TCT is highly sensitive in detecting thoracic injuries after blunt chest trauma and is superior to routine CXR in visualzing lung contusions, pneumothorax, and hemothorax. Early TCT influences therapeutic management in a significant number of patients. We therefore recommend TCT in the initial diagnostic work-up of patients with multiple injuries and with suspected chest trauma because early and exact diagnosis of all thoracic injuries along with sufficient therapeutic consequences may reduce complications and improve outcome of severely injured patients with blunt chest trauma.

Intermittent prone positioning was not able to reduce the duration of mechanical ventilation in this limited number of patients. However the oxygenation improved significantly over the first four days of treatment, and the prevalence of ARDS and pneumonia were reduced.

ObjectiveTo investigate the relation of the biallelic Nco1 restriction fragment length polymorphism in the first intron of the tumor necrosis factor (TNF) ␤ gene with the development of severe sepsis in multiply injured patients. Summary Background DataThe biallelic Nco1 polymorphism of the TNF␤ gene has been described to be associated with autoimmune diseases and with the mortality rate in severe sepsis. Therefore, the Nco1 polymorphism may be associated with the clinical finding that despite comparable risk factors, posttraumatic sepsis develops in some patients but not others. MethodsThe study group consisted of 110 patients with severe blunt trauma (Injury Severity Score Ն 17). Typing of each patient for the biallelic Nco1 polymorphism was performed by analyzing restriction fragments of an Nco1-digested DNA fragment obtained using polymerase chain reaction. Genotypes were then related to the occurrence of severe posttraumatic sepsis and TNF␣ serum concentrations. ResultsFifty-seven patients showed an uncomplicated posttraumatic recovery, and severe sepsis developed in 53 patients. The overall allele frequency (TNFB1 0.29, TNFB2 0.71) and genotype distribution (TNFB1 homozygous 7.3%, TNFB1/TNFB2 42.7%, TNFB2 homozygous 50%) were in agreement with the distribution in healthy volunteers. Genotype distribution in patients with an uncomplicated clinical course was significantly different from that in patients with severe posttraumatic sepsis. Development of severe posttraumatic sepsis was significantly increased in patients homozygous for the allele TNFB2. In patients with severe posttraumatic sepsis, TNF␣ serum concentrations were significantly higher in TNFB2-homozygous individuals compared with heterozygous and TNFB1-homozygous individuals. The age-and injury-matched odds ratio for the homozygous TNFB2 genotype compared with the heterozygous genotype was 5.22 (p ϭ 0.007, 95% confidence interval 1.6 to 17.9).

These data show that the degree of the initial inflammatory response corresponds with the development of posttraumatic organ failure. Besides anatomically and physiologically based trauma scores, these parameters might be used as indicators for the injury severity.

Although MOF incidence remains unchanged, there is a significant fall in MOF-related mortality in patients with severe trauma, and death from single organ failure is virtually absent. Severe brain injury is now the leading cause of death in patients with severe multiple injuries admitted to the ICU.

Age is a well-known risk factor in trauma patients. The aim of the present study was to define the age-dependent cut-off for increasing mortality in multiple injured patients. Pre-existing medical conditions in older age and impaired age-dependent physiologic reserve contributing to a worse outcome in multiple injured elderly patients are discussed as reasons for increased mortality. A retrospective clinical study of a statewide trauma data set from 1993 through 2000 included 5375 patients with an Injury Severity Score (ISS) > or = 16 who were stratified by age. The ISS and Abbreviated Injury Score (AIS) quantified the injury severity. Outcome measures were mortality, shock, multiple organ failure, and severe head injury. Mortality in this series increased beginning at age 56 years, and that increase was independent of the ISS. The mortality rate increased from 7.3% (patients 46-55 years of age) to 13.0% (patients ages 56-65 years) in patients with ISS 16-24; from 23.8% to 32.1% in those with ISS 25-50; and from 62.2% to 82.1% in those with ISS 51-75 (P < or = 0.05). Severe traumatic brain injury (sTBI) was the most frequent cause of death, with a significant peak in patients older than 75 years. The incidence of lethal multiple organ failure increased significantly beginning at age 56 years (P < or = 0.05), but it showed no further increase in patients aged 76 years or older. In contrast, the incidence of lethal shock showed a significant increase from age 76 years (P < or = 0.05), but not at age 56 years. However, from age 56 years, mortality increased significantly in patients who sustained multiple trauma-an increase that was independent of trauma severity.

The German Trauma Registry records processes and treatment results in severely injured patients. This information is fed back to participating hospitals. The continuous data feedback is associated with a continuous improvement of process and outcome quality in the treatment of severely injured patients.

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.