NT. The maximum increase per AIS point was 9% (95% confidence intervals [CI]: 3-16%). The effect of TBI on NT release was significant only at 108 h posttrauma with a 5% (95% CI: 1-10%) increase per AIS point. TBI induces a release of PCT and NT into the plasma, but this effect seems to be smaller for intra- than for extracranial injuries, probably due to more extensive surgery for abdominal and extremity injuries.

Pneumonia is the most common infectious complication in multiple trauma patients. In a prospective clinical cohort study, 266 multiply injured patients were examined for the development of pneumonia. Various risk factors were tested in uni- and multivariate analyses. Three different definitions of pneumonia were used in order to examine how results depended on definition. The incidence of pneumonia was 41%, but varied with definition (30-50%). Injuries to the thorax, head,and abdomen were associated with a significantly increased risk of pneumonia (adjusted relative risk: 1.77, 1.97,and 1.52, respectively).Furthermore, increasing age led to a higher risk of pneumonia. Although the primary analysis revealed a higher pneumonia risk in male patients (adjusted relative risk: 2.23; 95% CI: 1.43-3.05), this result could not be consistently reproduced when using other definitions of pneumonia. Trunk and head injuries and age are proven risk factors for developing posttraumatic pneumonia. The association between male gender and an increased rate of infectious complications remained questionable.

Objective and Design: In a prospective trial 266 multiple injured patients were included to evaluate clinical risk factors and immune parameters related to pneumonia., Methods: Clinical and humoral parameters were assessed and multivariate analysis performed., Results: The multivariate analysis (odds ratio with 95% confidence interval (CI)) revealed male gender (3.65), traumatic brain injury (TBI) (2.52), thorax trauma (AIS(thorax) > or = 3) (2.05), antibiotic prophylaxis (1.30), injury severity score (ISS) (1.03 per ISS point) and the age (1.02 per year) as risk factors for pneumonia. The main pathogens were Acinetobacter Baumannii (40%) and Staphylococcus aureus (25%). A tendency towards higher Procalcitonin (PCT) and Interleukin (IL)-6 levels two days after trauma was observed for pneumonia patients., Conclusion: The immune parameters (PCT, IL-6, IL-10, soluble tumor necrosis factor p-55 and p-75) could not confirm the diagnosis of pneumonia earlier than the clinical parameters.

Background: Our knowledge about the bidirectional interactions between brain and whole organism after trauma is still limited. It was the purpose of this prospective clinical study to determine the influence of severe head trauma (SHT) as well as trauma in different anatomic injury regions on posttraumatic inflammatory mediator levels from patients with multiple injuries., Methods: Thirty-five healthy controls, 33 patients with an isolated SHT, 47 patients with multiple injuries without SHT, and 45 patients with both SHT and multiple injuries were studied. The posttraumatic plasma levels of soluble tumor necrosis factor receptors p55 and p75, interleukin (IL)-6, IL-10, and polymorphonuclear neutrophil (PMN) elastase were monitored using enzyme-linked immunosorbent assay technique. The influence of head injuries as well as thorax, abdomen, and extremity injuries on the mediator release from patients with multiple injuries was investigated by multivariate linear regression models., Results: The soluble tumor necrosis factor receptor p55/p75 ratio was significantly elevated within 3 hours of trauma in all three injury groups and returned to reference ratios after 12 hours. The lowest increase was found in patients suffering from an isolated SHT. Lowest mediator levels in this patient population were also found for IL-6, IL-10, and PMN elastase during the first 36 hours after trauma. Additional injuries to the head, thorax, abdomen, and extremity modulated mediator levels to a different degree. No specific effect was found for SHT when compared with other injury groups. Thorax injuries caused the quickest rise in mediator levels, whereas abdominal injuries significantly increased PMN elastase levels 12 to 24 hours after trauma., Conclusion: Traumatic injuries cause the liberation of various mediators, without any specific association between anatomic injury pattern and the pattern of mediator release.

Two cases of severe spinal cord injuries to professional horse-racing jockeys are presented. There is only one comprehensive study conducted to ascertain the nature and incidence of injuries in the literature. The pathomechanism and surgical therapy of vertebral trauma in jockeys was analysed.